Atlas of Sciatica - Etiologies, Diagnosis, and Management (Feb 12, 2024)_(3031449835)_(Springer) 9783031449833, 9783031449840

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Ali Akhaddar

Atlas of Sciatica Etiologies, Diagnosis, and Management

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Atlas of Sciatica

Ali Akhaddar

Atlas of Sciatica Etiologies, Diagnosis, and Management

Ali Akhaddar Department of Neurosurgery Avicenne Military Hospital of Marrakech Mohammed V University in Rabat Marrakech, Morocco

ISBN 978-3-031-44983-3    ISBN 978-3-031-44984-0 (eBook) https://doi.org/10.1007/978-3-031-44984-0 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Paper in this product is recyclable.

To His Majesty Mohammed VI, King of Morocco “To serve the country and contribute to the advancement of universal science.” To my Parent, my Wife, and my Children, with love To my Teachers, with gratitude To my Patients, who are my inspiration

Foreword 1

This book, Atlas of Sciatica, is authored and edited by Ali Akhaddar, MD, IFAANS [a Full Professor of Neurosurgery at the Medical School, Mohammed V University in Rabat (Morocco) and Head of the Department of Neurosurgery at Avicenne Military Hospital of Marrakech (Morocco)]. Let me begin with a bit about Dr. Akhaddar. He is an accomplished clinical and academic neurosurgeon. His body of work is second to only a very few. He wrote this book, utilizing his broad and deep experience foundation, combined with a herculean effort that focused on the production of the penultimate treatise on sciatica. The book has one author, Ali Akhaddar. He, alone, amassed and assembled this treatise. It is a one of a kind work that stands heads and shoulders above any other work on this subject. It is composed of 111 chapters that cover every conceivable aspect of sciatica. Not only it is an exhaustive treatise, but it is also extraordinarily compressive. Nothing, I mean nothing, has been left uncovered. This book represents a great “read” for the clinician who is a student of the subject. Perhaps more importantly, it provides a wonderful source of information as a stand-alone reference book. One only needs to peruse the table of contents to appreciate its value as a reference source. This book will stand as the ultimate treatise on sciatica for years and decades to come. In a sense, the book is timeless. I enthusiastically applaud Ali Akhaddar for this contribution to the readers of this work. For all of us who care for or study spinal pathology, we thank Dr. Akhaddar for his contribution. We are indebted to him for helping each of us to become better at what we do and for enhancing the care and well-being of our patients. Department of Neurosurgery, Neurological Institute Cleveland Clinic, Cleveland, OH, USA

Edward C. Benzel

Founder of the World Spinal Column Society (The ex-World Spine Society) Cleveland, USA Editor-in-Chief of World Neurosurgery Cleveland, USA vii

Foreword 2

Sciatic pain, as a description, reflects the leg pain distributing in the sciatic nerve area or its roots in the lower lumbosacral plexus, a widespread symptom. It is generally associated with back pain. Creating a detailed text and atlas on sciatic pain is an excellent task, for it needs to gather information and interpret many challenging points. Diagnostic problems of sciatic pain are many. It is not just because the anatomic sources of the pain are variable but also because it commonly gains chronicity and starts to show different characteristics. The success rates of various treatment models could be more gratifying. Even lumbar disc herniation, one of the most frequent reasons for sciatic pain, can have diagnostic and treatment failures. Dr. Ali Akhaddar’s book is a masterpiece, including prevalent and uncommon sources of sciatic pain, their treatment options, and discussion for the improvement of outcomes. A total of 111 chapters have been gathered in parts that are named as “General Considerations,” “Lumbosacral Discogenic Sciatica,” “Spinal Non-discogenic Sciatica,” “Extraspinal Intrapelvic Sciatica,” and “Extraspinal Extrapelvic Sciatica.” Many surgical and nonsurgical disciplines, like spine surgeons, neurological surgeons, orthopedic surgeons, neurologists, physical therapists, pain physicians, rheumatologists, and

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Foreword 2

neuroscientists, will benefit from the vast information in this textbook. I congratulate Dr. Ali Akhaddar for creating a comprehensive review of sciatic pain. Sanko University Neurosurgery Department Gaziantep, Turkey Ege University Neurosurgery Department Izmir, Turkey Past President, Turkish Neurosurgical Society Izmir, Turkey Past President, World Spinal Column Society Izmir, Turkey Honorary President, Middle East Spine Society Izmir, Turkey Past Chairman, WFNS Spine Committee Izmir, Turkey

Mehmet Zileli

Preface

Blessed are the wise who savor the pleasures of the mind. Ibn Sina (Avicenna) [980–1037] A great project must represent a happy nightmare that illuminates your sleep, excites your awakening, and sleepwalks your day. Ali Akhaddar (The author)

Sciatica is among the most common symptoms encountered in clinical medicine worldwide. This usual pain is found on the borders of many medical and surgical specialties and can occur in different circumstances. Sciatic pain may precede, coincide with, or follow the diagnosis of a specific disease. All such pathological conditions may complicate the diagnostic process. In this momentum, it seems that sciatica has not revealed all its mysteries to us yet. Unfortunately, patients, and even many clinicians, still use the term “sciatica” to describe any painful disorder arising from the lower back or the hip and radiating down to the lower limb, but sciatica is much more than just a lower limb pain. The topic of this Atlas is as old as the “sciatica of Atlas,” one of the most legendary Titans in Greek mythology. Furthermore, despite more than 250 years after the first classic monograph written on sciatica by the Italian anatomist Domenico Cotugno (1736–1822), that condition continues to be a mysterious painful symptom for many patients, and a frustrating one for some of their physicians. Certainly, discogenic and spinogenic origins account for some, but not all, of the pain and discomfort that accompanies this situation. Indeed, extraspinal causes of sciatica as well as pseudosciatic pain (the so-called SPINO or sciatic pain in name only) are usually overlooked and even confused for a panoply of other causes. Management of sciatica is often challenging due to its various etiologies, different forms of presentations, and mimicking conditions. To offer the best chance for the patient to recover, it is crucial to accomplish an accurate diagnosis and to propose an adequate timely treatment. Otherwise, this “popular” symptom can result in serious functional consequences and permanent neurologic deficits. Classically, sciatic pains are arranged by the anatomical location concerned and the panoply of etiologies involved. Due to its long pathway, the sciatic nerve can be compressed and affected in diverse anatomical regions from its origin to its dividing branches and by various causes. Accordingly, the development of this pain requires good anatomic and physiologic knowledge as well as main concepts of pathophysiology which are necessary to understand the different clinical signs and symptoms. Unfortunately, nowadays, some cases are still diagnosed late. In addition, surgery is still performed unnecessarily for several patients whose situations are ultimately identified as being non-discogenic or extraspinal in origin. The same errors continue to be made even though today’s diagnostic tools are much more advanced in great measure because of improved imaging techniques and electrophysiological methods. Treating physicians must pay attention to the patient’s detailed history and the results of the clinical examination before asking for further paraclinical investigations. Presently, the spectrum of treatment, that has greatly profited from modern minimally invasive procedures, goes from conservative methods to decompressive surgical approaches. Nevertheless, after the enthusiasm of the first “eureka,” surgery for lumbar herniated discs is not always easy with its share of complications and poor results for both the surgeon and his/ xi

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her patient. Overall, early diagnosis of causes inducing sciatic or pseudo-sciatic pain is crucial because timely therapeutic management, in addition to preventing further neurologic damage and unnecessary spinal surgery, may have an important impact on the patient’s functional outcome and even his/her survival. Curiously, in recent years, very few medical books are dedicated to sciatic pain as a sole subject. On the opposite, there are many popular books for pain relief addressed to “patients.” It is not clear why sciatic pain did not receive much attention in recent medical literature, unlike in pain popularization books. Each of our patients is a real lesson for the others

On the grounds of all these considerations, a need has become evident for a modern illustrative book about sciatica from a medical, imaging, and surgical perspective. This Atlas book written with one hand required about 5 years of preparation. It is the result of a quarter-century practice in neurosurgery and spinal surgery and a detailed evaluation of hundreds of sciatica-­ like diseases in our department. Although some of these patients have haunted my sleep, many of them have brought me satisfaction that almost nothing else can replace. I also remembered that every patient every day represents a different challenge, a new learning experience, and a true lesson for others. Neurosurgeons, spinal surgeons, neurologists, rheumatologists, radiologists, emergency physicians, algiatrists, rehabilitation physicians, other clinicians, and neuroscientists worldwide will find a comprehensive visual encyclopedia about discogenic sciatica, non-discogenic sciatica, extraspinal (i.e., intrapelvic or extrapelvic) sciatica as well as pseudo-sciatica and sciatica mimics. The Atlas of Sciatica contains 1003 figures in more than 2800 separate illustrations and 92 tables. Most of the figures are original and taken from real-life personal clinical cases collected over 25 years of field practice in sciatica. To the best of my knowledge, no book hitherto published covers such a variety of figures and illustrations about this topic. The main goal is to deliver more information in less space than other text-heavy traditional books. The 111 chapters of this book cover the key variety of clinical presentations, mimic forms, and etiologies of sciatic pain seen in medical, imaging, and surgical practices. This book also tries to demystify the concern regarding atypical presentations, differential diagnoses, and unusual etiologies of sciatica. The purpose is to give a possible all-inclusive overview of sciatic pain even though I know that I have inevitably left some diseases off the list. I am also aware that some clinical presentations, related forms, and causes are too rare or even exceptional to be useful. Besides documenting the work, the present Atlas has a teaching value. The format makes it easily accessible and includes a definition and some generalities of each form and etiology as well as the main clinical presentations, paraclinical features, treatment options, complications, and prognosis. It will help the reader to choose the most appropriate way to recognize and manage this special multipart pain. Regardless of readers’ specialization and level of knowledge, I pray deeply they will enjoy using this book and find it helpful in their daily practice. Marrakech, Morocco July 2023

Ali Akhaddar, M.D., IFAANS

Acknowledgments

The author would like to acknowledge the following personalities for their continuous support and encouragement: • Pr. Major General Mohamed Abbar, MD. Health Inspector of the Moroccan Royal Armed Forces • Pr. Brigadier General Belkacem Chagar, MD. Chief Medical Officer of Avicenne Military Hospital. Marrakech, Morocco • Pr. Mohamed Boucetta, MD. Mentor and Former Chairman. Department of Neurosurgery. Mohammed V Military Teaching Hospital. Rabat, Morocco. “When the scarcity of words associates discipline in the workplace with the precision of gesture and the generosity of heart…” • Pr. Brahim Lekehal, MD. Dean of the Faculty of Medicine and Pharmacy, Mohammed V University in Rabat, Morocco • Pr. Mohamed Zyani, MD, Pr. Redouane Niamane, MD, and Pr. Haddou Ammar, MD, from Avicenne Military Hospital, Marrakech, Morocco • Pr. Abdellah El Maghraoui, MD. Former Chairman, Department of Rheumatology. Mohammed V Military Teaching Hospital, Rabat, Morocco • Mrs. Khadija Akhaddar, DESS (specialized graduate diploma) in Public Administration, working in the Federal Public Service of the Government of Canada, Ottawa, Canada The author wishes also to thank the following colleagues for providing this book with some illustrations and pictures: • Pr. Salah Bellasri, MD, Pr. Badr Slioui, MD, Pr. Redouane Roukhsi, MD, Pr. Nabil Hammoune, MD, and Pr. El Mehdi Atmane, MD, Department of Medical Imaging, Avicenne Military Hospital, Marrakech, Morocco • Dr. Mohamed Amine Azami, MD, and Pr. Issam Rharrassi, MD, Department of Pathology, Avicenne Military Hospital, Marrakech, Morocco • Dr. Achraf Moussa, MD, Pr. Hassan Baallal, MD, and Pr. Hatim Belfquih, MD, Department of Neurosurgery, Avicenne Military Hospital, Marrakech, Morocco • Pr. Abad Cherif El Asri, MD, Department of Neurosurgery, Mohammed V Military Teaching Hospital, Rabat, Morocco • Pr. Hafid Arabi, MD, Department of Physical Medicine and Functional Rehabilitation, Mohammed V Military Teaching Hospital, Rabat, Morocco • Pr. Redouane Niamane, MD, Department of Rheumatology, Avicenne Military Hospital, Marrakech, Morocco • Pr. Youssef Benyass, MD, Department of Orthopedic Surgery, Avicenne Military Hospital, Marrakech, Morocco • Pr. Adil Arrob, MD, Department of Burns and Plastic Surgery, Avicenne Military Hospital, Marrakech, Morocco

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Also, the author would like to express his gratitude to the following for their assistance in the preparation of the text and the illustrations: • Ms. Hiba Akhaddar, Master’s student and Computer Science Researcher, Gina Cody School of Engineering and Computer Science, Concordia University, Montreal, Canada • Mr. Ahmed Akhaddar, Schoolboy at Hilali Targa International School, Marrakech, Morocco • The team of Springer-Nature in the USA for coordinating various phases of this project, especially Richard Lansing (Editorial Director, New  York, USA), Kristopher Spring (Publishing Editor, New Jersey, USA), Lee Klein (Senior Editor, Philadelphia, USA), the copyeditor, and the artists who worked on this Atlas The author respectfully thanks and extends its deep appreciation to Professor Edward Benzel, MD (Cleveland, USA) and Professor Mehmet Zileli, MD (Turkey), for kindly agreeing to write the forewords of this Atlas book. Finally, the author would like to thank all the staff in the Department of Neurosurgery and all the medical doctors involved directly or indirectly in managing patients with sciatic pain at Avicenne Military Hospital of Marrakech. Special thanks to the radiologists, rheumatologists, neurologists, anesthesiologists, pathologists, physiotherapists, and medical assistants who also manage our patients.

Acknowledgments

Contents

Part I General Considerations 1 Definitions of Sciatica�����������������������������������������������������������������������������������������������    3 1.1 Origin of the Term “Sciatica” ���������������������������������������������������������������������������    3 1.2 Definitions of the Term “Sciatica”���������������������������������������������������������������������    3 Further Reading ���������������������������������������������������������������������������������������������������������    5 2 Historical Aspects of Sciatica�����������������������������������������������������������������������������������    7 2.1 Introduction�������������������������������������������������������������������������������������������������������    7 2.2 Biblical Period���������������������������������������������������������������������������������������������������    8 2.3 Greco-Roman Period�����������������������������������������������������������������������������������������   10 2.4 Arabic and Persian Civilization�������������������������������������������������������������������������   13 2.5 Eighteenth Century �������������������������������������������������������������������������������������������   17 2.6 Nineteenth Century �������������������������������������������������������������������������������������������   18 2.7 Twentieth Century���������������������������������������������������������������������������������������������   19 Further Reading ���������������������������������������������������������������������������������������������������������   22 3 Anatomy  and Physiology of the Sciatic Nerve�������������������������������������������������������   25 3.1 Generality and Relevance ���������������������������������������������������������������������������������   25 3.2 Origin and Course of the Sciatic Nerve�������������������������������������������������������������   25 3.3 The Lumbosacral Spine�������������������������������������������������������������������������������������   29 3.4 The Lumbosacral Nerve Roots �������������������������������������������������������������������������   40 3.5 The Intervertebral Foraminal Area���������������������������������������������������������������������   41 3.6 The Major Branches of the Sciatic Nerve���������������������������������������������������������   42 3.7 The Motor and Sensory Supply of the Sciatic Nerve����������������������������������������   42 3.8 Variant Anatomy of the Sciatic Nerve���������������������������������������������������������������   43 Further Reading ���������������������������������������������������������������������������������������������������������   45 4 Epidemiology  and Etiologies of Sciatica�����������������������������������������������������������������   47 4.1 Generalities and Relevance �������������������������������������������������������������������������������   47 4.2 Epidemiology�����������������������������������������������������������������������������������������������������   48 4.3 Risk Factors�������������������������������������������������������������������������������������������������������   48 4.4 Classifications and Etiologies ���������������������������������������������������������������������������   49 Further Reading ���������������������������������������������������������������������������������������������������������   55 5 Pathophysiological  Mechanisms of Sciatica�����������������������������������������������������������   57 5.1 Generalities and Relevance �������������������������������������������������������������������������������   57 5.2 Compression Mechanisms���������������������������������������������������������������������������������   58 5.3 Vascular Mechanisms�����������������������������������������������������������������������������������������   59 5.4 Inflammatory Mechanisms���������������������������������������������������������������������������������   59 5.5 Immunological Mechanisms�����������������������������������������������������������������������������   59 5.6 Neurophysiological Effects�������������������������������������������������������������������������������   59 5.7 Psychological Disorders�������������������������������������������������������������������������������������   59 5.8 Other Mechanisms���������������������������������������������������������������������������������������������   60 xv

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Further Reading ���������������������������������������������������������������������������������������������������������   61 6 Natural  History of Sciatica���������������������������������������������������������������������������������������   63 6.1 Generalities and Relevance �������������������������������������������������������������������������������   63 6.2 Natural History of Sciatica Related to Lumbar Disk Herniation�����������������������   63 Further Reading ���������������������������������������������������������������������������������������������������������   66 7 Main  Clinical Presentations of Sciatica �����������������������������������������������������������������   69 7.1 Generalities and Relevance �������������������������������������������������������������������������������   69 7.2 Patient History���������������������������������������������������������������������������������������������������   69 7.3 Physical Examinations and Findings�����������������������������������������������������������������   71 7.4 Psychological and Psychiatric Disorders�����������������������������������������������������������   90 Further Reading ���������������������������������������������������������������������������������������������������������   90 8 Clinical  Differential Diagnoses of Sciatica (Sciatic Pain in Name Only)�������������   93 8.1 Generalities and Relevance �������������������������������������������������������������������������������   93 8.2 Spinal Conditions�����������������������������������������������������������������������������������������������   94 8.2.1 Spinal Lesions Without Neurological Involvement�������������������������������   94 8.2.2 Myelopathies�����������������������������������������������������������������������������������������   96 8.2.3 Other Spinal Radiculopathies ���������������������������������������������������������������   97 8.3 Extraspinal Conditions���������������������������������������������������������������������������������������  101 8.3.1 Pelvic, Abdominal, and Thoracic Diseases�������������������������������������������  101 8.3.2 Other Plexopathies���������������������������������������������������������������������������������  101 8.3.3 Extrapelvic (Lower Limb) Diseases �����������������������������������������������������  101 8.3.4 Other Peripheral Neuropathies���������������������������������������������������������������  105 8.3.5 Fibromyalgia Syndrome������������������������������������������������������������������������  105 8.4 Intracranial Diseases �����������������������������������������������������������������������������������������  113 8.5 Psychological and Psychiatric Disorders�����������������������������������������������������������  113 Further Reading ���������������������������������������������������������������������������������������������������������  114 9 Paraclinic  Evaluations of Sciatica���������������������������������������������������������������������������  117 9.1 Generalities and Relevance �������������������������������������������������������������������������������  117 9.2 Neurophysiological Studies�������������������������������������������������������������������������������  124 9.3 Imaging Modalities �������������������������������������������������������������������������������������������  125 9.3.1 Plain Radiography���������������������������������������������������������������������������������  125 9.3.2 Myelography �����������������������������������������������������������������������������������������  125 9.3.3 Discography�������������������������������������������������������������������������������������������  127 9.3.4 Computed Tomography Scan�����������������������������������������������������������������  128 9.3.5 Magnetic Resonance Imaging���������������������������������������������������������������  128 9.3.6 Other Imaging Investigations�����������������������������������������������������������������  133 9.4 Laboratory Investigations�����������������������������������������������������������������������������������  145 9.5 Epidural and Selective Lumbosacral Nerve Blocks�������������������������������������������  145 Further Reading ���������������������������������������������������������������������������������������������������������  145 10 Neuroimaging  Differential Diagnoses of Common Lumbar Disk Herniations�������������������������������������������������������������������������������������������������������  147 10.1 Generalities and Relevance �����������������������������������������������������������������������������  147 10.2 Synovial Cyst���������������������������������������������������������������������������������������������������  148 10.3 Discal Cyst�������������������������������������������������������������������������������������������������������  149 10.4 Epidural Gas Pseudocyst���������������������������������������������������������������������������������  150 10.5 Osteophytes�����������������������������������������������������������������������������������������������������  151 10.6 Ossifications of the Posterior Longitudinal Ligament�������������������������������������  152 10.7 Discitis�������������������������������������������������������������������������������������������������������������  153 10.8 Epidural Abscess���������������������������������������������������������������������������������������������  155 10.9 Conjoined Nerve Root Anomalies�������������������������������������������������������������������  156

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10.10 Enlarged Nerve Roots �������������������������������������������������������������������������������������  157 10.11 Apophyseal Ring Fracture (Posterior Ring Apophysis Separation) ���������������  159 10.12 Postoperative Disorders�����������������������������������������������������������������������������������  160 10.13 Tumors and Pseudotumors (Epidural Non-vertebral) �������������������������������������  164 10.14 Tumors (Nerve Root Tumors)�������������������������������������������������������������������������  165 10.15 Epidural Hematoma�����������������������������������������������������������������������������������������  167 10.16 Epidural Varices (Venous Plexus Engorgement)���������������������������������������������  168 10.17 Epidural Cavernous Hemangiomas�����������������������������������������������������������������  168 10.18 Rare Lesions�����������������������������������������������������������������������������������������������������  169 Further Reading ���������������������������������������������������������������������������������������������������������  171 11 Nonsurgical  Treatment of Discogenic Sciatica�������������������������������������������������������  173 11.1 Generalities and Relevance �����������������������������������������������������������������������������  173 11.2 Medications (Pharmacological Therapies)������������������������������������������������������  173 11.3 Activity Modifications�������������������������������������������������������������������������������������  174 11.4 Physical Therapy Programs for Rehabilitation �����������������������������������������������  174 11.5 Therapeutic Injections�������������������������������������������������������������������������������������  174 11.6 Complementary and Alternative Therapies�����������������������������������������������������  176 11.7 Patient Education���������������������������������������������������������������������������������������������  177 Further Reading ���������������������������������������������������������������������������������������������������������  177 12 Surgical  Treatment of Discogenic Sciatica�������������������������������������������������������������  179 12.1 Generalities and Relevance �����������������������������������������������������������������������������  179 12.2 Open Approaches���������������������������������������������������������������������������������������������  179 12.3 Intradiscal Surgical Procedures�����������������������������������������������������������������������  189 12.3.1 Chemonucleolysis �������������������������������������������������������������������������������  189 12.3.2 Automated Percutaneous Lumbar Discectomy�����������������������������������  189 12.3.3 Intradiscal Endothermal Therapy (IDET) �������������������������������������������  190 12.3.4 Coblation Nucleoplasty�����������������������������������������������������������������������  190 12.3.5 Percutaneous Laser Disk Decompression (PLDD)�����������������������������  190 12.4 Endoscopic Disk Surgery���������������������������������������������������������������������������������  190 12.4.1 Transforaminal Endoscopic Approach�������������������������������������������������  190 12.4.2 Interlaminar Endoscopic Approach�����������������������������������������������������  190 Further Reading ���������������������������������������������������������������������������������������������������������  191 13 Surgical  Complications of Discogenic Sciatica�������������������������������������������������������  193 13.1 Definition and Relevance���������������������������������������������������������������������������������  193 13.2 Dural Tear �������������������������������������������������������������������������������������������������������  194 13.3 Infection�����������������������������������������������������������������������������������������������������������  198 13.4 Radicular Injury�����������������������������������������������������������������������������������������������  202 13.5 Neurological Complications ���������������������������������������������������������������������������  202 13.6 Recurrence (Re-herniation) Relapsing LDH���������������������������������������������������  202 13.7 Epidural Fibrosis���������������������������������������������������������������������������������������������  203 13.8 Arachnoiditis���������������������������������������������������������������������������������������������������  204 13.9 Failed Back Surgery Syndrome�����������������������������������������������������������������������  205 13.10 Wrong Side or Wrong Level Exploration �������������������������������������������������������  205 13.11 Lesions from Operative Positioning ���������������������������������������������������������������  207 13.12 Hardware Devices and Instrumentations���������������������������������������������������������  208 13.13 Spinal Instability ���������������������������������������������������������������������������������������������  208 13.14 Compressing Epidural Hematoma�������������������������������������������������������������������  208 13.15 Wound Complications�������������������������������������������������������������������������������������  208 13.16 Thromboembolic Problems�����������������������������������������������������������������������������  208 13.17 Reoperation �����������������������������������������������������������������������������������������������������  208 13.18 Pseudarthrosis �������������������������������������������������������������������������������������������������  209

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13.19 Retroperitoneal Blood Vessels and Visceral Injuries���������������������������������������  209 13.20 Other Surgical Errors and Rare Complications�����������������������������������������������  210 13.21 Nonsurgical (Medical) Complications�������������������������������������������������������������  214 13.22 Mortality ���������������������������������������������������������������������������������������������������������  214 13.23 Conclusion�������������������������������������������������������������������������������������������������������  215 Further Reading ���������������������������������������������������������������������������������������������������������  215 14 Surgical  Outcomes of Discogenic Sciatica �������������������������������������������������������������  217 14.1 Generalities and Relevance �����������������������������������������������������������������������������  217 14.2 Postoperative Management �����������������������������������������������������������������������������  217 14.3 Postoperative Complications (c.f. Chap. 13 About Surgical Complications of Discogenic Sciatica)�����������������������������������������������������������  222 14.4 Sequels�������������������������������������������������������������������������������������������������������������  222 14.5 Surgical Results�����������������������������������������������������������������������������������������������  222 Further Reading ���������������������������������������������������������������������������������������������������������  225 15 Sciatica  in Popular Cultures �����������������������������������������������������������������������������������  227 15.1 Traditional Therapeutic Practices �������������������������������������������������������������������  227 15.2 Sciatica in Nonmedical Literature�������������������������������������������������������������������  232 Further Reading ���������������������������������������������������������������������������������������������������������  234 Part II Lumbosacral Discogenic Sciatica 16 Central  and Subarticular Lumbar Disk Herniations �������������������������������������������  239 16.1 Definition and Relevance���������������������������������������������������������������������������������  239 16.2 Clinical Presentations���������������������������������������������������������������������������������������  243 16.3 Imaging Features���������������������������������������������������������������������������������������������  246 16.4 Treatment Options�������������������������������������������������������������������������������������������  255 16.5 Outcome and Prognosis�����������������������������������������������������������������������������������  258 Further Reading ���������������������������������������������������������������������������������������������������������  258 17 Foraminal  and Extraforaminal (Far Lateral) Lumbar Disk Herniations�����������  261 17.1 Generalities and Relevance �����������������������������������������������������������������������������  261 17.2 Main Particularities of Foraminal and Extraforaminal Lumbar Disk Herniations ���������������������������������������������������������������������������������������������  262 17.3 Imaging Features���������������������������������������������������������������������������������������������  263 17.4 Treatment Options and Prognosis �������������������������������������������������������������������  269 Further Reading ���������������������������������������������������������������������������������������������������������  276 18 Migrated  Lumbar Disk Herniations�����������������������������������������������������������������������  279 18.1 Generalities and Relevance �����������������������������������������������������������������������������  279 18.2 Clinical Presentations���������������������������������������������������������������������������������������  280 18.3 Paraclinic Features�������������������������������������������������������������������������������������������  280 18.4 Treatment Options and Prognosis �������������������������������������������������������������������  293 Further Reading ���������������������������������������������������������������������������������������������������������  294 19 Sequestrated  Lumbar Disk Herniations�����������������������������������������������������������������  297 19.1 Generalities and Relevance �����������������������������������������������������������������������������  297 19.2 Clinical Presentations���������������������������������������������������������������������������������������  298 19.3 Paraclinical Features ���������������������������������������������������������������������������������������  298 19.4 Treatment Options and Prognosis �������������������������������������������������������������������  310 Further Reading ���������������������������������������������������������������������������������������������������������  311 20 Massive  (Giant) Lumbar Disk Herniations �����������������������������������������������������������  313 20.1 Generalities and Relevance �����������������������������������������������������������������������������  313 20.2 Clinical Presentations���������������������������������������������������������������������������������������  314

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20.3 Imaging Features���������������������������������������������������������������������������������������������  314 20.4 Treatment Options and Prognosis �������������������������������������������������������������������  324 Further Reading ���������������������������������������������������������������������������������������������������������  325 21 Posterior  Epidural Migration of Lumbar Disk Herniations���������������������������������  327 21.1 Generalities and Relevance �����������������������������������������������������������������������������  327 21.2 Clinical Presentations���������������������������������������������������������������������������������������  328 21.3 Imaging Features���������������������������������������������������������������������������������������������  328 21.4 Treatment Options and Prognosis �������������������������������������������������������������������  333 Further Reading ���������������������������������������������������������������������������������������������������������  334 22 Sciatica  Due to High Lumbar Disk Herniations and Spinal Stenosis �����������������  335 22.1 Generalities and Relevance �����������������������������������������������������������������������������  335 22.2 Clinical Presentations���������������������������������������������������������������������������������������  336 22.3 Paraclinical Features ���������������������������������������������������������������������������������������  336 22.4 Treatment Options and Prognosis �������������������������������������������������������������������  342 Further Reading ���������������������������������������������������������������������������������������������������������  342 23 Anterior  Retroperitoneal Lumbar Disk Herniations �������������������������������������������  345 23.1 Generalities and Relevance �����������������������������������������������������������������������������  345 23.2 Clinical Presentations���������������������������������������������������������������������������������������  346 23.3 Imaging Features���������������������������������������������������������������������������������������������  346 23.4 Treatment Options and Prognosis �������������������������������������������������������������������  349 Further Reading ���������������������������������������������������������������������������������������������������������  350 24 Pediatric  Lumbar Disk Herniations�����������������������������������������������������������������������  351 24.1 Generalities and Relevance �����������������������������������������������������������������������������  351 24.2 Clinical Presentations���������������������������������������������������������������������������������������  355 24.3 Imaging Features���������������������������������������������������������������������������������������������  357 24.4 Treatment Options and Prognosis �������������������������������������������������������������������  358 24.5 Outcomes and Prognosis���������������������������������������������������������������������������������  359 Further Reading ���������������������������������������������������������������������������������������������������������  360 25 Pregnant  Women with Lumbar Disk Herniations�������������������������������������������������  361 25.1 Generalities and Relevance �����������������������������������������������������������������������������  361 25.2 Clinical Presentations���������������������������������������������������������������������������������������  362 25.3 Imaging Features���������������������������������������������������������������������������������������������  362 25.4 Treatment Options�������������������������������������������������������������������������������������������  362 25.5 Outcomes and Prognosis���������������������������������������������������������������������������������  363 Further Reading ���������������������������������������������������������������������������������������������������������  363 26 Spontaneous  Regression of Lumbar Disk Herniations�����������������������������������������  365 26.1 Generalities and Relevance �����������������������������������������������������������������������������  365 26.2 Clinical Presentations���������������������������������������������������������������������������������������  367 26.3 Paraclinical Features ���������������������������������������������������������������������������������������  368 26.4 Treatment Options and Prognosis �������������������������������������������������������������������  370 Further Reading ���������������������������������������������������������������������������������������������������������  371 27 Posterior Ring Apophysis Separation���������������������������������������������������������������������  373 27.1 Generalities and Relevance �����������������������������������������������������������������������������  373 27.2 Clinical Presentations���������������������������������������������������������������������������������������  375 27.3 Imaging Features���������������������������������������������������������������������������������������������  375 27.4 Treatment Options and Prognosis �������������������������������������������������������������������  391 Further Reading ���������������������������������������������������������������������������������������������������������  398

xx

28 Recurrent  Lumbar Disk Herniations���������������������������������������������������������������������  401 28.1 Generalities and Relevance �����������������������������������������������������������������������������  401 28.2 Clinical Presentations���������������������������������������������������������������������������������������  401 28.3 Imaging Features���������������������������������������������������������������������������������������������  402 28.4 Treatment Options and Prognosis �������������������������������������������������������������������  413 Further Reading ���������������������������������������������������������������������������������������������������������  414 29 Discal Cysts���������������������������������������������������������������������������������������������������������������  417 29.1 Generalities and Relevance �����������������������������������������������������������������������������  417 29.2 Clinical Presentations���������������������������������������������������������������������������������������  417 29.3 Imaging Features���������������������������������������������������������������������������������������������  417 29.4 Treatment Options and Prognosis �������������������������������������������������������������������  418 Further Reading ���������������������������������������������������������������������������������������������������������  419 30 Intradural  Lumbar Disk Herniations���������������������������������������������������������������������  421 30.1 Generalities and Relevance �����������������������������������������������������������������������������  421 30.2 Clinical Presentations���������������������������������������������������������������������������������������  422 30.3 Imaging Features���������������������������������������������������������������������������������������������  422 30.4 Treatment Options and Prognosis �������������������������������������������������������������������  425 Further Reading ���������������������������������������������������������������������������������������������������������  426 31 Intraradicular  Lumbar Disc Herniations���������������������������������������������������������������  427 31.1 Generalities and Relevance �����������������������������������������������������������������������������  427 31.2 Clinical Presentations���������������������������������������������������������������������������������������  428 31.3 Imaging Features���������������������������������������������������������������������������������������������  428 31.4 Treatment Options and Prognosis �������������������������������������������������������������������  429 Further Reading ���������������������������������������������������������������������������������������������������������  430 32 Sciatic  Double Crush Syndrome at the Same Root Site ���������������������������������������  431 32.1 Generalities and Relevance �����������������������������������������������������������������������������  431 32.2 Clinical Presentations���������������������������������������������������������������������������������������  431 32.3 Paraclinic Features�������������������������������������������������������������������������������������������  432 32.4 Treatment Options and Prognosis �������������������������������������������������������������������  433 Further Reading ���������������������������������������������������������������������������������������������������������  433 33 Sciatica  Due to Contralateral Lumbar Disc Herniations �������������������������������������  435 33.1 Generalities and Relevance �����������������������������������������������������������������������������  435 33.2 Clinical Presentations���������������������������������������������������������������������������������������  436 33.3 Paraclinic Features�������������������������������������������������������������������������������������������  436 33.4 Treatment Options and Prognosis �������������������������������������������������������������������  437 Further Reading ���������������������������������������������������������������������������������������������������������  438 Part III Spinal Non-discogenic Sciatica 34 Lumbar Spinal Stenosis�������������������������������������������������������������������������������������������  441 34.1 Generalities and Relevance �����������������������������������������������������������������������������  441 34.2 Clinical Presentations���������������������������������������������������������������������������������������  461 34.3 Paraclinic Features�������������������������������������������������������������������������������������������  462 34.4 Treatment Options and Prognosis �������������������������������������������������������������������  464 Further Reading ���������������������������������������������������������������������������������������������������������  474 35 Lumbar Spondylolysis ���������������������������������������������������������������������������������������������  477 35.1 Generalities and Relevance �����������������������������������������������������������������������������  477 35.2 Clinical Presentations���������������������������������������������������������������������������������������  478 35.3 Paraclinic Features�������������������������������������������������������������������������������������������  478 35.4 Treatment Options and Prognosis �������������������������������������������������������������������  488 Further Reading ���������������������������������������������������������������������������������������������������������  492

Contents

Contents

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36 Lumbar Spondylolisthesis ���������������������������������������������������������������������������������������  495 36.1 Generalities and Relevance �����������������������������������������������������������������������������  495 36.2 Clinical Presentations���������������������������������������������������������������������������������������  509 36.3 Paraclinic Features�������������������������������������������������������������������������������������������  510 36.4 Treatment Options and Prognosis �������������������������������������������������������������������  514 Further Reading ���������������������������������������������������������������������������������������������������������  519 37 Lumbar Degenerative Scoliosis�������������������������������������������������������������������������������  521 37.1 Generalities and Relevance �����������������������������������������������������������������������������  521 37.2 Clinical presentations���������������������������������������������������������������������������������������  521 37.3 Imaging Features���������������������������������������������������������������������������������������������  522 37.4 Treatment Options and Prognosis �������������������������������������������������������������������  528 Further Reading ���������������������������������������������������������������������������������������������������������  529 38 Lumbosacral  Extraforaminal Stenosis (Far-Out Syndrome)�������������������������������  531 38.1 Generalities and Relevance �����������������������������������������������������������������������������  531 38.2 Clinical Presentations���������������������������������������������������������������������������������������  534 38.3 Paraclinic Features�������������������������������������������������������������������������������������������  534 38.4 Treatment Options and Prognosis �������������������������������������������������������������������  535 Further Reading ���������������������������������������������������������������������������������������������������������  536 39 Lumbosacral Vertebral Tumors�������������������������������������������������������������������������������  537 39.1 Generalities and Relevance �����������������������������������������������������������������������������  537 39.2 Clinical Presentations���������������������������������������������������������������������������������������  538 39.3 Paraclinic Features�������������������������������������������������������������������������������������������  538 39.4 Treatment Options and Prognosis �������������������������������������������������������������������  556 Further Reading ���������������������������������������������������������������������������������������������������������  556 40 Epidural Nonvertebral Tumors�������������������������������������������������������������������������������  559 40.1 Generalities and Relevance �����������������������������������������������������������������������������  559 40.2 Clinical Presentations���������������������������������������������������������������������������������������  568 40.3 Paraclinic Features�������������������������������������������������������������������������������������������  568 40.4 Treatment Options and Prognosis �������������������������������������������������������������������  569 Further Reading ���������������������������������������������������������������������������������������������������������  570 41 Spinal Epidural Lipomatosis�����������������������������������������������������������������������������������  571 41.1 Generalities and Relevance �����������������������������������������������������������������������������  571 41.2 Clinical Presentations���������������������������������������������������������������������������������������  571 41.3 Imaging Features���������������������������������������������������������������������������������������������  571 41.4 Treatment Options and Prognosis �������������������������������������������������������������������  575 Further Reading ���������������������������������������������������������������������������������������������������������  575 42 Intradural Lumbosacral Tumors�����������������������������������������������������������������������������  577 42.1 Generalities and Relevance �����������������������������������������������������������������������������  577 42.2 Clinical Presentations���������������������������������������������������������������������������������������  578 42.3 Imaging Features���������������������������������������������������������������������������������������������  579 42.4 Treatment Options and Prognosis �������������������������������������������������������������������  594 Further Reading ���������������������������������������������������������������������������������������������������������  595 43 Conus Medullaris Lesions ���������������������������������������������������������������������������������������  597 43.1 Generalities and Relevance �����������������������������������������������������������������������������  597 43.2 Etiologies���������������������������������������������������������������������������������������������������������  599 43.3 Clinical Presentations���������������������������������������������������������������������������������������  604 43.4 Imaging Features���������������������������������������������������������������������������������������������  605 43.5 Treatment Options and Prognosis �������������������������������������������������������������������  606 Further Reading ���������������������������������������������������������������������������������������������������������  606

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44 Intraspinal Funicular Sciatica���������������������������������������������������������������������������������  609 44.1 Generalities and Relevance �����������������������������������������������������������������������������  609 44.2 Clinical Presentations���������������������������������������������������������������������������������������  609 44.3 Imaging Features���������������������������������������������������������������������������������������������  610 44.4 Treatment Options and Prognosis �������������������������������������������������������������������  617 Further Reading ���������������������������������������������������������������������������������������������������������  618 45 Axial  Spondyloarthritis (Spinal Ankylosing Spondylitis)�������������������������������������  619 45.1 Generalities and Relevance �����������������������������������������������������������������������������  619 45.2 Clinical Presentations���������������������������������������������������������������������������������������  619 45.3 Paraclinic Features�������������������������������������������������������������������������������������������  620 45.4 Treatment Options and Prognosis �������������������������������������������������������������������  625 Further Reading ���������������������������������������������������������������������������������������������������������  626 46 Spinal Pigmented Villonodular Synovitis���������������������������������������������������������������  627 46.1 Generalities and Relevance �����������������������������������������������������������������������������  627 46.2 Clinical Presentations���������������������������������������������������������������������������������������  627 46.3 Paraclinic Features�������������������������������������������������������������������������������������������  627 46.4 Treatment Options and Prognosis �������������������������������������������������������������������  629 Further Reading ���������������������������������������������������������������������������������������������������������  629 47 Spinal  Paget’s Disease and Sciatica�������������������������������������������������������������������������  631 47.1 Generalities and Relevance �����������������������������������������������������������������������������  631 47.2 Clinical Presentations���������������������������������������������������������������������������������������  631 47.3 Paraclinic Features�������������������������������������������������������������������������������������������  632 47.4 Treatment Options and Prognosis �������������������������������������������������������������������  634 Further Reading ���������������������������������������������������������������������������������������������������������  634 48 Spinal Rheumatoid Arthritis�����������������������������������������������������������������������������������  637 48.1 Generalities and Relevance �����������������������������������������������������������������������������  637 48.2 Clinical Presentations���������������������������������������������������������������������������������������  637 48.3 Paraclinic Features�������������������������������������������������������������������������������������������  638 48.4 Treatment Options and Prognosis �������������������������������������������������������������������  638 Further Reading ���������������������������������������������������������������������������������������������������������  639 49 Spinal  Diffuse Idiopathic Skeletal Hyperostosis (Forestier’s Disease)�����������������  641 49.1 Generalities and Relevance �����������������������������������������������������������������������������  641 49.2 Clinical Presentations���������������������������������������������������������������������������������������  641 49.3 Paraclinic Features�������������������������������������������������������������������������������������������  642 49.4 Treatment Options and Prognosis �������������������������������������������������������������������  643 Further Reading ���������������������������������������������������������������������������������������������������������  644 50 Lumbar  Spinal Gout and Pseudogout��������������������������������������������������������������������  645 50.1 Generalities and Relevance �����������������������������������������������������������������������������  645 50.2 Clinical Presentations���������������������������������������������������������������������������������������  645 50.3 Paraclinic Features�������������������������������������������������������������������������������������������  646 50.4 Treatment Options and Prognosis �������������������������������������������������������������������  647 Further Reading ���������������������������������������������������������������������������������������������������������  647 51 Spinal  Langerhans Cell Histiocytosis (Eosinophilic Granuloma) �����������������������  649 51.1 Generalities and Relevance �����������������������������������������������������������������������������  649 51.2 Clinical Presentations���������������������������������������������������������������������������������������  649 51.3 Paraclinic Features�������������������������������������������������������������������������������������������  650 51.4 Treatment Options and Prognosis �������������������������������������������������������������������  651 Further Reading ���������������������������������������������������������������������������������������������������������  651

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52 Vertebral  Osteomyelitis and Spondylodiscitis �������������������������������������������������������  653 52.1 Generalities and Relevance �����������������������������������������������������������������������������  653 52.2 Clinical Presentations���������������������������������������������������������������������������������������  654 52.3 Imaging Features���������������������������������������������������������������������������������������������  655 52.4 Laboratory Findings�����������������������������������������������������������������������������������������  666 52.5 Treatment Options and Prognosis �������������������������������������������������������������������  666 Further Reading ���������������������������������������������������������������������������������������������������������  667 53 Spinal Epidural Abscesses���������������������������������������������������������������������������������������  669 53.1 Generalities and Relevance �����������������������������������������������������������������������������  669 53.2 Clinical Presentations���������������������������������������������������������������������������������������  670 53.3 Imaging Features���������������������������������������������������������������������������������������������  670 53.4 Laboratory Findings�����������������������������������������������������������������������������������������  672 53.5 Treatment Options and Prognosis �������������������������������������������������������������������  672 Further Reading ���������������������������������������������������������������������������������������������������������  673 54 Spinal Subdural Abscesses���������������������������������������������������������������������������������������  675 54.1 Generalities and Relevance �����������������������������������������������������������������������������  675 54.2 Clinical Presentations���������������������������������������������������������������������������������������  675 54.3 Imaging Features���������������������������������������������������������������������������������������������  676 54.4 Laboratory Findings�����������������������������������������������������������������������������������������  676 54.5 Treatment Options and Prognosis �������������������������������������������������������������������  677 Further Reading ���������������������������������������������������������������������������������������������������������  677 55 Lumbar Adhesive Arachnoiditis �����������������������������������������������������������������������������  679 55.1 Generalities and Relevance �����������������������������������������������������������������������������  679 55.2 Clinical Presentations���������������������������������������������������������������������������������������  680 55.3 Imaging Features���������������������������������������������������������������������������������������������  681 55.4 Treatment Options and Prognosis �������������������������������������������������������������������  683 Further Reading ���������������������������������������������������������������������������������������������������������  683 56 Arachnoiditis Ossificans�������������������������������������������������������������������������������������������  685 56.1 Generalities and Relevance �����������������������������������������������������������������������������  685 56.2 Clinical Presentations���������������������������������������������������������������������������������������  685 56.3 Imaging Features���������������������������������������������������������������������������������������������  686 56.4 Treatment Options and Prognosis �������������������������������������������������������������������  687 Further Reading ���������������������������������������������������������������������������������������������������������  687 57 Bertolotti’s Syndrome�����������������������������������������������������������������������������������������������  689 57.1 Generalities and Relevance �����������������������������������������������������������������������������  689 57.2 Clinical Presentations���������������������������������������������������������������������������������������  690 57.3 Paraclinic Features�������������������������������������������������������������������������������������������  690 57.4 Treatment Options and Prognosis �������������������������������������������������������������������  695 Further Reading ���������������������������������������������������������������������������������������������������������  696 58 De  Anquin’s Disease (Spinous Engagement Syndrome)���������������������������������������  697 58.1 Generalities and Relevance �����������������������������������������������������������������������������  697 58.2 Clinical Presentations���������������������������������������������������������������������������������������  698 58.3 Imaging Features���������������������������������������������������������������������������������������������  698 58.4 Treatment Options and Prognosis �������������������������������������������������������������������  699 Further Reading ���������������������������������������������������������������������������������������������������������  700 59 Lumbosacral  Conjoined Nerve Roots���������������������������������������������������������������������  701 59.1 Generalities and Relevance �����������������������������������������������������������������������������  701 59.2 Clinical Presentations���������������������������������������������������������������������������������������  702 59.3 Imaging Features���������������������������������������������������������������������������������������������  702 59.4 Treatment Options and Prognosis �������������������������������������������������������������������  706 Further Reading ���������������������������������������������������������������������������������������������������������  707

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60 Tethered  Spinal Cord Syndrome�����������������������������������������������������������������������������  709 60.1 Generalities and Relevance �����������������������������������������������������������������������������  709 60.2 Clinical Presentations���������������������������������������������������������������������������������������  714 60.3 Imaging Features���������������������������������������������������������������������������������������������  715 60.4 Treatment Options and Prognosis �������������������������������������������������������������������  717 Further Reading ���������������������������������������������������������������������������������������������������������  718 61 Ventriculus Terminalis (Fifth Ventricle)�����������������������������������������������������������������  721 61.1 Generalities and Relevance �����������������������������������������������������������������������������  721 61.2 Clinical Presentations���������������������������������������������������������������������������������������  721 61.3 Imaging Features���������������������������������������������������������������������������������������������  722 61.4 Treatment Options and Prognosis �������������������������������������������������������������������  723 Further Reading ���������������������������������������������������������������������������������������������������������  723 62 Spinal Dural Ectasia�������������������������������������������������������������������������������������������������  725 62.1 Generalities and Relevance �����������������������������������������������������������������������������  725 62.2 Clinical Presentations���������������������������������������������������������������������������������������  726 62.3 Imaging Features���������������������������������������������������������������������������������������������  726 62.4 Treatment Options and Prognosis �������������������������������������������������������������������  727 Further Reading ���������������������������������������������������������������������������������������������������������  727 63 Spinal Arachnoid Cysts �������������������������������������������������������������������������������������������  729 63.1 Definition and Relevance���������������������������������������������������������������������������������  729 63.2 Clinical Presentations���������������������������������������������������������������������������������������  729 63.3 Imaging Features���������������������������������������������������������������������������������������������  730 63.4 Treatment Options and Prognosis �������������������������������������������������������������������  731 Further Reading ���������������������������������������������������������������������������������������������������������  732 64 Tarlov Cysts���������������������������������������������������������������������������������������������������������������  733 64.1 Generalities and Relevance �����������������������������������������������������������������������������  733 64.2 Clinical Presentations���������������������������������������������������������������������������������������  735 64.3 Imaging Features���������������������������������������������������������������������������������������������  735 64.4 Treatment Options and Prognosis �������������������������������������������������������������������  741 Further Reading ���������������������������������������������������������������������������������������������������������  741 65 Lumbosacral  Spine Fractures and Dislocations�����������������������������������������������������  743 65.1 Generalities and Relevance �����������������������������������������������������������������������������  743 65.2 Clinical Presentations���������������������������������������������������������������������������������������  744 65.3 Paraclinic Features�������������������������������������������������������������������������������������������  744 65.4 Treatment Options and Prognosis �������������������������������������������������������������������  751 Further Reading ���������������������������������������������������������������������������������������������������������  752 66 Spinal Pathologic Fractures�������������������������������������������������������������������������������������  755 66.1 Generalities and Relevance �����������������������������������������������������������������������������  755 66.2 Clinical Presentations���������������������������������������������������������������������������������������  756 66.3 Paraclinic Features�������������������������������������������������������������������������������������������  756 66.4 Treatment Options and Prognosis �������������������������������������������������������������������  761 Further Reading ���������������������������������������������������������������������������������������������������������  762 67 Sacral Stress Fractures���������������������������������������������������������������������������������������������  763 67.1 Generalities and Relevance �����������������������������������������������������������������������������  763 67.2 Clinical Presentations���������������������������������������������������������������������������������������  764 67.3 Paraclinic Features�������������������������������������������������������������������������������������������  764 67.4 Treatment Options and Prognosis �������������������������������������������������������������������  765 Further Reading ���������������������������������������������������������������������������������������������������������  766

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68 Penetrating  Lumbosacral Spine Injuries���������������������������������������������������������������  767 68.1 Generalities and Relevance �����������������������������������������������������������������������������  767 68.2 Clinical Presentations���������������������������������������������������������������������������������������  768 68.3 Paraclinic Features�������������������������������������������������������������������������������������������  768 68.4 Treatment Options�������������������������������������������������������������������������������������������  771 68.5 Outcomes and Prognosis���������������������������������������������������������������������������������  772 Further Reading ���������������������������������������������������������������������������������������������������������  772 69 Spinal Epidural Hematomas�����������������������������������������������������������������������������������  775 69.1 Generalities and Relevance �����������������������������������������������������������������������������  775 69.2 Clinical Presentations���������������������������������������������������������������������������������������  776 69.3 Imaging Features���������������������������������������������������������������������������������������������  776 69.4 Treatment Options and Prognosis �������������������������������������������������������������������  777 Further Reading ���������������������������������������������������������������������������������������������������������  777 70 Spinal Subdural Hematomas�����������������������������������������������������������������������������������  779 70.1 Generalities and Relevance �����������������������������������������������������������������������������  779 70.2 Clinical Presentations���������������������������������������������������������������������������������������  779 70.3 Imaging Features���������������������������������������������������������������������������������������������  779 70.4 Treatment Options and Prognosis �������������������������������������������������������������������  781 Further Reading ���������������������������������������������������������������������������������������������������������  781 71 Spinal Subarachnoid Hematomas���������������������������������������������������������������������������  783 71.1 Generalities and Relevance �����������������������������������������������������������������������������  783 71.2 Clinical Presentations���������������������������������������������������������������������������������������  783 71.3 Imaging Features���������������������������������������������������������������������������������������������  784 71.4 Treatment Options and Prognosis �������������������������������������������������������������������  784 Further Reading ���������������������������������������������������������������������������������������������������������  784 72 Lumbar Epidural Varices�����������������������������������������������������������������������������������������  787 72.1 Generalities and Relevance �����������������������������������������������������������������������������  787 72.2 Clinical Presentations���������������������������������������������������������������������������������������  788 72.3 Imaging Features���������������������������������������������������������������������������������������������  788 72.4 Treatment Options and Prognosis �������������������������������������������������������������������  789 Further Reading ���������������������������������������������������������������������������������������������������������  789 73 Ligamentum Flavum Hematomas���������������������������������������������������������������������������  791 73.1 Generalities and Relevance �����������������������������������������������������������������������������  791 73.2 Clinical Presentations���������������������������������������������������������������������������������������  791 73.3 Imaging Features���������������������������������������������������������������������������������������������  791 73.4 Treatment Options and Prognosis �������������������������������������������������������������������  792 Further Reading ���������������������������������������������������������������������������������������������������������  793 74 Spinal Cavernous Angioma (Cavernoma)���������������������������������������������������������������  795 74.1 Generalities and Relevance �����������������������������������������������������������������������������  795 74.2 Clinical Presentations���������������������������������������������������������������������������������������  795 74.3 Paraclinic Features�������������������������������������������������������������������������������������������  796 74.4 Treatment Options and Prognosis �������������������������������������������������������������������  798 Further Reading ���������������������������������������������������������������������������������������������������������  798 75 Spinal Hygromas�������������������������������������������������������������������������������������������������������  799 75.1 Generalities End Relevance�����������������������������������������������������������������������������  799 75.2 Clinical Presentations���������������������������������������������������������������������������������������  799 75.3 Imaging Features���������������������������������������������������������������������������������������������  799 75.4 Treatment Options and Prognosis �������������������������������������������������������������������  799 Further Reading ���������������������������������������������������������������������������������������������������������  800

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76 Postoperative  Spinal Etiologies of Sciatica�������������������������������������������������������������  801 76.1 Generalities and Relevance �����������������������������������������������������������������������������  801 76.2 Clinical Presentations���������������������������������������������������������������������������������������  821 76.3 Paraclinic Evaluations�������������������������������������������������������������������������������������  822 76.4 Treatment Options�������������������������������������������������������������������������������������������  822 76.5 Outcome and Prognosis�����������������������������������������������������������������������������������  823 Further Reading ���������������������������������������������������������������������������������������������������������  823 77 Extradural  Fibrous Entrapment of Lumbosacral Nerve Roots���������������������������  825 77.1 Generalities and Relevance �����������������������������������������������������������������������������  825 77.2 Clinical Presentations���������������������������������������������������������������������������������������  825 77.3 Imaging Features���������������������������������������������������������������������������������������������  825 77.4 Treatment Options and Prognosis �������������������������������������������������������������������  825 Further Reading ���������������������������������������������������������������������������������������������������������  826 78 Nerve  Roots Herniation and Entrapment���������������������������������������������������������������  827 78.1 Generalities and Relevance �����������������������������������������������������������������������������  827 78.2 Clinical Presentations���������������������������������������������������������������������������������������  831 78.3 Imaging Features���������������������������������������������������������������������������������������������  831 78.4 Treatment Options and Prognosis �������������������������������������������������������������������  831 Further Reading ���������������������������������������������������������������������������������������������������������  832 79 Synovial  Cysts of the Facet Joints���������������������������������������������������������������������������  835 79.1 Generalities and Relevance �����������������������������������������������������������������������������  835 79.2 Clinical Presentations���������������������������������������������������������������������������������������  836 79.3 Imaging Features���������������������������������������������������������������������������������������������  836 79.4 Treatment Options and Prognosis �������������������������������������������������������������������  842 Further Reading ���������������������������������������������������������������������������������������������������������  843 80 Ligamentum  Flavum Cystic Lesions�����������������������������������������������������������������������  845 80.1 Generalities and Relevance �����������������������������������������������������������������������������  845 80.2 Clinical Presentations���������������������������������������������������������������������������������������  845 80.3 Imaging Features���������������������������������������������������������������������������������������������  845 80.4 Treatment Options and Prognosis �������������������������������������������������������������������  848 Further Reading ���������������������������������������������������������������������������������������������������������  849 81 Ligamentum Flavum Ossifications�������������������������������������������������������������������������  851 81.1 Generalities and Relevance �����������������������������������������������������������������������������  851 81.2 Clinical Presentations���������������������������������������������������������������������������������������  851 81.3 Imaging Features���������������������������������������������������������������������������������������������  852 81.4 Treatment Options and Prognosis �������������������������������������������������������������������  854 Further Reading ���������������������������������������������������������������������������������������������������������  854 82 Posterior  Longitudinal Ligament Cysts�����������������������������������������������������������������  857 82.1 Generalities and Relevance �����������������������������������������������������������������������������  857 82.2 Clinical Presentations���������������������������������������������������������������������������������������  857 82.3 Imaging Features���������������������������������������������������������������������������������������������  858 82.4 Treatment Options and Prognosis �������������������������������������������������������������������  859 Further Reading ���������������������������������������������������������������������������������������������������������  859 83 Posterior  Longitudinal Ligament Ossifications�����������������������������������������������������  861 83.1 Generalities and Relevance �����������������������������������������������������������������������������  861 83.2 Clinical Presentations���������������������������������������������������������������������������������������  861 83.3 Imaging Features���������������������������������������������������������������������������������������������  861 83.4 Treatment Options and Prognosis �������������������������������������������������������������������  866 Further Reading ���������������������������������������������������������������������������������������������������������  867

Contents

Contents

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84 Baastrup Disease�������������������������������������������������������������������������������������������������������  869 84.1 Generalities and Relevance �����������������������������������������������������������������������������  869 84.2 Clinical Presentations���������������������������������������������������������������������������������������  870 84.3 Imaging Features���������������������������������������������������������������������������������������������  870 84.4 Treatment Options and Prognosis �������������������������������������������������������������������  873 Further Reading ���������������������������������������������������������������������������������������������������������  874 85 Spinal  Epidural Gas Pseudocysts ���������������������������������������������������������������������������  875 85.1 Generalities and Relevance �����������������������������������������������������������������������������  875 85.2 Clinical Presentations���������������������������������������������������������������������������������������  875 85.3 Imaging Features���������������������������������������������������������������������������������������������  875 85.4 Treatment Options and Prognosis �������������������������������������������������������������������  879 Further Reading ���������������������������������������������������������������������������������������������������������  879 Part IV Extraspinal Intrapelvic Sciatica 86 Sciatic Lumbosacral Plexopathies���������������������������������������������������������������������������  883 86.1 Generalities and Relevance �����������������������������������������������������������������������������  883 86.2 Etiologies���������������������������������������������������������������������������������������������������������  884 86.3 Clinical Presentations���������������������������������������������������������������������������������������  889 86.4 Paraclinic Features�������������������������������������������������������������������������������������������  889 86.5 Treatment Options and Prognosis �������������������������������������������������������������������  890 Further Reading ���������������������������������������������������������������������������������������������������������  890 87 Abdominopelvic and Retroperitoneal Tumors�������������������������������������������������������  893 87.1 Generalities and Relevance �����������������������������������������������������������������������������  893 87.2 Clinical Presentations���������������������������������������������������������������������������������������  898 87.3 Paraclinic Features�������������������������������������������������������������������������������������������  899 87.4 Treatment Options�������������������������������������������������������������������������������������������  900 87.5 Prognosis���������������������������������������������������������������������������������������������������������  900 Further Reading ���������������������������������������������������������������������������������������������������������  900 88 Intrapelvic  and Retroperitoneal Vascular Lesions �����������������������������������������������  903 88.1 Generalities and Relevance �����������������������������������������������������������������������������  903 88.2 Clinical Presentations���������������������������������������������������������������������������������������  904 88.3 Paraclinic Features�������������������������������������������������������������������������������������������  904 88.4 Treatment Options�������������������������������������������������������������������������������������������  905 88.5 Outcome and Prognosis�����������������������������������������������������������������������������������  905 Further Reading ���������������������������������������������������������������������������������������������������������  905 89 Pelvic  and Intrapelvic Infections�����������������������������������������������������������������������������  907 89.1 Definition and Relevance���������������������������������������������������������������������������������  907 89.2 Clinical Presentations���������������������������������������������������������������������������������������  908 89.3 Imaging Features���������������������������������������������������������������������������������������������  908 89.4 Laboratory Findings�����������������������������������������������������������������������������������������  912 89.5 Treatment Options and Prognosis �������������������������������������������������������������������  912 Further Reading ���������������������������������������������������������������������������������������������������������  913 90 Non-discogenic  Sciatica in Pregnancy���������������������������������������������������������������������  915 90.1 Generalities and Relevance �����������������������������������������������������������������������������  915 90.2 Clinical Presentations���������������������������������������������������������������������������������������  916 90.3 Imaging Features���������������������������������������������������������������������������������������������  916 90.4 Treatment Options�������������������������������������������������������������������������������������������  916 Further Reading ���������������������������������������������������������������������������������������������������������  917

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91 Sciatic Endometriosis�����������������������������������������������������������������������������������������������  919 91.1 Generalities and Relevance �����������������������������������������������������������������������������  919 91.2 Clinical Presentations���������������������������������������������������������������������������������������  920 91.3 Paraclinic Features�������������������������������������������������������������������������������������������  920 91.4 Treatment Options�������������������������������������������������������������������������������������������  921 91.5 Prognosis���������������������������������������������������������������������������������������������������������  922 Further Reading ���������������������������������������������������������������������������������������������������������  922 92 Sacroiliac Joint Disorders ���������������������������������������������������������������������������������������  923 92.1 Generalities and Relevance �����������������������������������������������������������������������������  923 92.2 Clinical Presentations���������������������������������������������������������������������������������������  929 92.3 Paraclinic Features�������������������������������������������������������������������������������������������  932 92.4 Treatment Options and Prognosis �������������������������������������������������������������������  932 Further Reading ���������������������������������������������������������������������������������������������������������  932 93 Sciatic Hernias�����������������������������������������������������������������������������������������������������������  935 93.1 Generalities and Relevance �����������������������������������������������������������������������������  935 93.2 Clinical Presentations���������������������������������������������������������������������������������������  936 93.3 Paraclinic Features�������������������������������������������������������������������������������������������  936 93.4 Treatment Options and Prognosis �������������������������������������������������������������������  937 Further Reading ���������������������������������������������������������������������������������������������������������  937 Part V Extraspinal Extrapelvic Sciatica 94 Sciatic Peripheral Neuropathies �����������������������������������������������������������������������������  941 94.1 Generalities and Relevance �����������������������������������������������������������������������������  941 94.2 Etiologies���������������������������������������������������������������������������������������������������������  941 94.3 Clinic Presentations�����������������������������������������������������������������������������������������  944 94.4 Paraclinic Features�������������������������������������������������������������������������������������������  944 94.5 Treatment Options and Prognosis �������������������������������������������������������������������  945 Further Reading ���������������������������������������������������������������������������������������������������������  945 95 Deep  Gluteal Syndrome (Including Piriformis Syndrome)�����������������������������������  947 95.1 Generalities and Relevance �����������������������������������������������������������������������������  947 95.2 Clinical Presentations���������������������������������������������������������������������������������������  950 95.3 Paraclinic Features�������������������������������������������������������������������������������������������  951 95.4 Treatment Options and Prognosis �������������������������������������������������������������������  952 Further Reading ���������������������������������������������������������������������������������������������������������  953 96 Gluteal Intramuscular Injections ���������������������������������������������������������������������������  955 96.1 Generalities and Relevance �����������������������������������������������������������������������������  955 96.2 Clinical Presentations���������������������������������������������������������������������������������������  955 96.3 Paraclinic Features�������������������������������������������������������������������������������������������  956 96.4 Treatment Options and Prognosis �������������������������������������������������������������������  956 96.5 Prevention �������������������������������������������������������������������������������������������������������  956 Further Reading ���������������������������������������������������������������������������������������������������������  957 97 Prolonged  Immobilization and Incorrect Positioning�������������������������������������������  959 97.1 Generalities and Relevance �����������������������������������������������������������������������������  959 97.2 Clinical Presentations���������������������������������������������������������������������������������������  961 97.3 Paraclinic Features�������������������������������������������������������������������������������������������  961 97.4 Treatment Options�������������������������������������������������������������������������������������������  961 97.5 Prognosis���������������������������������������������������������������������������������������������������������  962 Further Reading ���������������������������������������������������������������������������������������������������������  962

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98 Lower  Limb Compartment Syndromes�����������������������������������������������������������������  963 98.1 Generalities and Relevance �����������������������������������������������������������������������������  963 98.2 Clinical Presentations���������������������������������������������������������������������������������������  964 98.3 Paraclinic Features�������������������������������������������������������������������������������������������  964 98.4 Treatment Options�������������������������������������������������������������������������������������������  964 98.5 Outcomes and Prognosis���������������������������������������������������������������������������������  965 Further Reading ���������������������������������������������������������������������������������������������������������  965 99 Traumatic  Sciatic Nerve Lesions�����������������������������������������������������������������������������  967 99.1 Generalities and Relevance �����������������������������������������������������������������������������  967 99.2 Clinical Presentations���������������������������������������������������������������������������������������  968 99.3 Paraclinic Features�������������������������������������������������������������������������������������������  970 99.4 Treatment Options�������������������������������������������������������������������������������������������  970 99.5 Outcomes and Prognosis���������������������������������������������������������������������������������  970 Further Reading ���������������������������������������������������������������������������������������������������������  971 100 Heterotopic Ossification Around the Hip Joint�����������������������������������������������������  973 100.1 Generalities and Relevance �����������������������������������������������������������������������������  973 100.2 Clinical Presentations���������������������������������������������������������������������������������������  974 100.3 Paraclinic Features�������������������������������������������������������������������������������������������  974 100.4 Treatment Options and Prognosis �������������������������������������������������������������������  975 Further Reading ���������������������������������������������������������������������������������������������������������  976 101 Extrapelvic Musculoskeletal and Soft Tissues Tumors�����������������������������������������  977 101.1 Generalities and Relevance �����������������������������������������������������������������������������  977 101.2 Clinical Presentations���������������������������������������������������������������������������������������  978 101.3 Paraclinic Features�������������������������������������������������������������������������������������������  978 101.4 Treatment Options�������������������������������������������������������������������������������������������  984 101.5 Prognosis���������������������������������������������������������������������������������������������������������  984 Further Reading ���������������������������������������������������������������������������������������������������������  984 102 Intrinsic Tumors of the Sciatic Nerve���������������������������������������������������������������������  987 102.1 Generalities and Relevance �����������������������������������������������������������������������������  987 102.2 Clinical Presentations���������������������������������������������������������������������������������������  988 102.3 Paraclinic Features�������������������������������������������������������������������������������������������  988 102.4 Treatment Options�������������������������������������������������������������������������������������������  990 102.5 Prognosis���������������������������������������������������������������������������������������������������������  990 Further Reading ���������������������������������������������������������������������������������������������������������  990 103 Extrapelvic Ganglion and Synovial Cysts���������������������������������������������������������������  993 103.1 Generalities and Relevance �����������������������������������������������������������������������������  993 103.2 Clinical Presentations���������������������������������������������������������������������������������������  993 103.3 Imaging Features���������������������������������������������������������������������������������������������  994 103.4 Treatment Options and Prognosis �������������������������������������������������������������������  994 Further Reading ���������������������������������������������������������������������������������������������������������  995 104 Extrapelvic Vascular Lesions�����������������������������������������������������������������������������������  997 104.1 Generalities and Relevance �����������������������������������������������������������������������������  997 104.1.1 Persistent Sciatic Artery Aneurysm �������������������������������������������������  997 104.1.2 Gluteal Artery Aneurysms and Pseudoaneurysms���������������������������  998 104.1.3 Gluteal Venous Varicosities �������������������������������������������������������������  998 104.2 Clinical Presentations���������������������������������������������������������������������������������������  998 104.3 Paraclinic Features�������������������������������������������������������������������������������������������  998 104.4 Treatment Options�������������������������������������������������������������������������������������������  999 104.5 Outcome and Prognosis����������������������������������������������������������������������������������� 1000 Further Reading ��������������������������������������������������������������������������������������������������������� 1000

xxx

105 Extrapelvic Hematomas������������������������������������������������������������������������������������������� 1001 105.1 Generalities and Relevance ����������������������������������������������������������������������������� 1001 105.2 Clinical Presentations��������������������������������������������������������������������������������������� 1001 105.3 Paraclinic Features������������������������������������������������������������������������������������������� 1002 105.4 Treatment Options������������������������������������������������������������������������������������������� 1002 105.5 Outcome and Prognosis����������������������������������������������������������������������������������� 1003 Further Reading ��������������������������������������������������������������������������������������������������������� 1003 106 Common Peroneal Nerve Entrapment������������������������������������������������������������������� 1005 106.1 Generalities and Relevance ����������������������������������������������������������������������������� 1005 106.2 Clinical Presentations��������������������������������������������������������������������������������������� 1006 106.3 Paraclinic Features������������������������������������������������������������������������������������������� 1007 106.4 Treatment Options and Prognosis ������������������������������������������������������������������� 1008 Further Reading ��������������������������������������������������������������������������������������������������������� 1008 107 Herpes Zoster Virus (Shingles) Infection��������������������������������������������������������������� 1011 107.1 Generalities and Relevance ����������������������������������������������������������������������������� 1011 107.2 Clinical Presentations��������������������������������������������������������������������������������������� 1011 107.3 Paraclinic Features������������������������������������������������������������������������������������������� 1013 107.4 Treatment Options and Prognosis ������������������������������������������������������������������� 1013 Further Reading ��������������������������������������������������������������������������������������������������������� 1014 108 Decompression Sickness������������������������������������������������������������������������������������������� 1015 108.1 Generalities and Relevance ����������������������������������������������������������������������������� 1015 108.2 Clinical Presentations��������������������������������������������������������������������������������������� 1016 108.3 Paraclinic Features������������������������������������������������������������������������������������������� 1016 108.4 Treatment Options and Prognosis ������������������������������������������������������������������� 1016 Further Reading ��������������������������������������������������������������������������������������������������������� 1017 109 Sciatic Double Crush Syndrome Involving Different Sites����������������������������������� 1019 109.1 Generalities and Relevance ����������������������������������������������������������������������������� 1019 109.2 Clinical Presentations��������������������������������������������������������������������������������������� 1020 109.3 Paraclinic Features������������������������������������������������������������������������������������������� 1020 109.4 Treatment Options and Prognosis ������������������������������������������������������������������� 1021 Further Reading ��������������������������������������������������������������������������������������������������������� 1021 110 Phantom Sciatic Pain����������������������������������������������������������������������������������������������� 1023 110.1 Generalities and Relevance ����������������������������������������������������������������������������� 1023 110.2 Clinical Presentations��������������������������������������������������������������������������������������� 1024 110.3 Imaging Features��������������������������������������������������������������������������������������������� 1024 110.4 Treatment Options and Prognosis ������������������������������������������������������������������� 1025 Further Reading ��������������������������������������������������������������������������������������������������������� 1025 111 Intracranial Funicular Sciatica������������������������������������������������������������������������������� 1027 111.1 Generalities and Relevance ����������������������������������������������������������������������������� 1027 111.2 Clinical Presentations��������������������������������������������������������������������������������������� 1029 111.3 Imaging Features��������������������������������������������������������������������������������������������� 1029 111.4 Treatment Options and Prognosis ������������������������������������������������������������������� 1032 Further Reading ��������������������������������������������������������������������������������������������������������� 1033 Index����������������������������������������������������������������������������������������������������������������������������������� 1035

Contents

About the Author

Ali Akhaddar, M.D., IFAANS  This book is authored and edited by Ali Akhaddar, MD, IFAANS, who is a Full Professor of Neurosurgery at the Medical School, Mohammed V University in Rabat (Morocco) and Head of the Department of Neurosurgery at Avicenne Military Hospital of Marrakech (Morocco) since 2013. He received his MD degree (1997) and completed his neurosurgical residency (2003) at the Medical School of Mohammed V University in Rabat. During his training, he spent 1 year at the Department of Neurosurgery of Angers University Hospital (France). He was an Expert Member of the Scientific Committees of the National Scientific and Technological Research Center of Morocco (CNRST) from 2011 to 2017. Dr. Akhaddar is an International Fellow of the American Association of Neurological Surgeons (AANS), a member of the Congress of Neurological Surgeons (CNS), and the French-speaking Society of Neurosurgery (SNCLF). His fields of expertise and research interests include central nervous system infections, spinal surgery, pituitary tumors, stereotactic surgery, history of medicine, and medical writing. Professor Akhaddar has received many awards during his career, including from the Moroccan Society of Neurosurgery (2007), the World Federation of Neurosurgical Societies [Traveling Fellowship Award: Nagoya 2007, Boston 2009 and Seoul 2013], the University of Mohammed V in Rabat (2011 and 2017), and the French Society of Hospitals’ History (SFHH) (2014). In 2020, he was awarded the COMSTECH Best Scientific Book Award by the Organisation of Islamic Cooperation (OIC) in Islamabad (Pakistan) for his book entitled Atlas of Infections in Neurosurgery and Spinal Surgery. Dr. Akhaddar is the Associate Editor-in-Chief of Surgical Neurology International [Infection] and a reviewer for a number of well-respected medical journals. He has authored and edited 14 previous books (including 7 with Springer-Nature and 1 translated into Chinese). He is also the author of more than 350 papers published in peer-reviewed journals [197 papers indexed in PubMed* and 254 indexed in Scopus* (Author ID: 22978603700), ORCID iD: http://orcid.org/0000-­0001-­5743-­2777] and more than 40 book chapters. Books authored and co-edited by Springer: • • • • • • • •

Cranial Osteomyelitis. A Akhaddar. 2016 Tuberculosis of the Central Nervous System. M Turgut, A Akhaddar, AT Turgut, RK Garg. 2017 Atlas of Infections in Neurosurgery and Spinal Surgery. A Akhaddar. 2017 Fungal Infections of the Central Nervous System. M Turgut, S Challa, A Akhaddar. 2019 Subdural Hematoma. M Turgut, A Akhaddar, WA Hall, AT Turgut. 2021 Arachnoid Cysts. M Turgut, A Akhaddar, AT Turgut, WA Hall. 2023 The present book: Atlas of Sciatica. A Akhaddar. 2024 Lesions of the Scalp and Cranial Vault. M Turgut, A Akhaddar, AT Turgut, WA Hall. In Progress

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Abbreviations

? Unknown AD Anno Domini in Latin (in the year of our Lord) ADC Apparent diffusion coefficient AKA Also known as AKSP Ankylosing spondylitis ARLDH Anterior retroperitoneal lumbar disc herniation AVF Arteriovenous fistulae AVM Arteriovenous malformation BC Before Christ c.f. confer in Latin (referring to) CES Cauda equina syndrome CISS Constructive interference in steady state (sequence) CML Conus medullaris lesion CNR Conjoined nerve root CPNE Common peroneal nerve entrapment CRP C-reactive protein CSF Cerebrospinal fluid CT Computed tomography CTA Computed tomographic angiography DAS De Anquin’s disease (or spinous engagement syndrome) DCS Double crush syndrome DEXA Dual-energy X-ray absorptiometry DGS Deep gluteal syndrome DISH Diffuse idiopathic skeletal hyperostosis (Forestier’s disease) DNA Deoxyribonucleic acid DS Decompression sickness DWI Diffusion weighted image (sequence) e.g. Exempli gratia in Latin (for example) EMG Electromyogram ENVT Epidural non-vertebral tumor EOG Eosinophilic granuloma ESR Erythrocyte sedimentation rate FAIR Hip flexion, adduction, and internal rotation (test) FDG-PET Fluorodeoxyglucose-positron emission tomography FELDH Extraforaminal and foraminal lumbar disc herniation Fig. Figure FLAIR Fluid attenuated inversion recovery (sequence) GABA Gamma-aminobutyric acid GArt Gluteal artery GILID Giant lumbar intervertebral disc herniation GIMIJ Gluteal intramuscular injection GSW Gunshot wounds xxxiii

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HE HIV HOS HSV i.e. IDEA IDET IDLSTum INGC L LCH LDH LEV LF LFO LSES LSFD LSS LSTum LSTV MALDH MigLDH MODAL MPNST MPR MR MRA MRI n.a NAP NCV NDA NF-1 NII NSAID OPLL PCR PEMLIF PLDD PLL PLN PLP PRAS PSA PVNS RAR R-LDH ROM S SeqLDH SLR SpCA SPECT

Abbreviations

Hematoxylin and eosin stain Human immunodeficiency virus Heterotopic ossification Herpes simplex virus Id est in Latin (that is) Intradiscal electrothermal annuloplasty Intradiscal endothermal therapy Intradural lumbosacral tumors Intraneural ganglionic cyst Lumbar vertebra Langerhans cell histiocytosis Lumbar disc herniation Lumbar epidural varices Ligamentum flavum Ligamentum flavum ossification Lumbosacral extraforaminal stenosis Lumbosacral spine fractures and dislocations Lumbar spinal stenosis Lumbosacral spinal tumors Lumbosacral transitional vertebra Massive lumbar disc herniation Migrated lumbar disc herniation Musculo-Osteo-Disco-Articular-Ligament complex Malignant peripheral nerve sheath tumor Multiplanar reconstructions Magnetic resonance Magnetic resonance angiography Magnetic resonance imaging Not available Nerve action potential Nerve conduction velocity No Data Available Neurofibromatosis type 1 Nerve injection injury Non-steroidal anti-inflammatory drug Ossification of the posterior longitudinal ligament Polymerase chain reaction Posterior epidural migration of lumbar intervertebral disc fragment Percutaneous laser disc decompression Posterior longitudinal ligament Percutaneous lumbar nucleoplasty Phantom limb pain Posterior ring apophysis separation Persistent sciatic artery Pigmented villonodular synovitis Rheumatoid arthritis Recurrent lumbar disc herniation Range-of-motion (exercise) Sacral vertebra Sequestrated lumbar disc herniation Straight leg raising Spinal cavernous angioma Single photon emission computed tomography

Abbreviations

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SPF SPINO SSF STIR TNF TSCS VTER VZV WHO

Spinal pathologic fractures Sciatic Pain In Name Only Sacral stress fractures Short tau inversion recovery (sequence) Tumor necrosis factor Tethered spinal cord syndrome Ventriculus terminalis Varicella Zoster Virus World Health Organization

Part I General Considerations

1

Definitions of Sciatica

“Language is the source of all misunderstandings” Antoine de Saint-Exupéry [1900–1944, French writer and aviator]

1.1 Origin of the Term “Sciatica” The word “sciatica” is associated with the “sciatic nerve,” which is related to the anatomic region of the hip. The name “hip” refers to “ischia/ischiaticus” in Latin. The suffix “ica” indicates a disability of the “ischia.” With time, the vowel “i” was deleted in the everyday language so that only the word “sciatica” remains. “Ischia” derives also from the antique Greek ισχία and “ischiadikos.” The oldest use of the term “ischiacos” probably dates back to the fifth-century BC by the Hellenic Hippocrates of Kos [460–377 BC] (c.f. Chap. 2 about Historical Aspects of Sciatica). According to the Online Etymology Dictionary, the word “sciatica” comes from Medieval Latin sciaticus [sciatic], a corruption of Latin ischiadicus [of pain in the hip], from Greek iskhiadikos, from iskhias (genitive iskhiados) [pain in the hips], from iskhion [hip joint]. The word “ischialgia” from the Greek ischion [hip] and algos [pain] meaning pain in the hip is an obsolete term but still nowadays used by some German, Polish, and Russian authors to describe true sciatic pain. Interestingly, pain in the region of the ischium is currently named “ischiodynia.” Sciatic pain has long been wrongly attributed to the “hip” because the “buttock” (AKA gluteal area) is the most generally painful region in radicular sciatica, sometimes even more common and severe than low back pain. Indeed, L5 and S1 radiculopathy usually show symptoms at the upper and lower buttock areas, respectively. “Scelalgia” is another old term signifying leg pain from the Greek skelos [leg] and algos [pain] for “pain in the leg.” Nevertheless, this word is now obsolete and very rarely used in working medical language.

Anatomically speaking, the sciatic nerve is also called the ischiadic nerve, the ischiatic nerve, or nervus ischiadicus in Latin terminology.

1.2 Definitions of the Term “Sciatica” Webster’s dictionary defines sciatica as “pain along the course of a sciatic nerve or its branches and especially in the leg caused by compression, inflammation, or reflex mechanisms; broadly: pain in the lower back, buttocks, hips, or adjacent parts—not used technically.” Dorland’s medical dictionary defines sciatica as “pain along the course of the sciatic nerve, usually a neuritis. It is attended with paresthesia of the thigh and leg, tenderness along the course of the nerve, and sometimes by wasting of the calf muscle.” According to the Oxford Medical Dictionary, sciatica is “pain radiating from the buttock into the thigh, calf, and occasionally the foot. Although it is in the distribution of the sciatic nerve, sciatica is rarely due to disease of this nerve. Pain felt down the back and lateral aspect of the thigh, leg, and foot is often caused by degeneration or displacement of an intervertebral disk, which encroaches upon and irritates a lower lumbar or an upper sacral spinal nerve root.” For many scholars, sciatica is specific to the pain, and/or paresthesia, which is a direct result of the sciatic nerve root (L4 to S3) or sciatic nerve (the largest nerve of the body) irritation. Most cases of sciatica result from an inflammatory or mechanical condition. “Sciatica” is not a disease, even if, for a long time, physicians have considered this neuropathic pain as an illness.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_1

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Despite these definitions and the evolution of ideas (c.f. Chap. 2 about Historical Aspects of Sciatica) (Fig. 1.1), there is sometimes some confusion between sciatic pain and other pains “radiating” from the low back somewhere down in the lower extremity such as femoral neuralgia and cruralgia. In addition, it is occasionally difficult to clearly distinguish between sciatica and lower limb pain “referred” from the low back. In this context, other various terms have been proposed and used, in particular: • • • • • • •

Sciatic pain Sciatic neuralgia Sciatic neuropathy Lumbar radicular pain Lumbar radiculopathy Lumbosacral radicular pain Lumbosacral radiculitis

• • • • • • •

Lumbosacral radicular syndrome Radicular leg pain Ischiadic pain Ischiatic pain Cotunnius disease Cotugno’s syndrome Cotugno’s disease

For some authors, lumbosacral radicular pain remains the more appropriate term for sciatica secondary to lumbar disk herniation (namely discogenic sciatica). Finally, after reading the literature there is still a lack of agreement between patients, between patients and doctors, and even among doctors themselves on generally used “sciatica” and “sciatic pain” terminologies (Fig. 1.1). This certainly poses difficulties in the management of some patients suffering from this symptomatic disorder.

Fig. 1.1  Word cloud: Translating the word “Sciatica” in different current languages

Further Reading

Further Reading Aguilar-Shea AL, Gallardo-Mayo C, Sanz-González R, Paredes I.  Sciatica. Management for family physicians. J Family Med Prim Care. 2022;11:4174–9. https://doi.org/10.4103/jfmpc. jfmpc_1061_21. Alter R. Genesis, translation and commentary. New York: WW Norton; 1996. Genesis 31/3–5:166. Genesis 32/24–33 with footnoting: 180–3. Aygen G, Karasu A, Ofluoglu AE, Pait G, Toplamaoglu H.  The first Anatolian contribution to treatment of sciatica by Serefeddin Sabuncuoglu in the 15th century. Surg Neurol. 2009;71:130–3. https://doi.org/10.1016/j.surneu.2007.09.007. Bequeathed to Francesco Melzi; from whose heirs purchased by Pompeo Leoni, c.1582–90; Thomas Howard, 14th Earl of Arundel, by 1630; Probably acquired by Charles II; Royal Collection by 1690. Cotugno D.  De Ischiade Nervosa Commentarius. Napoli: Fratres Simonii; 1764. Cowan J.  The relation of sciatica to the sacro-iliac joint. Br Med J. 1923;1(3244):372–3. https://doi.org/10.1136/bmj.1.3244.372. Deyo RA, Mirza SK. Clinical practice. Herniated lumbar intervertebral disk. N Engl J Med. 2016;374:1763–72. https://doi.org/10.1056/ NEJMcp1512658. Dyck P.  Lumbar nerve root: the enigmatic eponyms. Spine (Phila Pa 1976). 1984;9:3–6. https://doi.org/10.1097/00007632-­ 198401000-­00003. Fairbank JC. Sciatic: an archaic term. BMJ. 2007;335:112. https://doi. org/10.1136/bmj.39275.951343.BE. Fardon D. Biblical pain: did Jacob have sciatica? Spine J. 2002;2:228. https://doi.org/10.1016/s1529-­9430(02)00172-­9. Fourré A, Monnier F, Ris L, Telliez F, Michielsen J, Roussel N, et al. Low-back related leg pain: is the nerve guilty? How to differentiate the underlying pain mechanism. J Man Manip Ther. 2023;31:57–63. https://doi.org/10.1080/10669817.2022.2092266. Freiburg AH, Vinke TA. Sciatica and the sacroiliac joint. J Bone Joint Surg Am. 1934;16-A:126–36. Hashemi M, Halabchi F.  Changing concept of sciatica: a historical overview. Iran Red Crescent Med J. 2016;18:e21132. https://doi. org/10.5812/ircmj.21132. Hippocrates. The genuine works of Hippocrates. Translated by Adams Francis from the Greek with a preliminary discourse and annotations. New York: William Wood and Company; 1929. Hoenig LJ.  Jacob’s limp. Semin Arthritis Rheum. 1997;26:684–8. https://doi.org/10.1016/s0049-­0172(97)80004-­2. Karampelas I, Boev AN III, Fountas KN, Robinson JS Jr. Sciatica: a historical perspective on early views of a distinct medical syn-

5 drome. Neurosurg Focus. 2004;16:E6. https://doi.org/10.3171/ foc.2004.16.1.7. Konstantinou K, Dunn KM. Sciatica: review of epidemiological studies and prevalence estimates. Spine (Phila Pa 1976). 2008;33:2464–72. https://doi.org/10.1097/BRS.0b013e318183a4a2. Kuraishi K, Hanakita J, Takahashi T, Minami M, Watanabe M, Uesaka T, et al. Study on the area of pain and numbness in cases with lumbosacral radiculopathy. No Shinkei Geka. 2012;40:877–85. Law J, Martin E. Concise medical dictionary (Oxford quick reference). 10th ed. Oxford, UK: Oxford University Press; 2020. Minaee B, Abbassian A, Nasrabadi AN, Rostamian A.  Prognostic factors of sciatica in the Canon of Avicenna. Rheumatol Int. 2013;33:3095–6. https://doi.org/10.1007/ s00296-­0 12-­2 574-­2 . Missori P, Domenicucci M, Currà A. Bloodletting from the ankle vein to treat sciatic pain. Pain Med. 2015;16:30–6. https://doi.org/10.1111/ pme.12445. Postacchini F. Presidential lecture, European Spine Society, 1995. The role of Europe in the spine—past and future perspectives. Eur Spine J. 1995;4:323–6. https://doi.org/10.1007/BF00300290. Robinson JS.  Sciatica and the lumbar disk syndrome: a historic perspective. South Med J. 1983;76:232–8. https://doi. org/10.1097/00007611-­198302000-­00022. Schmid AB, Tampin B, Baron R, Finnerup NB, Hansson P, Hietaharju A, et al. Recommendations for terminology and the identification of neuropathic pain in people with spine-related leg pain. Outcomes from the NeuPSIG working group. Pain. 2023;164:1693. https://doi. org/10.1097/j.pain.0000000000002919. Stafford MA, Peng P, Hill DA. Sciatica: a review of history, epidemiology, pathogenesis, and the role of epidural steroid injection in management. Br J Anaesth. 2007;99:461–73. https://doi.org/10.1093/ bja/aem238. Stynes S, Konstantinou K, Dunn KM.  Classification of patients with low back-related leg pain: a systematic review. BMC Musculoskelet Disord. 2016;17:226. https://doi.org/10.1186/ s12891-­016-­1074-­z. Sweetman BJ. The words we use: where did lumbago and sciatica come from? Int Musculoskelet Med. 2011;33(1):26–9. https://doi.org/10. 1179/175361511X12965803070865. Truumees E. A history of lumbar disc herniation from Hippocrates to the 1990s. Clin Orthop Relat Res. 2015;473:1885–95. https://doi. org/10.1007/s11999-­014-­3633-­7. Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica, with an analysis of 100 cases. Lancet. 1928;212:1119–23. https:// doi.org/10.1016/S0140-­6736(00)84887-­4. Zhang Y.  The needling technique and clinical application of point Zhibian. J Tradit Chin Med. 2004;24:182–4.

2

Historical Aspects of Sciatica

“To better understand something, you must first deep dive into its past. However, the history of medicine is too short to fully understand sciatica” A. Akhaddar [The author] “The history of sciatica is, it must be confessed, the record of pathological ignorance and therapeutic failure” Henry William Fuller [1820–1873, English physician]

2.1 Introduction From “Sciatica of Atlas” to “Atlas of Sciatica.” Tracing the history of sciatica is not easy because humans have experienced this condition since ancient times by Greek, Roman, Arabic, Jewish, and Persian physicians as evident in their manuscripts. We could say that this topic is as old as the “sciatica of Atlas,” one of the most legendary Titans in Greek mythology. Atlas was condemned by Zeus to

hold up the sky on his shoulders for eternity; Atlas would have felt pain in his lumbar and hip (Fig. 2.1)! Understanding the concept of this pain is the result of a long historical evolution, starting with the hip joint, passing through its neurogenic nature, and finally recognizing the lumbar intervertebral disks’ involvement. This process took more than 35 centuries before developing our current therapies. This chapter reviews the main historical steps in the evolution of the “sciatica concepts” from ancient eras to modern times.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_2

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a

b

Fig. 2.1  Atlas the legendary Titan in Greek mythology. He was condemned to hold up the heavens or the sky on his shoulders for eternity (a, b). In yellow, it is the area of sciatic pain (b). [(a): Available under the Creative Commons Attribution 4.0 International (CC BY-­NC-­ND

4.0) from www.laceramicaantica.org. (b): Available under the Creative Commons Attribution 4.0 International (CC BY-­SA 4.0) from National Archaeological Museum in Naples, Italy, 2019]

2.2 Biblical Period

musculoskeletal damage to his hip. These injuries caused a temporary limping gait. Since that time, according to Halacha (Jewish Law), the descendants of Jacob (renamed Israel) were prohibited from eating for devotion to the “hip nerve” or “sciatic tendon” which crosses the hip joint. “Gid hanasheh” corresponds to the term sciatic nerve in Judaism (Hebrew). In the same context, some Native American communities, such as Cherokees, supposed if they consumed the sciatic nerve of animals they killed, then they would have a cramp when attempting to run.

The first citation of a “neurological pain” in the lower limb was attributed to the wrestling between the prophet Jacob and the Angel more than 15 centuries before our era. According to the bible (Genesis 32, 23–33), the Angel touched Jacob at the joint of his hip, causing him severe pain along the “big nerve” which persisted for a few days (Fig.  2.2). Jacob seems to have sustained a neurological injury to his sciatic nerve (may be neurapraxia) as well as

2.2 Biblical Period Fig. 2.2  Depiction of Jacob Wrestling with the Angel at Penuel, by Eugène Delacroix (1798–1863). Fresco of Eugène Delacroix in Église Saint-­Sulpice Church (Paris) (1861). [Available under the Creative Commons Attribution-­Share Alike 3.0 (CC BY-­SA 3.0), unported license from Gloumouth1, 2005]

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2.3 Greco-Roman Period • Hellenic Hippocrates of Kos [460–377 BC] (Fig. 2.3), the Father of medicine, was probably the first physician to use the word “sciatica” deriving from the Greek “ischios” or “ischiacos” (which means hip) in his legendary treatise

Fig. 2.3  Hippocrates (460–370 BC). Bust Greek and Roman Portraits Hekler, Anton Published: 1912. [Available under the Creative Commons Attribution 4.0 International (CC BY 4.0). From Wellcome Library, London, 2014, http://wellcomeimages.org]

2  Historical Aspects of Sciatica

De affectionibus (Treatise of diseases) (c.f. Chap. 1 about Definitions of Sciatica). However, he attributed the pain to a diseased or subluxated hip joint. In the Treatise of Predictions, Hippocrates noted that sciatica would last at least 1 year in aging patients and the pain disappears after 40  days in younger patients. Also, he noticed that this symptom was seen more frequently in summer and fall (probably a time of more strong exercises). Hippocrates treated this symptom with warm water therapy applied to the painful region, fumigations, fasting cure, laxatives, and ingestion of donkey milk. The author considers cauterization if the pain is fixed at one point and the prescribed therapies failed. Interestingly, he noticed that pain radiating to the foot was a good predictive sign, while pain localized to the hip was less expected to improve spontaneously. • The Greek physician Soranus of Ephesus [98–138  AD] wrote in his lost book De morbis acutis et chronicis (On Acute and Chronic Diseases) the first description of sciatica caused by wearing heavy objects. The North-­African Roman physician Caelius Aurelianus [fifth century AD], based on his Latin translation of the survived works of Soranus of Ephesus, described in his book Tardarum sive chronicarum passionum (Of the slow or chronic sufferings) the importance of exercise therapy (physiotherapy) and a form of spinal traction therapy designed for sciatica. For Caelius Aurelianus, sciatic pain may be accompanied by constipation, claudication, and posture alterations. However, occasionally he mistook sciatica for “psoitis.” • In the second century AD, Claudius Galenus or Galen [129–216 AD] (Fig. 2.4) described spinal deformities and curvatures and invented the terms “scoliosis,” “lordosis,” and “kyphosis,” and he tried to treat them. According to the concept of “humoral medicine,” Galen attempted to cure sciatica by bloodletting (also known as venesection or phlebotomy) to remove the “noxious humors” or “bad fluids” (Fig. 2.5). • The Byzantine physician Paulus Aegineta, or Paul of Aegina [625–690 AD] (Fig. 2.6), considered the Father of early medical writing, best known for writing the medical encyclopedia Epitomae medicae libri septem (Medical Compendium in seven books), detailed description of sciatica, but he confused this condition with gout. Moreover, Paul of Aegina described the practice of cauterization on the hip joint (AKA ischiatic joint).

2.3 Greco-Roman Period Fig. 2.4  Galen or Claudius Galenus (129–216 AD). Lithograph by P. R. Vignéron. [Available under the Creative Commons Attribution 4.0 International (CC BY 4.0). From Wellcome Library, London, http:// wellcomeimages.org]

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Fig. 2.5  Galen or Claudius Galenus (129–216 AD). Galen cupping a patient. [Courtesy of National Library of Medicine. Available at: http:// resource.nlm.nih.gov/101407467. (This work is in the public domain in the United States because it was first published before 1926)]

2.4 Arabic and Persian Civilization

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Fig. 2.6  Paulus Aegineta or Paul of Aegina [625–690  AD]. [Courtesy of National Library of Medicine. Available at: http://resource.nlm.nih. gov/101436686. (This work is in the public domain in the United States because it was first published before 1926)]

2.4 Arabic and Persian Civilization • The oldest Arabic/Persian writing about pain in the hip joint and sciatic was probably done by Yuhanna ibn Masawaih (AKA Mesue or Janus Damascenus) [777– 857] (Fig. 2.7). He was a Persian or Assyrian Nestorian Christian physician who first reported bloodletting from the “sciatic vein” (or small saphenous vein) for “pain in the hip and sciatic.” He wrote: “Galen recommended phlebotomy, and among the veins that may be bled, there is a vein between the little toe and the second toe of the

foot, for matters in the lower parts. In fact, in this case, the benefit of this vein is greater than that of the sciatic and saphenous veins…” • In the book entitled Firdous al-Hikmah (Paradise of Wisdom), one of the first encyclopedias of medicine produced by Ali ibn Sahl Rabban Al Tabari [838–870], this Persian Jewish physician described the cause, risk factors, and some therapies for sciatic pain. • Al Tabari’s famous student is Muhammad ibn Zakariya al Razi [864–925/935], known as the Galen of the Arabs, who added more descriptions about sciatica in his

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Fig. 2.7  Yuhanna ibn Masawaih or Mesue [777–857]. [Available under the Creative Commons Attribution 4.0 International (CC BY 4.0). From Wellcome Library, London, http:// wellcomeimages.org]

renowned book of medicine Al Havi (Liber Elhavy or Continens). Al Razi in Baghdad recognized that he had cured 1000 patients with sciatica generally by bleeding one of the lower members. Later, additional comprehensive explanations were found in the famous book Qanun fi al Tibb (The Canon of Medicine) written by al Husayn ibn Abdullah ibn Sina (Avicenna) [980–1037], who was considered the Leading medieval Islamic doctor (Figs. 2.8 and 2.9). However, Avicenna was known as less physically aggressive than its predecessors.

• In his book Kitab al Tesrif, the Andalusian physician Khalaf ibn al-Abbas Al-Zahrawi (Abulcasis) [936–1013], considered to be the Father of modern surgery, recommended the practice of the cautery and illustrated a number of instruments used, but he overlooked bleeding (Fig.  2.10). For Abulcasis, cauterization was applied in the hip region and the lower limb along the era of pain radiation. • The Andalucian Jewish physician Musa ibn Maymun [1138–1204], AKA Maimonides, used bloodletting to

2.4 Arabic and Persian Civilization

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a

Fig. 2.8 (a) Avicenna or Ibn Sina (980–1037) (Courtesy of National Library of Medicine. Available at: http://resource.nlm.nih. gov/101408284). (b) The opening decoration and invocation to Allah from a sixteenth-century manuscript of Avicenna’s Canon of Medicine.

a

b

[Copied in 1006 H./1597–98 A.D. (This work is in the public domain in the United States because it was first published before 1926. From Medical Historical Library of Yale. http://www.library.yale.edu/oacis/ scopa/scopa_ibnsina_ms5.html)]

b

Fig. 2.9  Avicenna medal from Monnaie de Paris (Currency of Paris) (Sculpted by Victor Douek, 1972) (a). Private collection of A. Akhaddar. Arabic and French transcription meaning “Blessed are the wise who savor the pleasures of the mind” (b)

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Fig. 2.10  Khalaf ibn al-Abbas Al-Zahrawi (Abulcasis) [936–1013]. Albucasis blistering a patient in the hospital at Cordova, 1100 AD. Oil By: Ernest Board (1877–1934). [Available under the Creative Commons

Attribution 4.0 International (CC BY 4.0). From Wellcome Library, London, 2014, http://wellcomeimages.org]

treat one patient with sciatica. He wrote: “I know that, after removing blood from the foot in one day, … the disease called sciatica was cured.” • Most Arabic and Persian physicians named sciatica “Ergho Nasaa” which means “Pain in vein pathway in the lower limb.” Al Tabari and Avicenna believed that Ergho Nasaa disorder is a pain in the nerve (or vein) that descends from the hip to the foot and toes due to unfavorable humors mixed in blood. They also used bloodletting to dispose of the infused substances which were correlated to a sciatic nerve disorder. Arabic, Persian, and Islamic medicine were known to use traction and manipulation, local cauterization, cupping, bloodletting, and opioids. Some of these methods had been copied and practiced by European physicians for centuries. • The Persian physician Mansur ibn Muhammad ibn Ahmad ibn Yusuf ibn Ilyas is best known for writing one of the

earliest illustrated treatises on human anatomy “Tashrih-i badan-i insan” [Anatomy of the Human Body or Mansur’s Anatomy]. The first version of Mansur’s anatomy was composed in 1396 with illustrations about the human body including the nervous system (Fig. 2.11). • Pietro Andrea Gregorio Mattioli or Mattioli of Siena [1501–1577] was an Italian physician and naturalist. In his book entitled Dioscoride (Commentaria in sex libros Pedacii Dioscoridis), he described the use and effects of some plants for the treatment of many diseases including sciatica (e.g., peucedanus). • Until the eighteenth century, no distinction was made between pain arising in the hip joint and spine. Also, the concept of “humoral medicine” was the main accepted idea correlated to a sciatic nerve problem. In addition, according to the history of traditional Chinese medicine, acupuncture was reported to be effective in relieving diverse pain including sciatica for several centuries.

2.5 Eighteenth Century

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2.5 Eighteenth Century • In 1764, the Italian anatomist and physician Domenico Cotugno [1736–1822] wrote the first book on sciatica in his monography entitled De Ischiade Nervosa Commentarius (comments on nervous ischialgia) (Fig. 2.12). He was the first to distinguish “neurological” sciatica from its arthritis origin (ischias arthritica) with which it was previously confused. Furthermore, he separates “sciatica postica” (sciatic pain) from “sciatica antica” (crural pain). Cotugno’s syndrome or disease was then applied to unilateral neuralgia along the distribution of the sciatic nerve. According to Cotugno, some patients in his time were also treated with electricity, opium, and cauterization with a small pointed cautery. • In 1784, the Italian physician Giuseppe Petrini described three types of sciatica: tibial, sural, and combined. In his monograph entitled Della sciatica nervosa e del nuevo metodo di guarirla (on nervous sciatica and the new method to cure it), he supposed that the tibial sciatica was more common than the sural one and he recapitulated all the treatment procedures used for the sciatic pain.

Fig. 2.11 Illustration of the nervous system from Mansur ibn Muhammad ibn Ahmad ibn Yusuf ibn Ilyas (between 1393 and 1409). The arrows point to the main nerve of the lower limb. [Courtesy of National Library of Medicine. Available at: https://www.nlm.nih.gov/ exhibition/historicalanatomies/Images/1200_pixels/p1911b.jpg. (This work is in the public domain in the United States because it was first published before 1926)]

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2  Historical Aspects of Sciatica

Fig. 2.12  Domenico Cotugno [1736–1822]. Lithograph by Luigi Rossi (1853–1923). [Available under the Creative Commons Attribution 4.0 (CC BY 4.0). From Wellcome Library, London, 2014, http://wellcomeimages.org]

2.6 Nineteenth Century

the leg in patients with sciatica. This maneuver was published by his student Jean Joseph Forst in 1881 in his doctoral thesis entitled Contribution à l’étude Clinique de la • In 1841, the French physician François-Louis-Isidore sciatique (contribution to the clinical study of sciatica). Valleix [1807–1855] provided in his work Traité des According to Forst, Lasègue’s maneuver was to help in névralgies, ou, Affections douloureuses des nerfs (Treatise differentiating hip pain from sciatic pain. Also, Lasègue on neuralgia, or, painful disorders of the nerves) a remarktries to distinguish sciatica from hysteria. Sixteen years ably detailed description of the topography of painful following Lasègue’s finding, the Serbian doctor Lazar points along the course of the sciatic nerve. Accessible to Lazarevic [1851–1891] described sciatic scoliosis and the palpation, Valleix points are known to be painful in straight leg raise test as it is accomplished today. patients with sciatic pain. He considered sciatica, or femo• In 1874, Doctor CJ Mill from Scotland published an interropopliteal neuralgia, as a “functional neuralgia.” esting case of extraspinal sciatica. The patient had been • In 1857, the famous German pathologist Rudolf Virchow treated unsuccessfully for hip pain, extending in the ipsi[1821–1902] (Fig.  2.13) described one case of post-­ lateral leg along the route of the sciatic nerve. At postmortraumatic “fractured intervertebral disk” in a patient who tem examination, the hip joint was sound. However, there had died secondary to trauma. This examined lesion, was a cystic lesion in the posterior iliac region protruding known as “Virchow’s tumor” was discovered during the through the sacro-sciatic opening and extending into the necropsy. pelvis. The sciatic nerve was under great pressure, and the • In 1864, Ernest-Charles Lasègue [1816–1883] (Fig. 2.14), pelvic viscera were displaced. a French neurologist, noticed a pain provoked by lifting

2.7 Twentieth Century

19

Fig. 2.14  Ernest-Charles Lasègue (1816–1883). (Available under the Open Licence 1.0. Courtesy of Bibliothèque interuniversitaire de santé BIU, Paris) Fig. 2.13  Rudolf Ludwig Karl Virchow (1821–1902). Photograph by J.  C. Schaarwächter, 1891. [Available under the Creative Commons Attribution 4.0 (CC BY 4.0). From Wellcome Library, London, http:// wellcomeimages.org]

2.7 Twentieth Century With the introduction of anesthesia in the late 1840s and aseptic techniques in 1867, surgical treatments for the spine rapidly expanded. The first successful removal of a herniated intervertebral disk was probably done in 1901 by the German neurosurgeon Fedor Krause [1857–1937] (Fig.  2.15), following the advice of the neurologist Hermann Oppenheim [1857–1919] via a lumbar midline laminectomy and a transdural resection of a “cartilaginous lesion” which has been thought to represent a tumor. The patient had immediate total relief of pain. • In 1912, the French neurologist Joseph Jules Dejerine [1849–1917] reported that some sciatica have a root distribution and not a truncal one. He predicted that inflammation of the intrathecal nerve roots can produce motor loss with or without sensory damage in the lower extremi-

ties. However, Dejerine misattributed this condition to neurosyphilis. • In 1918, the Italian physician Arnone listed various clinical signs or maneuvers for distinguishing true sciatica from pseudo-sciatic pain. However, these criteria are not currently used because they are inconstant and inconclusive. • In the 1920s, many practitioners such as the British doctor Yeoman considered the involvement of the sacroiliac joint in the pathophysiology of sciatica. It was reported that sciatica might result from sacroiliitis due to inflammation within the piriformis muscle and consequent irritation of the sciatic nerve. This mechanism was considered the most likely source of idiopathic low back pain and sciatica. • In 1922, the American military surgeon Alfred Washington Adson [1887–1951] of the Mayo Clinic removed a disk protrusion at the L4–L5 intervertebral level of a dentist

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2  Historical Aspects of Sciatica

•

• Fig. 2.15  Fedor Krause (1857–1937). (Courtesy of National Library of Medicine. Available at: http://resource.nlm.nih.gov/101420883)

•

•

•

•

suffering from intractable sciatic pain with a good postoperative result. The German pathologist Christian Georg Schmorl [1861– 1932] is remembered for his work about protrusions of the intervertebral disk into the vertebral body known as “Schmorl’s nodes” as well as degeneration of the nucleus pulposus and the posterior disk prolapse in the spinal canal (1925). However, his works did not contain clinical links. Also in the 1920s, it was supposed that sciatica has been caused by inflammation of the sciatic nerve itself; however, when the nerve had been explored, it was not seen inflamed. In 1927, Wiedhoff noted that anesthetic blocking of the sciatic nerve failed to relieve the pain but that sacral anesthesia did, indicating that the responsible lesion was located higher. In 1927, Vittorio Putti [1880–1940] (Fig. 2.16), an Italian orthopedic surgeon, made a valuable contribution using the term “arthritis or vertebral sciatica.” He also recognized degenerative modifications of the intervertebral foramen as a cause of sciatic compression. In 1930, the English physician and future cardiologist William Evans [1895–1988], published his results obtained in the treatment of sciatic pain by intrasacral

•

•

•

extradural injection of novocaine concerning 40 patients. The use of corticosteroids will only be made from the 1960s. Before the legendary Mixter and Barr’s publication in the New England Journal of Medicine in 1934, some surgeons operated on patients with “benign tumor adjacent to a lumbar disk” or with “unrecognized cartilaginous material inside the lumbar canal,” but at that time, they could not realize that the lesions were “intervertebral disk herniations.” Reported are as follows: –– The couple Jacque Calvé [1857–1954]/Marcel Galland [1888–1963]. –– Maurice Robineau [1870–1950]. –– Otto Veraguth [1870–1944]. –– Charles Albert Elsberg [1871–1948]. –– Vittorio Putti [1880–1940]. –– Walter Edward Dandy [1886–1946]. –– Alfred Washington Adson [1887–1951]. –– The duo Théophile Alajouanine [1890–1980]/Daniel Petit-Dutaillis [1889–1968]. In 1933, the American neurosurgeon William Jason Mixter [1880–1958] and the orthopedic surgeon Joseph Seaton Barr [1901–1963] (Fig. 2.17), finally clarified the etiopathogenic mechanism of lumbar discogenic sciatica. They also propagated the discectomy technic using laminectomy and a transdural approach as the standard therapy in light of their landmark paper entitled Rupture of the intervertebral disc with involvement of the spinal canal and published in the New England Journal of Medicine in 1934. In 1938, J Grafton Love [1903–1987] and Maurice Walsh published their results on 100 patients operated on for a lumbar disk herniation. Furthermore and for the first time, they reported a herniated disk recurrence. Facing discogenic sciatica, the pain has been attributed for a long time to pressure on the nerve root(s). But since the 1950s, this concept began to be contested. In 1956, the Australian rheumatologist Michael Kelly [1905–1967], believed that pressure on a nerve would induce damage to neurological function rather than “pain.” Over the same period, the Swedish orthopedist Olov Lindahl [1919– 1961] and the neuroanatomist Bror Rexed [1914–2002] suggested that the source of the nerve root pain is an inflammatory reaction rather than direct contact pressure on the damaged nerve roots. From the 1990s, other factors, in particular, immunological and even neurophysiological (e.g., glutamate), will be revealed in the development of sciatic neuralgia. Diagnostic imaging has played a crucial role in understanding degenerative disk disease and its potential symp-

2.7 Twentieth Century

21

Fig. 2.16  Vittorio Putti (1880–1940). Photograph, 1928 (?). [Available under the Creative Commons Attribution only licence (CC BY 4.0). From Wellcome Library, London, http://wellcomeimages.org]

toms particularly “discogenic sciatica.” Modern imaging had also a crucial role in identifying extraspinal sciatica lesions. What a path traveled over the past century! The beginning had started with X-rays radiography until the development of high-resolution magnetic resonance neurography. The following major applications have been instrumental in observing the spine and its contents as well as detecting many origins of sciatic pain (Table 2.1). However, a causal relationship between clinical symptoms and imaging results is sometimes difficult to establish despite technological development. • In the last decades, treatment of the lumbar disk herniation experienced a significant and rapid development including techniques of extradural interlaminar approach [1939], chemonucleolysis [1964], percutaneous discectomy [1975/1985], microsurgical discectomy [1977], posterior instrumented lumbar fusion [1950s–1970s],

laser discectomy [1986], lumbar disk arthroplasty [1950s–1990s], percutaneous endoscopic and microendoscopic lumbar discectomy [1980s/2000s], tubular retractor systems [2000s], and, shortly, the introduction of robotic lumbar microdiscectomy. Minimally invasive spinal surgery is actually in constant improvement and offers many attractive techniques in appropriate selective patients with successful results. Despite technological development and improvement in sciatica pain management, this painful disorder still hides many secrets. A significant number of patients still experience diagnostic delays, inadequate therapeutic adaptations, and refractory sciatic pain and related complications. More clinical and scientific basic research may be essential for the development of new management strategies for the various etiologies of sciatica.

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Further Reading

Fig. 2.17  Joseph Seaton Barr (1901–1964). (Courtesy of National Library of Medicine. Available at: http://resource.nlm.nih. gov/101409920) Table 2.1  Major imaging applications in the observation of the spine and its contents Imaging procedure X-rays

Discovery year 1895

Authors Wilhelm Conrad Röntgen (1845–1923)a Myelography 1919–1922 Jean-Athanase Sicard (1872–1929) Jacques Forestier (1890–1978) Discography 1948 Knut Lindblom (1905–1963) Spinal epidural venography 1950s–1960s Developed by many authors Computed tomography 1972 Godfrey Newbold (CT) scan Hounsfield (1919–2004)a Allan MacLeod Cormack (1924–1998)a Myelo-CT scan (computer-­ 1976 Giovanni Di Chiro assisted myelography) (1926–1997) Dieter Schellinger (1937–2019) Magnetic resonance 1970s–1980s Paul Christian imaging (MRI) Lauterbur (1929–2007)a Peter Mansfield (1933–2017)a  Nobel prize winners

a

Alajouanine TH, Petit-Dutaillis D. Compression de la queue de cheval par une tumeur du disque intervertébral. Ablation suivie de guérison. Bull Mem Soc Nat Chir. 1929;55:937–40. Allan DB, Waddell G. An historical perspective on low back pain and disability. Acta Orthop Scand Suppl. 1989;234:1–23. https://doi. org/10.3109/17453678909153916. Alter R. Genesis, translation and commentary. New York: WW Norton; 1996. Genesis 31/3–5:166. Genesis 32/24–33 with footnoting: 180–3. Aygen G, Karasu A, Ofluoglu AE, Pait G, Toplamaoglu H.  The first Anatolian contribution to treatment of sciatica by Serefeddin Sabuncuoglu in the 15th century. Surg Neurol. 2009;71(1):130–3. https://doi.org/10.1016/j.surneu.2007.09.007. Bequeathed to Francesco Melzi; from whose heirs purchased by Pompeo Leoni, c.1582–90; Thomas Howard, 14th Earl of Arundel, by 1630; Probably acquired by Charles II; Royal Collection by 1690. Caspar W.  A new surgical procedure for lumbar disc herniation causing less tissue damage through a microsurgical approach. Berlin: Springer; 1977. p.  74–80. https://doi. org/10.1007/978-­3-­642-­66578-­3_15. Chedid KJ, Chedid MK.  The “tract” of history in the treatment of lumbar degenerative disc disease. Neurosurg Focus. 2004;16:E7. https://doi.org/10.3171/foc.2004.16.1.8. Choy DS, Ascher PW, Ranu HS, Saddekni S, Alkaitis D, Liebler W, et  al. Percutaneous laser disc decompression. A new therapeutic modality. Spine (Phila Pa 1976). 1992;17:949–56. https://doi. org/10.1097/00007632-­199208000-­00014. De Ischiade CD.  Nervosa Commentarius. Napoli: Fratres Simonii; 1764. Cowan J.  The relation of sciatica to the sacro-iliac joint. Br Med J. 1923;1:372–3. https://doi.org/10.1136/bmj.1.3244.372. Dandy WE. Loose cartilage from intervertebral disk simulating tumour of the spinal cord. Arch Surg. 1929;19:660–3. Di Chiro G, Schellinger D.  Computed tomography of spinal cord after lumbar intrathecal introduction of metrizamide (computer-­ assisted myelography). Radiology. 1976;120:101–4. https://doi. org/10.1148/120.1.101. Evans W.  Intrasacral epidural injection in the treatment of sciatica. Lancet. 1930;216:1225–9. https://doi.org/10.1016/ S0140-­6736(00)86498-­3. Fardon D. Biblical pain: did Jacob have sciatica? Spine J. 2002;2:228. https://doi.org/10.1016/s1529-­9430(02)00172-­9. Freiburg AH, Vinke TA. Sciatica and the sacroiliac joint. J Bone Joint Surg Am. 1934;16-A:126–36. Fuller HW. On rheumatism, rheumatic gout and sciatica: the pathology, symptoms and treatment. London: John Churchill; 1852. Goebert HW Jr, Jallo SJ, Gardner WJ, Wasmuth CE, Bitte EM. Sciatica: treatment with epidural injections of procaine and hydrocortisone. Cleve Clin Q. 1960;27:191–7. https://doi.org/10.3949/ ccjm.27.4.191. Harrington JF, Messier AA, Bereiter D, Barnes B, Epstein MH.  Herniated lumbar disc material as a source of free glutamate available to affect pain signals through the dorsal root ganglion. Spine (Phila Pa 1976). 2000;25:929–36. https://doi. org/10.1097/00007632-­200004150-­00006. Hashemi M, Halabchi F.  Changing concept of sciatica: a historical overview. Iran Red Crescent Med J. 2016;18:e21132. https://doi. org/10.5812/ircmj.21132. Hippocrates. The genuine works of Hippocrates. Translated by Adams Francis from the Greek with a preliminary discourse and annotations. New York: William Wood and Company; 1929. Hoenig LJ.  Jacob’s limp. Semin Arthritis Rheum. 1997;26:684–8. https://doi.org/10.1016/s0049-­0172(97)80004-­2.

Further Reading Karampelas I, Boev AN III, Fountas KN, Robinson JS Jr. Sciatica: a historical perspective on early views of a distinct medical syndrome. Neurosurg Focus. 2004;16:E6. https://doi.org/10.3171/ foc.2004.16.1.7. Kelly M. Is pain due to pressure on nerves? Spinal tumors and the intervertebral disk. Neurology. 1956;6:32–6. https://doi.org/10.1212/ wnl.6.1.32. Kirkes WS.  On rheumatism, rheumatic gout, and sciatica: their pathology, symptoms, and treatment. Br Foreign Med Chir Rev. 1853;11:149–59. Lindahl O, Rexed B. Histologic changes in spinal nerve roots of operated cases of sciatica. Acta Orthop Scand. 1951;20:215–25. https:// doi.org/10.3109/17453675108991169. Lindblom K.  Diagnostic puncture of intervertebral disks in sciatica. Acta Orthop Scand. 1948;17:231–9. https://doi. org/10.3109/17453674808988943. Longatti P.  Bicentenary of Domenico Cotugno: the four experiments that marked a turning point on the modern research of cerebrospinal fluid. Childs Nerv Syst. 2022;38:1839–43. https://doi.org/10.1007/ s00381-­022-­05666-­6. Mayer HM, Brock M.  Percutaneous endoscopic discectomy: surgical technique and preliminary results compared to microsurgical discectomy. J Neurosurg. 1993;78:216–25. https://doi.org/10.3171/ jns.1993.78.2.0216. Mill CJ.  Case of sciatica depending on pressure by an intrapelvic tumour. Edinb Med J. 1874;20:402–4. Minaee B, Abbassian A, Nasrabadi AN, Rostamian A.  Prognostic factors of sciatica in the Canon of Avicenna. Rheumatol Int. 2013;33:3095–6. https://doi.org/10.1007/s00296-­012-­2574-­2. Missori P, Domenicucci M, Currà A. Bloodletting from the ankle vein to treat sciatic pain. Pain Med. 2015;16:30–6. https://doi.org/10.1111/ pme.12445. Mixter WJ, Barr JS.  Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med. 1934;211:210–5. https:// doi.org/10.1056/NEJM193408022110506.

23 Naderi S, Acar F, Arda MN. History of spinal disorders and Cerrahiyetül Haniye (Imperial Surgery): a review of a Turkish treatise written by Serefeddin Sabuncuoğlu in the 15th century. Historical vignette. J Neurosurg. 2002;96S:352–6. Pearce JM.  A brief history of sciatica. Spinal Cord. 2007;45:592–6. https://doi.org/10.1038/sj.sc.3102080. Postacchini F. Presidential lecture, European Spine Society, 1995. The role of Europe in the spine—past and future perspectives. Eur Spine J. 1995;4:323–6. https://doi.org/10.1007/BF00300290. Robinson JS.  Sciatica and the lumbar disk syndrome: a historic perspective. South Med J. 1983;76:232–8. https://doi. org/10.1097/00007611-­198302000-­00022. Rutkowski MD, Winkelstein BA, Hickey WF, Pahl JL, DeLeo JA. Lumbar nerve root injury induces central nervous system neuroimmune activation and neuroinflammation in the rat: relationship to painful radiculopathy. Spine (Phila Pa 1976). 2002;27:1604–13. https://doi.org/10.1097/00007632-­200208010-­00003. Stafford MA, Peng P, Hill DA. Sciatica: a review of history, epidemiology, pathogenesis, and the role of epidural steroid injection in management. Br J Anaesth. 2007;99:461–73. https://doi.org/10.1093/ bja/aem238. Sweetman BJ. The words we use: where did lumbago and sciatica come from? Int Musculoskelet Med. 2011;33:26–9. https://doi.org/10.117 9/175361511X12965803070865. Truumees E. A history of lumbar disc herniation from Hippocrates to the 1990s. Clin Orthop Relat Res. 2015;473:1885–95. https://doi. org/10.1007/s11999-­014-­3633-­7. Wiedhoff O. Klein Wochen. 1927;6:739. Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica, with an analysis of 100 cases. Lancet. 1928;212:1119–23. https:// doi.org/10.1016/S0140-­6736(00)84887-­4. Zhang Y.  The needling technique and clinical application of point Zhibian. J Tradit Chin Med. 2004;24:182–4.

3

Anatomy and Physiology of the Sciatic Nerve

3.1 Generality and Relevance The sciatic nerve (AKA ischiadic nerve, ischiatic nerve, or nervus ischiadicus in Latin), about the thickness of a finger, is the largest and longest nerve in the human body. It has a long course right from its origin in the lumbosacral spinal canal to its division in the apex of the popliteal fossa. It is a mixed nerve having both motor and sensory fibers. Indeed, it controls the muscles in the back of the knee and lower leg and provides sensation to the back of the thigh, lower leg, and the sole of the foot. Due to its significant length, the sciatic nerve can be affected in different anatomical regions (e.g., lumbosacral radiculopathies, plexopathies, and mononeuropathies) and by various causes. However, a thorough understanding of the regional anatomy and physiology of the sciatic nerve and its major branches is essential for managing any patient with sciatica.

3.2 Origin and Course of the Sciatic Nerve The sciatic nerve originates in the lumbosacral spinal canal from the ventral rami of the fourth lumbar (L4) to the third sacral (S3) spinal nerves and contains fibers from both the posterior and anterior divisions of the lumbosacral plexus (Fig. 3.1). The sacral plexus is a network of nerves formed by the lumbosacral trunk (originating from L4 to L5) and sacral spinal nerves (from S1 to S4) (Fig.  3.2). The sacral plexus is positioned on the posterior pelvic wall, posterior to the internal iliac vessels and ureter, and anterior to the piriformis muscle. The plexus gives several ramifications including the anterior and posterior branches and one terminal branch. These branches provide the motor and sensory innervation for the posterior thigh, most of the lower leg, the entire foot,

and part of the pelvis. The five main nerves that originate from the sacral plexus can be remembered with this saying “Some Irish Sailor Pesters Polly” (Fig. 3.2). S: Superior gluteal nerve I: Inferior gluteal nerve S: Sciatic nerve P: Posterior cutaneous nerve P: Pudendal nerve After leaving the lumbosacral vertebra, the nerve fibers converge in the posterior pelvic region to form a single nerve (i.e., the sciatic nerve) that descends posteriorly and leaves the pelvis through the greater sciatic foramen (AKA sciatic notch). Then, it passes inferior to the piriformis muscle (Fig. 3.3), accompanied by some important anatomical structures known as “PIN–PINS” (Table 3.1). Covered by the gluteus maximus, the sciatic nerve next runs medial and posterior to the hip joint between the ischial tuberosity and the greater trochanter of the femur. After that, it continues its course downward through the posterior compartment of the thigh. It runs between the long head of the biceps femoris muscle and the adductor magnus muscle, and laterally to the semitendinosus and semimembranosus muscles. At the apex of the popliteal fossa (approximately 6 cm above the popliteal fossa), the sciatic nerve bifurcates by dividing into its two terminal branches: the tibial nerve and the peroneal (AKA common fibular) nerve (Fig. 3.4). Before dividing, the nerve gives off articular and muscular branches to the hip joint and the thigh (ischial part of adductor magnus and hamstring muscles, which are biceps femoris, semitendinosus, and semimembranosus). Within the sciatic nerve, fibers that eventually form the peroneal nerve frequently are separated from those that distally become the tibial nerve. The peroneal division of the sciatic nerve, which has fewer and larger fascicles and less

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_3

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Fig. 3.1  Anterior view of the lumbosacral spine showing the origin of the sciatic nerve in the lumbosacral spinal canal from the fourth lumbar (L4) to the third sacral (S3) spinal nerves

supportive tissue, runs lateral to the tibial division. The two divisions physically separate from each other in the mid-­ thigh to form their respective nerves. The peroneal division is more susceptible to stretch injury and compression. Recently, it was found that there was also a clear somatotopic distribution of nerve fascicles along the entire course of

the sciatic nerve. Fascicles emerging from the L5 nerve root were organized in anterolateral parts, while fascicles emerging from S1 looked posteromedially in cross-sections of the sciatic nerve. Studying any peripheral nerve should always consider its histological architecture (Fig. 3.5).

3.2 Origin and Course of the Sciatic Nerve Fig. 3.2  Configuration of the sacral plexus and its 12 branches. Superior gluteal nerve, inferior gluteal nerve, sciatic nerve, posterior femoral cutaneous nerve, pudendal nerve, nerve to lumbar plexus (A), nerve to perineum and levator ani (B), perforating cutaneous nerve (C), nerve to obturator internis and superior gemellus (D), nerve to quadratus femoris and inferior gemellus (E), and nerve to piriformis (F)

Fig. 3.3  Posterior view of the pelvis showing the relationship between sciatic nerve and piriformis muscle

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28 Table 3.1  Anatomical structures (PIN–PINS as an acronym) that pass from the greater sciatic notch below the piriformis muscle P: Posterior femoral cutaneous nerve I: Inferior gluteal artery, vein, and nerve N: Nerve to quadratus femoris P: Pudendal nerve I: Internal pudendal artery and vein N: Nerve to obturator internus S: Sciatic nerve Fig. 3.4  Posterior view of the lower limb showing the course of sciatic nerve. Note the division of the sciatic nerve into its two terminal branches: the tibial nerve and the common peroneal nerve

3  Anatomy and Physiology of the Sciatic Nerve

3.3 The Lumbosacral Spine

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Fig. 3.5 Histological structures of a typical peripheral nerve

3.3 The Lumbosacral Spine Spine is not just an arrangement of vertebrae, it is an ingenious musculo-osteo-disco-articular-ligament (MODAL) complex. Strong as a bull, balanced as a giraffe, agile like a snake; take care of him and he will surprise you! A. Akhaddar [The author]

The anatomy of the lumbosacral spine consists of five lumbar vertebrae with an overall lumbar lordotic curvature and five fused sacral vertebrae (i.e., sacrum) with soft intervertebral disks in between each lumbar vertebra supporting and serving in the flexible movements of the lumbar spine (Figs. 3.6, 3.7, and 3.8). Each vertebra is composed of two parts: the anterior segment consisting of the vertebral body and the posterior segment representing the vertebral arch that encircles the spinal canal posteriorly. The vertebral arch is formed by two pedicles, two laminae, two transverse processes, two posterior joint masses (each one containing superior and inferior articular processes), and the spinous process (Fig. 3.9). Each vertebra is connected to adjacent ones by a disco-ligamentous system composed, from front to back, of anterior longitudinal ligament, intervertebral disk, posterior longitudinal ligament, yellow ligament (AKA ligamentum flavum), interspinous ligament, and supraspinous ligament (Fig. 3.10). Each superior articular process of one vertebra articulates with a synovial joint with the inferior articular process of the vertebra directly above. The sacrum articulates with four different bones: the lumbar spine rostrally, the coccyx caudally, and bilaterally with the ilium through the sacroiliac joint. The lower lumbar spine and the upper part of the sacrum can occasionally contain transitional anatomy where the L5 vertebral body may sometimes be “sacralized” (with L5 fused to the sacrum, AKA sacralization), or S1 may be “lumbarized” (with a well-developed disk seen between S1 and S2, AKA lumbarization) (Fig. 3.11). Recognizing the lumbosacral transitional vertebra when counting vertebral levels is important for spinal imaging and surgery (Figs. 3.12 and 3.13) (see also Chap. 57 about Bertolotti’s Syndrome). The

posterior vertebral arch may present a failure of fusion on the midline, often with the absence of the spinous process of L5 or S1. This last condition is called spina bifida occulta (Figs. 3.14 and 3.15). Occasionally, the posterior facet joints (AKA zygapophyseal joints) may be asymmetric and have different orientations known as facet tropism (Fig.  3.16). This special tropism may induce spinal instability and pathological changes in the intervertebral disk structures. The intervertebral disk is composed of three parts: the nucleus pulposus, the annulus fibrosus, and the cartilaginous endplates. In the child, the nucleus pulposus is semiliquid, but with age, degeneration and dehydration occur; consequently, the disk becomes more solid and fibrous and loses its height (Figs. 3.17 and 3.18). Displacement of lumbar disk material beyond the normal margin of the intervertebral disk space is referred to as a lumbar disk herniation. The lumbar spine is surrounded by the paraspinal muscles (AKA paravertebral muscles), which play a fundamental role in spine stabilization and mobility (Fig. 3.19). Paraspinal muscles represent the second biggest muscle mass of the human body just after the muscles of the thigh. They are divided into three categories: 1. Extrinsic Muscles: Latissimus dorsi and serratus muscles, which cover the intrinsic muscles. 2. Abdominal Muscles: Psoas major muscles and quadratus lumborum muscles. 3. Intrinsic Muscles: They are divided into three groups: (a) Deep Layer: Rotators lumborum, interspinalis, and intertransversarii muscles. (b) Middle Layer: Multifidus muscle. (c) Superficial Layer: Sacrospinalis muscle formed by the longissimus and Iliocostalis muscles. Some authors divided intrinsic muscles into only two groups: the erector spinae group (namely longissimus and Iliocostalis muscles) and the transversospinalis group (namely multifidus and rotatores muscles).

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3  Anatomy and Physiology of the Sciatic Nerve

Fig. 3.6  Anterior view of the lumbosacral spine

Identification of posterior lumbosacral bony landmarks [including spinous processes, posterior sacrum, anterior superior iliac spine, and iliac crests, which usually correspond to the L4/L5 disk level] is imperative for guiding the

surgical approach and avoiding wrong intervertebral level although intraoperative fluoroscopy examination remains invaluable in the localization of the correct affected disk level (Fig. 3.20).

3.3 The Lumbosacral Spine Fig. 3.7  Posterior view of the lumbosacral spine

31

32 Fig. 3.8  Lateral view of the lumbosacral spine

Fig. 3.9  Normal axial view of a lumbar vertebra. Structures of the vertebra

3  Anatomy and Physiology of the Sciatic Nerve

3.3 The Lumbosacral Spine Fig. 3.10  Normal sagittal view of discoligamentous structures of the lumbosacral spine

Fig. 3.11  Anterior view of the lumbosacral spine showing the two main types of lumbosacral transitional vertebra (sacralization and lumbarization)

33

34 Fig. 3.12 Antero-posterior (a) and lateral (b) lumbosacral plain radiographs showing a sacralization of L5 (arrows)

3  Anatomy and Physiology of the Sciatic Nerve

a

b

3.3 The Lumbosacral Spine Fig. 3.13 Antero-posterior (a) and lateral (b) lumbosacral plain radiographs showing a lumbarization of S1

35

a

b

36 Fig. 3.14 Antero-posterior view of the lumbosacral spine on plain radiography showing a midline failure of the posterior vertebral arch of L5 with the absence of the spinous process (arrows) (a, b)

3  Anatomy and Physiology of the Sciatic Nerve

a

b

3.3 The Lumbosacral Spine

37

a

b

d

c

e

f

Fig. 3.15  Different forms of spina bifida occulta (arrows) on axial CT scan (a–f) Fig. 3.16  Facet joint asymmetry (a, b). These different orientations are known as facet tropism

a

b

38

Fig. 3.17  Axial view of the intervertebral disk showing its constituent parts Fig. 3.18  Sagittal view of the lumbar intervertebral space showing the constituent parts of the disk

3  Anatomy and Physiology of the Sciatic Nerve

3.3 The Lumbosacral Spine Fig. 3.19  Axial cross-­ sectional anatomy of the posterior lumbar musculature at the L4–L5 intervertebral disk space. Psoas major (P), quadratus lumborum (QL), rotators lumborum (RL), intertransversarii (IT), multifidus (M), and erector spinae muscular group formed by the longissimus (L) and Iliocostalis (IC) muscles. Note the proximity of the abdominal aorta (Ao) and inferior vena cava (IVC) with the anterior part of the disk space

Fig. 3.20  Identification of posterior lumbosacral bony landmarks [including spinous processes, posterior sacrum, anterior superior iliac spine, and iliac crests, which usually correspond to the L4/L5 disk level] for guiding the surgical approach and avoiding wrong disk level

39

40

3  Anatomy and Physiology of the Sciatic Nerve

3.4 The Lumbosacral Nerve Roots Within the spinal canal, the cauda equina is composed of about 20 nerve roots originating from the conus medullaris (i.e., termination of the spinal cord), which ends caudally at the T12–L1 vertebral level. All cauda equina nerve roots are contained by a cylindrical sac of dura mater and arachnoid and immersed by the cerebrospinal fluid (Fig.  3.21). This cylindrical sac (AKA thecal sac or dural sac) extends from the head to the inferior border of S2 (Fig. 3.10). As the cauda equina nerve roots exit the thecal sac at each spinal level, they move in pairs to the lateral recess on each side. The number of cauda equina nerve roots decreases as they extend inferiorly from about 20 nerve root pairs at L1– L2 to 11 nerve root pairs at L5–S1 and 1 coccygeal nerve root pair at S5–first coccygeal. The lumbar nerve roots follow a precise course within the spinal canal, which can be compared with an arm of

a

the upper limb positioned on small abduction. When LDH occurs, the nerve root may be compressed at its “shoulder” or its “armpit” (axillary part) depending on the topographic localization of the herniated disk material. An important anatomical fact should be considered to understand the difference between a traversing and exiting nerve root at a determinate intervertebral disk level. In the lumbar area, the intervertebral disk is located well below the pedicle of the vertebra. The nerve root exists in the spinal canal (through the foramen) below and in close proximity to the pedicle of its vertebra, whereas the traversing nerve root at an intervertebral disk level goes across the disk and exists the spinal canal at the next level below (Fig. 3.22). For example, the L5 nerve root is the traversing nerve root at the L4–L5 level and is the exiting nerve root at the L5–S1 level.

b

c

Fig. 3.21  Posterior operative view of the lumbosacral spine showing the cauda equina nerve roots (dotted oval shape) (a–c) following durotomy (arrows)

3.5 The Intervertebral Foraminal Area

41

Fig. 3.22  Posterior view of the lumbosacral spine showing the disposition of the nerve roots within the lumbosacral canal

Fig. 3.23  Conjoined nerve roots according to Neidre and MacNab’s classification. Type 1: two nerve roots derived from a common dural sheath. Type 2: two nerve roots in one lateral spinal foramina. Type 3: two adjacent nerve roots are connected by a connecting root (AKA nerve root anastomosis)

Sometimes, a developmental/embryological anomaly involves two adjacent nerve roots, which share a common root sleeve at some part during their running course from the thecal sac. This nerve root congenital anomaly is named “conjoined nerve root” and is most commonly observed in the lumbosacral region, mainly unilateral at L5 and S1 vertebral segments (c.f. Chap. 59 about Lumbosacral Conjoined Nerve Roots). The concerning neural exit foramina may be empty or sometimes contain two nerve roots instead of one. Occasionally, there is also an abnormal anastomosis between these conjoined nerve roots within the spinal canal (Fig. 3.23).

3.5 The Intervertebral Foraminal Area Each lumbar nerve root exits the thecal sac laterally and emerges from the lateral spinal recess formed by the inferior facet of the rostral vertebrae and the superior facet of the caudal vertebra. Then, the nerve root exists the spinal canal through the intervertebral foramen (singular of foramina, AKA neural foramina), which is present between every pair of vertebra laterally, one on each side (Fig. 3.24). It allows the passage of some anatomical structures out of and into the vertebral canal (Table 3.2).

3  Anatomy and Physiology of the Sciatic Nerve

42

a

b

Fig. 3.24  Anatomical borders and different structures that pass through the intervertebral foramina (a, b) Table 3.2  Anatomical structures that pass through the intervertebral foramina •  •  •  •  •  •  • 

Spinal nerve root Posterior root ganglia (AKA spinal ganglia) Sinu-vertebral nerve (AKA recurrent meningeal nerve) Segmental spinal artery (AKA root artery) Intervertebral veins Transforaminal ligaments (when present) Fat (adipose tissue)

The normal neural foramen has an appearance similar to a “keyhole” limited by the following borders (Fig. 3.24): • Anteriorly: Lower posterolateral aspect of a vertebral body and the intervertebral disk below. • Posteriorly: Facet joint and associated fibrous joint capsule. • Superiorly: Inferior vertebral notch of the pedicle above. • Inferiorly: Superior vertebral notch of the pedicle below. Lumbar nerve roots only occupy a certain part of the foraminal space. This proportion is around 25–30% for L5 and less than 22% for the other lumbar nerve roots.

3.6 The Major Branches of the Sciatic Nerve The tibial nerve and the peroneal nerve represent the two major branches of the sciatic nerve. The tibial nerve continues to descend in the posterior compartment of the leg and foot, while the peroneal nerve travels down in the lateral and anterior compartments of the leg and foot.

More precisely, the tibial nerve runs through the center of the popliteal fossa and passes below the tendinous arch of the soleus muscle. It continues its course in a neurovascular bundle through the posterior leg compartment and passes through the tarsal tunnel. At the level of the foot, the tibial nerve divides into two branches: medial and lateral plantar nerves that innervate the majority of the foot muscles. Contrary to the tibial nerve, the peroneal nerve runs laterally toward the head of the fibula where it is superficial and consequently vulnerable to injury and compression. At the level of the anterior compartment of the leg, the tibial nerve divides under the fibularis longus muscle into the superficial peroneal nerve and the deep peroneal nerve. The superficial division supplies the lateral compartment of the leg, while the deep division innervates the anterior compartment of the leg and the medial aspect of the foot. The deep peroneal nerve descends between the fibula and the superior part of the peroneus longus and continues its course deeply to the extensor digitorum longus and anterior to the interosseous membrane. All sciatic innervated muscles in the thigh are derived from the tibial division of the sciatic nerve except the short head of the biceps femoris, which is derived from the peroneal division. The sciatic nerve supplies all motor and sensory innervation below the knee excluding the sensation over the medial calf and foot, which is a saphenous sensory area.

3.7 The Motor and Sensory Supply of the Sciatic Nerve The motor and sensory supplies of the sciatic nerve are represented in Tables 3.3 and 3.4, respectively.

3.8 Variant Anatomy of the Sciatic Nerve

43

Table 3.3  Summary of the representation of the motor distribution of the sciatic nerve Nerve Thigh

Branch Tibial division (posterior compartment of the thigh)

Leg

Peroneal division (superficial and lateral to tibial division) Tibial nerve (superficial posterior and deep posterior compartments of the leg)

Superficial peroneal nerve (lateral compartment of the leg) Deep peroneal nerve (anterior compartment of the leg)

Ankle and foot

Medial plantar nerve

Lateral plantar nerve

Deep peroneal (lateral terminal branch)

Table 3.4  Summary of the representation of the sensory supply of the sciatic nerve Nerve Peroneal

Branch Deep peroneal nerve Superficial peroneal nerve Sural

Tibial

Lateral cutaneous nerve Medial plantar nerve Lateral plantar nerve Calcaneal nerve Sural nerve

Sensory supply Dorsal first web space Distal lateral leg Lateral foot Dorsum of foot Proximal lateral leg Medial plantar foot Lateral plantar foot Plantar heel Lateral foot

Motor supply •  Long head of biceps femoris • Semimembranosus • Semitendinosus •  Short head of biceps femoris • Gastrocnemius • Soleus • Popliteus •  Flexor digitorum longus •  Flexor hallucis longus •  Tibialis posterior •  Peroneus longus •  Peroneus brevis •  Extensor digitorum longus •  Extensor hallucis longus •  Tibialis anterior •  Peroneus tertius •  Flexor digitorum brevis •  Adductor hallucis •  Flexor hallucis brevis •  First lumbrical •  Abductor digiti minimi (Baxter’s nerve) •  Quadratus plantae •  Flexor digiti minimi brevis •  Adductor hallucis •  Second, third, and fourth lumbricals •  Dorsal and plantar interossei •  Extensor digitorum brevis •  Extensor hallucis brevis

3.8 Variant Anatomy of the Sciatic Nerve Some anatomical variations regarding topography, course, and division of the sciatic nerve should be considered especially during surgical and other clinical procedures in order to reduce the risk of iatrogenic injury. Among these anatomical variations, sciatic nerve division in relation to the piriformis muscle is the most frequent (Fig. 3.25). Occasionally, there are some variations in the division of sciatic nerve into the tibial nerve and the peroneal nerve. In most people (70–80% of cases), the sciatic nerve splits at the lower thigh or at the apex of the popliteal fossa. Sometimes, the nerve splits higher than usual within the pelvic region, gluteal area, upper thigh, or at the middle of the thigh (Table 3.5).

44

3  Anatomy and Physiology of the Sciatic Nerve

Fig. 3.25  Posterior view of the pelvis showing different variations of the sciatic nerve in relation to the piriformis muscle

Table 3.5  The main anatomical variants related to the division of the sciatic nerve in relation to the piriformis muscle in the deep gluteal region (according to Beaton and Anson) Type of variation a b c d e f

Description An undivided nerve below the undivided piriformis muscle (normal course) A divided sciatic nerve passing through and below the piriformis muscle A divided nerve passing above and below an undivided muscle An undivided sciatic nerve passing through the piriformis muscle heads A divided nerve passing through and above the muscle heads An undivided sciatic nerve passing above the undivided piriformis muscle

Reported incidence (%) 83.1 13.7 1.3 0.5 0.08 0.08

Further Reading

Further Reading Adibatti M, Sangeetha V.  Study on variant anatomy of sciatic nerve. J Clin Diagn Res. 2014;8:AC07–9. https://doi.org/10.7860/ JCDR/2014/9116.4725. Ailianou A, Fitsiori A, Syrogiannopoulou A, Toso S, Viallon M, Merlini L, et  al. Review of the principal extra spinal pathologies causing sciatica and new MRI approaches. Br J Radiol. 2012;85:672–81. https://doi.org/10.1259/bjr/84443179. Al-Khodairy AW, Bovay P, Gobelet C. Sciatica in the female patient: anatomical considerations, aetiology and review of the literature. Eur Spine J. 2007;16:721–31. https://doi.org/10.1007/ s00586-­006-­0074-­3. Atoni AD, Oyinbo CA, Francis DAU, Tabowei UL. Anatomic variation of the sciatic nerve: a study on the prevalence, and bifurcation loci in relation to the piriformis and popliteal fossa. Acta Med Acad. 2022;51:52–8. https://doi.org/10.5644/ama2006-­124.370. Barbosa ABM, Santos PVD, Targino VA, Silva NA, Silva YCM, Gomes FB, et al. Sciatic nerve and its variations: is it possible to associate them with piriformis syndrome? Arq Neuropsiquiatr. 2019;77:646– 53. https://doi.org/10.1590/0004-­282X20190093. Bäumer P, Weiler M, Bendszus M, Pham M.  Somatotopic fascicular organization of the human sciatic nerve demonstrated by MR neurography. Neurology. 2015;84:1782–7. https://doi.org/10.1212/ WNL.0000000000001526. Beaton LE, Anson BJ. The relation of the sciatic nerve and of its subdivisions to the piriformis muscle. Anat Rec. 1937;70:1–5. https://doi. org/10.1002/ar.1090700102. Berihu BA, Debeb YG.  Anatomical variation in bifurcation and trifurcations of sciatic nerve and its clinical implications: in selected university in Ethiopia. BMC Res Notes. 2015;8:633. https://doi. org/10.1186/s13104-­015-­1626-­6. Bharadwaj UU, Varenika V, Carson W, Villanueva-Meyer J, Ammanuel S, Bucknor M, et  al. Variant sciatic nerve anatomy in relation to the piriformis muscle on magnetic resonance neurography: a potential etiology for extraspinal sciatica. Tomography. 2023;9:475–84. https://doi.org/10.3390/tomography9020039. Carro LP, Hernando MF, Cerezal L, Navarro IS, Fernandez AA, Castillo AO.  Deep gluteal space problems: piriformis syndrome, ischiofemoral impingement and sciatic nerve release. Muscles Ligaments Tendons J. 2016;6:384–96. https://doi.org/10.11138/ mltj/2016.6.3.384. Choi YK.  Lumbar foraminal neuropathy: an update on non-­surgical management. Korean J Pain. 2019;32:147–59. https://doi. org/10.3344/kjp.2019.32.3.147. Currin SS, Mirjalili SA, Meikle G, Stringer MD.  Revisiting the surface anatomy of the sciatic nerve in the gluteal region. Clin Anat. 2015;28:144–9. https://doi.org/10.1002/ca.22449. David WS, Sadjadi R.  Clinical neurophysiology of lower extremity focal neuropathies. Handb Clin Neurol. 2019;161:207–16. https:// doi.org/10.1016/B978-­0-­444-­64142-­7.00050-­3. Demondion X, Lefebvre G, Fisch O, Vandenbussche L, Cepparo J, Balbi V.  Radiographic anatomy of the intervertebral cervical and lumbar foramina (vessels and variants). Diagn Interv Imaging. 2012;93:690–7. https://doi.org/10.1016/j.diii.2012.07.008. Distad BJ, Weiss MD.  Clinical and electrodiagnostic features of sciatic neuropathies. Phys Med Rehabil Clin N Am. 2013;24:107–20. https://doi.org/10.1016/j.pmr.2012.08.023. Gilchrist RV, Slipman CW, Bhagia SM. Anatomy of the intervertebral foramen. Pain Physician. 2002;5:372–8.

45 Haviarova Z, Matejcik V, Kuruc R, Líška J, Steno J. Extradural characteristics of the origins of lumbosacral nerve roots. J Neurol Surg A Cent Eur Neurosurg. 2019;80:109–15. https://doi. org/10.1055/s-­0038-­1673400. Ishii T, Kawagishi K, Hayashi S, Yamada S, Yoshioka H, Matsuno Y, et  al. A novel categorization of the muscular branches of the tibial nerve within the popliteal fossa. Ann Anat. 2023;245:151997. https://doi.org/10.1016/j.aanat.2022.151997. Jha AK, Baral P.  Composite anatomical variations between the sciatic nerve and the piriformis muscle: a Nepalese cadaveric study. Case Rep Neurol Med. 2020;2020:7165818. https://doi. org/10.1155/2020/7165818. Kambin P, Brager MD.  Percutaneous posterolateral discectomy. Anatomy and mechanism. Clin Orthop Relat Res. 1987;223:145–54. Kasapuram D, Ganapathy A, Harisha K, Bhukya S, Rani N, Singh S. Neuromuscular variations in the gluteal region—embryological basis and clinical significance. Clin Ter. 2021;172:91–3. https://doi. org/10.7417/CT.2021.2290. Khan H, Ling S, Ali S, Jonnalagadda P, Ramsey F, Weiner M, Awan O. Sciatic nerve variants in patients diagnosed with sciatica: is there a correlation? J Comput Assist Tomogr. 2019;43:953–7. https://doi. org/10.1097/RCT.0000000000000919. Krystkiewicz K, Maślanka M, Skadorwa T, Ciszek B, Tosik M, Furtak J. Meningovertebral ligaments could be a barrier for migration of a herniated intervertebral disc: an anatomical study. Front Surg. 2022;9:969244. https://doi.org/10.3389/fsurg.2022.969244. Muniz Neto FJ, Kihara Filho EN, Miranda FC, Rosemberg LA, Santos DCB, Taneja AK.  Demystifying MR Neurography of the lumbosacral plexus: from protocols to pathologies. Biomed Res Int. 2018;2018:9608947. https://doi.org/10.1155/2018/9608947. Natsis K, Totlis T, Konstantinidis GA, Paraskevas G, Piagkou M, Koebke J.  Anatomical variations between the sciatic nerve and the piriformis muscle: a contribution to surgical anatomy in piriformis syndrome. Surg Radiol Anat. 2014;36:273–80. https://doi. org/10.1007/s00276-­013-­1180-­7. Raj PP.  Intervertebral disc: anatomy-physiology-pathophysiology-­ treatment. Pain Pract. 2008;8:18–44. https://doi. org/10.1111/j.1533-­2500.2007.00171.x. Ribeiro FS, Bettencourt Pires MA, Silva Junior EX, Casal D, Casanova-­ Martinez D, Pais D, et al. Rethinking sciatica in view of a bilateral anatomical variation of the sciatic nerve, with low origin and high division: historical, anatomical and clinical approach. Acta Medica Port. 2018;31:568–75. https://doi.org/10.20344/amp.10567. Silav G, Arslan M, Comert A, Acar HI, Kahilogullari G, Dolgun H, et al. Relationship of dorsal root ganglion to intervertebral foramen in lumbar region: an anatomical study and review of literature. J Neurosurg Sci. 2016;60:339–44. Smoll NR.  Variations of the piriformis and sciatic nerve with clinical consequence: a review. Clin Anat. 2010;23:8–17. https://doi. org/10.1002/ca.20893. Tomaszewski KA, Graves MJ, Henry BM, Popieluszko P, Roy J, Pękala PA, et  al. Surgical anatomy of the sciatic nerve: a meta-analysis. J Orthop Res. 2016;34:1820–7. https://doi.org/10.1002/jor.23186. Wadhwa V, Thakkar RS, Maragakis N, Höke A, Sumner CJ, Lloyd TE, et  al. Sciatic nerve tumor and tumor-like lesions—uncommon pathologies. Skelet Radiol. 2012;41:763–74. https://doi. org/10.1007/s00256-­012-­1384-­7. Yuan SG, Wen YL, Zhang P, Li YK.  Ligament, nerve, and blood vessel anatomy of the lateral zone of the lumbar intervertebral foramina. Int Orthop. 2015;39:2135–41. https://doi.org/10.1007/ s00264-­015-­2831-­6.

4

Epidemiology and Etiologies of Sciatica

“Not all sciatic pains are discogenic or even spinogenic. Although unusual, extrapinal etiologies, whether intra- or extrapelvic, should be known.” A. Akhaddar [The author]

4.1 Generalities and Relevance Sciatica, whether acute or chronic, is among the top most common pain in humans with considerable medical and economic implications. Many people currently use the Internet and consult “Doctor Google” to obtain medical information about their conditions. Concerning sciatica, this term is in the top 20 search pain queries in the world, especially in the United States and Japan. There is also a clear increase in

public interest in the topic of sciatica. According to Google Trends, “sciatica” has had a twofold increase in search frequency worldwide on the Web, a sixfold increase on YouTube, and a threefold increase in Google images between 2008 and 2019. When you enter the term “sciatica” into Google Books Ngram [Michel et al.], a graph shows how the frequency of use of the word “sciatica” occurred in English books between 1800 and 2019 (Fig.  4.1). “Sciatica” is an old term in the

Fig. 4.1  A graph showing the frequency of use of the word “sciatica” in English books between 1800 and 2019 according to Google Books Ngram © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_4

47

48

literature that the frequency of use started to rise in the 1860s, and it peaked in the 1880s and continued to decline until 1972. Then, the frequency of utilization of the term increased slightly up to 2008 to gradually decrease since. It seems that books in English using the term “sciatica” appears less frequently in the literature since the end of World War II. Unfortunately, patients, and many clinicians similarly, use the term “sciatica” to describe any pain arising from the lower back and radiating down to the leg. In our practice, the majority of patients with supposed “sciatic pain,” with or without low back pain, are referred by general practitioners with the question of whether they had lumbosacral radiculopathy secondary to a lumbar disk herniation (LDH). Although the lumbar herniated disk is the most frequent cause of sciatica, many other non-discogenic etiologies should be considered whether they are spinal or extraspinal and even intracranial. Knowing epidemiological characteristics, risk factors, topographic localizations, and different potential etiologies of sciatica may help practitioners understand the occurrence of this symptom in the general population, better address the needs of patients, and facilitate patient management, especially for primary prevention.

4.2 Epidemiology Sciatica is a very common complaint with an annual incidence varying between 1% and 5%. However, its prevalence varies widely in the literature (mean of about 18%) with values ranging from 1.6% in the general population to 43% in a selected working population. This important variation is related to many reasons including data collection techniques, study designs, definitions of sciatica, populations considered (e.g., age, with or without low back pain, working people, and clinical assessment or self-reporting), and the different specified periods of study time. For example, the stricter the definition of sciatic symptoms in relation to pain distribution and duration, the lower the reported prevalence rate. Between 5% and 10% of patients with low back pain have sciatica. Regarding discogenic causes, the annual prevalence of disk-related sciatic pain in the general population is about 2.2%. Sciatica is an adult symptom with a peak incidence around the age of 40. It occasionally occurs before 20 years of age, but pediatric cases are rare. Most of the clinical studies report a clear male predominance (up to 60%). In the United Kingdom, the prevalence of sciatica was about 3.1% in men and 1.3% in women. However, evidence for an association between sciatica and gender is contradictory. There is no temporal, ethnic, or geographic predominance of sciatic pain worldwide.

4  Epidemiology and Etiologies of Sciatica

4.3 Risk Factors Many studies have been directed to identify the risk factors for developing sciatica. Among the best-identified factors associated with increased risk of sciatica are middle age, above-average height (taller individuals), smoking, mental stress, motor vehicle driving, physically strenuous work, and exposure to whole-body vibration (Table 4.1). A part of these factors is even interdependent, which adds to the complexity of the problem. On the opposite, walking, cycling to work, and leisure-time physical activity protect against sciatica. Other possible factors could be involved in discogenic sciatica including but not reserved to the following: • Asymmetry of lower extremities. • Facet joint tropism and orientation (Fig. 4.2). (Lateral LDHs may occur on the side in which the facet joint had a more sagittal orientation. Central LDHs have more symmetric facet joints than those with more lateral herniations). • Paravertebral muscle atrophy (especially fat infiltration of lumbar multifidus muscle) (Fig. 4.3). • Standing abnormalities. • Gait asymmetries. • Flat feet. Besides these factors mentioned above, a few other risk factors can be identified in various non-discogenic sciatic pain groups (c.f. Chapters dedicated to each specific etiology and disease). Identification of consistent potential risk factors, especially modifiable risk factors that could be controlled and changed, plays an important role in primary prevention. The role of genetic factors involved in susceptibility to sciatica has been discussed for a few years. Recently, some studies identified substantial genetic components associated with sciatic pain (e.g., NFIB, SLED1, CHRNB3, BEGAIN, SPTBN2, HRASLS2, and OSR2). In addition, some genetic variabilities may influence the risk of persistent sciatica and chronic outcome in newly diagnosed sciatic pain patients. Table 4.1  Main factors associated with the development of sciatica Personal factors • Age • Height •  Obesity and overweight •  Tobacco smoking •  Psychological factors such as mental stress Occupational •  Severe physical activity (e.g., frequent lifting factors and carrying heavy objects) •  Bending and twisting movements and postures •  Driving, including exposure to vibration from vehicles •  Prolonged sitting

4.4 Classifications and Etiologies Fig. 4.2  Facet joint tropism and orientation on axial CT scan (a, b). Lateral LDHs (arrow) may occur on the side in which the facet joint had a more sagittal orientation (β 10°, lower preoperative disk height index), factors related to the primary discectomy (larger annular defects and limited discectomy during primary surgery), and presence of lumbosacral transitional vertebrae. In order to minimize relapsing, some precautions are needed such as adequate postoperative care, correct rehabilitation, and even a special back school program. When done, repeat discectomy at the same level may need more extensive bone removal to adequately expose recurrent disk fragment(s) with subsequent risk of spinal instability (c.f. Chap. 28 about Recurrent Lumbar Disk Herniations).

13.7 Epidural Fibrosis Epidural or extradural fibrosis is the formation of epidural scar tissue. Up to 25% of patients with FBSS will have epidural fibrosis (AKA scar formation) (Fig.  13.16).

Discrimination between fibrotic scar and recurrent LDH is not always easy on spinal imaging. However, MRI with gadolinium administration is very helpful. Excessive cautery of epidural veins as well as epidural bleeding can be the cause of epidural fibrosis and therefore should be avoided. Fibrosis formed peridural can attach the dura and nerve roots to the surrounding structures and by this means cause compression or stretching of the nervous elements. Free autologous fat graft in the epidural space has been used in an attempt to reduce postoperative epidural fibrosis. Most treatments are conservative using pain control (e.g., analgesics, antidepressants, and GABA analogs) and physical therapies. Concomitant corticosteroids have also a beneficial effect. Removal of fibrosis and scar tissue may lead to poor results. However, some surgeons recommend surgical decompression for selective patients suffering from recalcitrant radicular pain. Finally, electrical nerve stimulation has also been suggested.

204 Fig. 13.16 Postoperative extradural fibrosis (epidural scar tissue) occurred 4 months after the initial surgery for discogenic sciatica. Axial post-gadolinium T1-weighted (a, b) and T2-weighted MR imaging (c, d). Note the epidural gadolinium enhancement (arrows). This patient improved on medical treatment and physical therapy alone

Fig. 13.17 Postoperative arachnoiditis occurred 6 months following the initial unilateral L4–L5 herniectomy/discectomy. Sagittal (a) and axial (b) T2-weighted MR imaging. There is a retraction of the thecal sac, and the nerve roots are adherent to the parietal arachnoid peripherally (arrows)

13  Surgical Complications of Discogenic Sciatica

a

b

c

d

a

13.8 Arachnoiditis Arachnoiditis is an inflammation within the arachnoid and subarachnoid spaces with scaring in the perineural structures leading to compression of the nerve roots within the cauda

b

equina (Fig.  13.17). Arachnoiditis is more commonly the result of surgical intervention and the healing process that occurs following surgery. This condition is usually associated with inflammatory changes and can result in progressive spinal and neurological radicular symptoms over several

13.10 Wrong Side or Wrong Level Exploration

weeks or months. Acute forms are rare. MRI is the neuroimaging procedure of choice for the diagnosis (c.f. Chap. 55 about Lumbar Adhesive Arachnoiditis). There are three main features: (a) Central conglomerations of adherent nerve roots into the dural sac. (b) “Empty thecal sac sign”: The thecal sac appears devoid of its cauda equina roots because nerve roots are adherent to the parietal arachnoid peripherally. (c) Subarachnoid space is filed with inflammatory soft tissue mass without CSF signal. Most therapeutic methods are conservative using pain control and physical therapies. Some other neuroinflammation suppressor agents have been suggested (e.g., naltrexone, ketorolac, and corticosteroid) but the results are controversial. The efficacy of decompressive surgical procedures (arachnoid dissection with or without duroplasty) remains debated and rarely used. Therefore, some authors recommended a simple decompressive laminectomy without durotomy.

13.9 Failed Back Surgery Syndrome Failed back surgery syndrome (FBSS) is defined as “a surgical end-stage after one or several operative interventions on the lumbar neuroaxis, indicated to relieve lower back pain, radicular pain or the combination of both without positive effect.” FBSS may occur in up to 40% of patients following lumbar spine surgery. Postoperative pain may persist for various reasons that should be managed consecutively (Table 13.2). Sometimes, the exact cause is unknown and the FBSS is then considered “idiopathic.” However, apart from organic etiologies, psychological factors should be taken into consideration in predicting postoperative low back pain. In this context, the patient should be reassured and appropriate analgesics must be given. However, facing severe and

205 Table 13.2  Various etiologies associated with failed back surgery syndrome Patho-anatomical

Physical and mechanical Neurophysiological

Peripheral pain generators Other etiologies

•  Stenosis (incorrect decompression) • Fibrosis •  Wrong level surgery •  Disk herniation •  Spinal instability • Pseudarthrosis •  Mechanical low back pain •  Myofascial pain •  Spinal deconditioning •  Flat back syndrome •  Neuropathic pain • Fibromyalgia •  Reflex sympathetic dystrophy • Radiculopathy •  Sacro-iliac joint dysfunction and pain •  Facet joint syndrome • Hardware • Pseudomeningocele • Arachnoiditis •  Synovial cyst •  Battered root syndrome (by excessive root retraction) • Discitis/osteomyelitis •  Vascular claudication

persistent sciatic pain, the onset of neurological weakness or cauda equina symptoms requires MRI control which can detect the causative etiology.

13.10 Wrong Side or Wrong Level Exploration In 1.2–3.3% of cases, postoperative symptoms are related to wrong disk level exploration during surgery (Figs. 13.18 and 13.19). To minimize this complication, it is important to correlate the level visualized by MRI and the same one seen on the lateral view of X-ray intraoperatively. Exploration of the wrong level happens less often in the L5–S1 level than in the higher segments. This condition requires rapid reoperation.

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Fig. 13.18  Case 4. This patient was operated on at another hospital for a massive/giant L4–L5 disk herniation (arrows) without any clinical improvement. Sagittal T1-weighted (a), T2-weighted MR imaging (b), in STIR sequences (c) and axial (d, e) T2-weighted MR imaging

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Fig. 13.19  Case 4. Postoperative MR imaging performed a month later shows L4–L4 wrong level exploration (arrows) (a–d). The L4–L5 symptomatic disk level has not been explored. The patient’s condition requires rapid reoperation with good immediate results

13.11 Lesions from Operative Positioning

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13.11 Lesions from Operative Positioning Ventral or kneeling operative positioning can induce skin lesions and some neurological structures (e.g., brachial plexus). Cutaneous edema or necrosis of the skin may occur on the thorax, scrotum, penis, face (Fig. 13.20a and 13.20b), and knees (Fig. 13.20c). Cervical myelopathy and ophthal-

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mological lesions (Fig.  13.21) are rarer. Postoperative leg pain and even sciatica can also be related to lesions secondary to incorrect surgical positioning (especially following a kneeling position). Proper head and whole-body operative positions should avoid these problems.

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Fig. 13.20  Postoperative facial swelling (a, b) mimicking local cellulitis in a young patient operated on for discogenic sciatica in a “knee-chest position”. Bullous pemphigoid of the knees developed after lumbar spinal decompression in a “knee-chest position” (c)

Fig. 13.21 Postoperative “red eye” (a, b) in a patient operated on for discogenic sciatica in a “knee-chest position.” Luckily, this patient did not present any visual disturbances

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13.12 Hardware Devices and Instrumentations

13  Surgical Complications of Discogenic Sciatica

• Wound dehiscence. • Delay or poor healing. • Infection (more or less deep and extensive) (Fig. 13.6). • Hematoma. The most important factor in preventing instrumentation-­ related complications is a systematic understanding of the Closure of the surgical wound should not be underestiapplicable surgical anatomy. Instrumentation-related commated and left to the care of the operating assistant. plications regarding insertion can be avoided by using the proper image guidance and intraoperative verification. For lumbar pedicle screw placement, palpation of all four walls and the floor of the bony channel is a critical portion of the 13.16 Thromboembolic Problems procedure. In addition, lumbar pedicle instrumentation can include During spine surgery, patients have a risk of thromboembolic pedicle fracture, dural injury, nerve root injury, and vascular complications, especially in the kneeling position. The rate of embolic complications in the literature ranges from 0.1% injury. Any instrumentation or hardware failure can lead to to 1%, whereas the rate of thrombosis of the lower limb seems to be, must be, much higher. Thrombosis prophylaxis threatening postoperative spinal instability. by early mobilization and the use of antithrombotic stockings must be considered. Additional low-dose heparin application remains a matter of debate because of possible 13.13 Spinal Instability bleeding into the spinal canal. Many authors recommend This is an excessive mobility between two vertebrae. latro- perioperative low-dose heparin prophylaxis. genic spinal lumbar instability may develop in 0.4% of operative patients with LDH. Most cases happen due to excessive facet joint removal 13.17 Reoperation with simultaneous discectomy. Patients with concomitant spinal canal stenosis, those with foraminal/extraforaminal Reoperation includes any additional surgical procedure LDH, and those with unsuspected spondylolysis are particu- regardless of indication during the postoperative period. A meta-analysis performed by Shriver et al. in 2015 found larly exposed to postoperative spinal instability. a mean 7.1% new operation rate for LDH after open discecCaution should be taken when performing posterior facetomy and 3.7% for microendoscopic discectomy with varitectomy. Resection of the inferior articular process of the able lengths of follow-up. superior vertebrae should not exceed one-third of the entire Most causes for reoperation are related to re-herniation facet joint. (recurrence), insufficient neurological decompression, missing disk fragment(s), or spinal instability. Indeed, inadequate decompression in the lateral recess or the neural 13.14 Compressing Epidural Hematoma foramen is the most common cause of poor surgical techIntraoperative excessive bleeding may be encountered in nique leading to FBSS. However, maximum decompression 3.5–7.1% of cases. However, compressing epidural hemato- may also lead to instability due to excessive articular surmas is much rare. The majority of cases do not require a face removal. Moreover, neurological compression from grafts and blood transfusion. Bleeding might be caused by arterial bleeding from the hardware needs to be re-explored urgently to avoid any back muscles or epidural veins, rarely from cancellous bone definitive problems. More rarely, for the presence of a crush syndrome (c.f. following bone resection. The intraoperative bleeding can be Chaps. 32 and 109 about Crush Syndrome), the new surgical reduced by positioning the patient prone or kneeling with a procedure consists of microdiscectomy, microendoscopic hanging abdomen as well as proper coagulation and using an discectomy, nucleolysis, laminectomy, and fusion. epidural tube drainage system whenever needed. In most cases, reoperation has greater possibilities for further complications and fibrosis. In addition, the presence of certain comorbidities, pre-­ 13.15 Wound Complications existing chronic pain disorders, or psychological conditions Postoperative wound problems are not rare and often include may all prevent a successful postoperative outcome. the following:

13.19 Retroperitoneal Blood Vessels and Visceral Injuries

13.18 Pseudarthrosis Pseudoarthrosis or false joint is a non-union mobile fracture occurring in 5–35% of cases after lumbar spine fusion (failed spinal fusion). This complication should be suspected when a patient presents with recurrent axial pain and/or radicular symptoms during long-term follow-up from fusion or in the presence of instrumentation failure. Acute presentations are unusual. Some risk factors are associated with decreased fusion rates such as alcoholism, osteoporosis, advanced age, malnutrition, and tobacco use. On imaging, some features, and characteristics are highly suggestive such as motion on dynamic films, absence of continuous trabecular bone between adjacent vertebrae, gas in the disk space, and peri-implant radiolucency. The treatment of pseudarthrosis varies but is almost always surgical. Asymptomatic patients may be observed and followed closely with radiographs and routine clinical evaluation. Primary principles of surgery include stabilization of the existing posterior fixation and re-grafting.

13.19 Retroperitoneal Blood Vessels and Visceral Injuries Retroperitoneal blood vessel injuries are rare with a reported incidence of less than 0.1%. Three main types of vascular injury may occur during posterior lumbar discectomy are as follows: Fig. 13.22 Intraoperative iatrogenic vessel injury during posterior lumbar discectomy. Left common iliac artery laceration (arrows) as seen on immediate abdominopelvic CT angiography (a, b). Note the adjacent retroperitoneal hematoma (dotted lines). The injury occurred due to direct iatrogenic damage produced by forceps used for discectomy (c)

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(a) Iatrogenic vascular laceration with bleeding from an artery and/or a vein. (b) Arteriovenous fistula formation. (c) Pseudoaneurysm (arterial) development. A vascular laceration is by far the least common but the most dangerous iatrogenic vascular complication (Fig. 13.22). This injury tends to occur intraoperatively due to direct iatrogenic damage and is often produced by the pituitary rongeur or forceps (Fig.  13.23). The vascular laceration usually becomes symptomatic and potentially ­ fatal during the surgical procedure or in the early postoperative period (mortality rate of 18.8%), while an arteriovenous fistula or pseudoaneurysm is often diagnosed later. In hemodynamically unstable patients, an emergent exploratory laparotomy is life-saving even without vascular imaging, although angiography with/without endovascular intervention may be used in stable patients. The endovascular procedure should be reserved for patients with stable vital signs. To avoid this life-threatening complication, some precautions should be bear in mind. Exploration of the intervertebral disk space should be done with the pituitary rongeur/ forceps closed, and the distal joint of the rongeur’s or forceps’s jaws (about 10 mm) is a useful marker not to exceed in depth. The anterior longitudinal ligament should not be damaged. Ureteral, bowel, and other retroperitoneal anatomic structures are rare.

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13.20 Other Surgical Errors and Rare Complications

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Although rare occurrence following lumbar discectomy, the following complications should be known: • Retained foreign bodies (e.g., nonabsorbable hemostatic materials, textiloma, tube drainage) (Figs.  13.24, 13.25, 13.26, 13.27, 13.28, 13.29, 13.30, and 13.31). • Surgical equipment failure (instrument breakages such as pituitary rongeur or forceps rupture). • Epidural radicular neuroma. • Epidural gas compression. • Discal cyst and pseudocyst (Fig. 13.32). • Radicular compression by free epidural fat-grafting. • Graft-related complications, especially bone sites such as iliac crest (hematoma, bone fracture, infection, or adjacent peripheral nerve injury). • Spinal epidural arteriovenous fistula.

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Fig. 13.23  A forceps in a closed and open position (a). Too deep penetration of the instrument can induce retroperitoneal blood vessels or visceral injuries (b) [aorta (Ao) and inferior venous cava (IVC)]

Fig. 13.24  Case 5. Intracanal retained foreign body granuloma (gossypiboma— retained surgical cottonoid) (stars) diagnosed 10 months following L4–L5 disk surgery performed in another hospital. Axial CT scan (a) and T2-weighted MR imaging (b)

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13.20 Other Surgical Errors and Rare Complications Fig. 13.25  Case 5. Sagittal T1-weighted (a) and T2-weighted MR imaging (b) in the same patient. This compressive epidural granuloma (arrows) can be confused with a re-herniation or an epidural abscess

Fig. 13.26  Case 6. Chronic low back pain in a 64-year-­ old man operated on 13 years previously for lumbar spinal stenosis. Axial (a) and sagittal (b) CT scan imaging showing a paravertebral granuloma on the left side (stars)

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Fig. 13.27  Case 6. Bilobed paraspinal granuloma (stars) as seen on sagittal T1-weighted (a) and T2-weighted MR imaging (b) and on axial post-­ gadolinium T1-weighted (c) and T2-weighted MR imaging (d)

Fig. 13.28  Case 6. Intraoperative view of the granuloma (a). The foreign body (likely a hemostatic compress) (stars) was surrounded by an important thick fibrous capsule (b)

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13.20 Other Surgical Errors and Rare Complications Fig. 13.29  Case 6. Histopathological images showing a granulomatous inflammatory reaction rich in foamy macrophages (black arrows) and foreign body-type multinucleated giant cells (yellow arrows) around cholesterol clefts (stars) and around foreign bodies (circle) (a, b) (hematoxylin and eosin stain, original magnification ×200). (Courtesy of Pr. Mohamed Amine Azami)

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Fig. 13.30  Case 7. This postoperative paraspinal granuloma (textiloma) (stars) was diagnosed 5 years following an initial surgery for an L4–L5 disk herniation combined with adjacent spinal stenosis. Sagittal

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T1-weighted (a) and T2-weighted MR imaging (b), and axial T1 post-­ gadolinium MR imaging (c)

13  Surgical Complications of Discogenic Sciatica

214 Fig. 13.31  Case 7. Intraoperative view of the granuloma (a). The foreign body (nonabsorbable materials) (stars) was surrounded by a large fibrous capsule (b)

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Fig. 13.32  A postoperative discal cyst (arrows) occurring after L4–L5 herniectomy and discectomy for disk herniation as seen on sagittal (a, b) and axial (c) T2-weighted MR imaging. (Courtesy of Pr. Abad Cherif El Asri)

13.21 Nonsurgical (Medical) Complications As with all other surgical procedures, surgery for discogenic sciatica is also associated with various general medical complications. However, these complications are unusual because the majority of patients are young adults and previously healthy. Deep vein thrombosis, pulmonary embolism, pneumonia, urinary retention, urinary tract infection, and gastroenteric disturbances are among the most common medical problems. Additional complications are less frequent (e.g., myocardial infarction, seizure, and ischemic stroke).

Clinicians and surgeons must keep in mind potential concomitant diseases, whether spinal, extraspinal, or systemic, to avoid further problems. Special attention must concern pre-existing chronic pain conditions or psychological disorders.

13.22 Mortality Mortality is a rare complication following surgery for discogenic sciatica (less than 0.1%). Hemorrhagic shock due to retroperitoneal blood vessel laceration and pulmonary embolism are the complications with the highest mortality rates.

Further Reading

13.23 Conclusion Surgical complications are frustrating events for both patients and surgeons. Possible surgical risks of complications during lumbar discectomy should be well known and clearly exposed to the patients or their families before the surgical procedure. Many possibilities exist for the management of these different complications encountered but none of them are considered standard of care. In order to prevent the majority of surgical complications, the following precautions have to be made correctly: • • • • • • •

Accurate diagnosis. Patient selection and information. Surgeon’s education and training. Preoperative planning. Step-by-step surgical technique. Infection prophylaxis. Postoperative care and follow-up.

Furthermore, special attention should be given to patient psychological factors such as anxiety, depression, and hypochondriasis as well as to social characteristics such as salary or wages, social and financial problems, and litigation. All these factors have a negative impact on surgical outcome. Finally, from a medicolegal standpoint of view, any negligence, inattention, and lack of care will result in serious malpractices in the surgical management of patients with sciatic pain.

Further Reading Ajiboye RM, Drysch A, Mosich GM, Sharma A, Pourtaheri S. Surgical treatment of recurrent lumbar disk herniation: a systematic review and meta-analysis. Orthopedics. 2018;41:e457–69. https://doi. org/10.3928/01477447-­20180621-­01. Akhaddar A.  Surgical site infections in spinal surgery. In: Atlas of infections in neurosurgery and spinal surgery. Cham, Switzerland: Springer; 2017. https://doi.org/10.1007/978-­3-­319-­60086-­4_22. Akhaddar A.  Letter to the Editor: Talking about our own complications: is it still a taboo subject in neurosurgery? World Neurosurg. 2020;142:579. https://doi.org/10.1016/j.wneu.2020.07.191. Akhaddar A, Boulahroud O, Naama O, Al-Bouzidi A, Boucetta M.  Paraspinal textiloma after posterior lumbar surgery: a wolf in sheep’s clothing. World Neurosurg. 2012;77:375–80. https://doi. org/10.1016/j.wneu.2011.07.017. Al-Saadi T, Al-Kindi Y, Allawati M, Al-Saadi H.  Intracranial hemorrhage following spinal surgery: a systematic review of a rare complication. Surg J (N Y). 2022;8:e98–e107. https://doi. org/10.1055/s-­0042-­1743525. Altschul D, Kobets A, Nakhla J, Jada A, Nasser R, Kinon MD, et al. Postoperative urinary retention in patients undergoing elective spinal surgery. J Neurosurg Spine. 2017;26:229–34. https://doi.org/10. 3171/2016.8.SPINE151371.

215 Anichini G, Landi A, Caporlingua F, Beer-Furlan A, Brogna C, Delfini R, et al. Lumbar endoscopic microdiscectomy: where are we now? An updated literature review focused on clinical outcome, complications, and rate of recurrence. Biomed Res Int. 2015;2015:417801. https://doi.org/10.1155/2015/417801. BenDebba M, Augustus van Alphen H, Long DM. Association between peridural scar and activity-related pain after lumbar discectomy. Neurol Res. 1999;21S1:S37–42. https://doi.org/10.1080/01616412 .1999.11741025. Bombieri FF, Shafafy R, Elsayed S.  Complications associated with lumbar discectomy surgical techniques: a systematic review. J Spine Surg. 2022;8:377–89. https://doi.org/10.21037/jss-­21-­59. Bydon M, Macki M, Abt NB, Sciubba DM, Wolinsky JP, Witham TF, et al. Clinical and surgical outcomes after lumbar laminectomy: an analysis of 500 patients. Surg Neurol Int. 2015;6:S190–3. https:// doi.org/10.4103/2152-­7806.156578. Clancy C, Quinn A, Wilson F. The aetiologies of failed back surgery syndrome: a systematic review. J Back Musculoskelet Rehabil. 2017;30:395–402. https://doi.org/10.3233/BMR-­150318. Cobanoğlu S, Imer M, Ozylmaz F, Memiş M. Complication of epidural fat graft in lumbar spine disc surgery: case report. Surg Neurol. 1995;44:479–81. https://doi.org/10.1016/0090-­3019(95)00222-­7. Daly CD, Lim KZ, Ghosh P, Goldschlager T.  Perioperative care for lumbar microdiscectomy: a survey of Australasian neurosurgeons. J Spine Surg. 2018;4:1–8. https://doi.org/10.21037/jss.2018.01.03. Erman T, Tuna M, Göçer AI, Idan F, Akgül E, Zorludemir S. Postoperative radicular neuroma. Case report. Neurosurg Focus. 2001;11:ecp. https://doi.org/10.3171/foc.2001.11.5.9. Fjeld OR, Grøvle L, Helgeland J, Småstuen MC, Solberg TK, Zwart JA, et  al. Complications, reoperations, readmissions, and length of hospital stay in 34 639 surgical cases of lumbar disc herniation. Bone Joint J. 2019;101-B:470–7. https://doi.org/10.1302/0301-­ 620X.101B4.BJJ-­2018-­1184.R1. Fu CF, Tian ZS, Yao LY, Yao JH, Jin YZ, Liu Y, et  al. Postoperative discal pseudocyst and its similarities to discal cyst: a case report. World J Clin Cases. 2021;9:1439–45. https://doi.org/10.12998/ wjcc.v9.i6.1439. Golinvaux NS, Bohl DD, Basques BA, Yacob A, Grauer JN. Comparison of the lumbar disc herniation patients randomized in SPORT to 6,846 discectomy patients from NSQIP: demographics, perioperative variables, and complications correlate well. Spine J. 2015;15:685–91. https://doi.org/10.1016/j.spinee.2014.12.008. Goodkin R, Laska LL.  Vascular and visceral injuries associated with lumbar disc surgery: medicolegal implications. Surg Neurol. 1998;49:358–70. https://doi.org/10.1016/s0090-­3019(97)00372-­8. Harper R, Klineberg E. The evidence-based approach for surgical complications in the treatment of lumbar disc herniation. Int Orthop. 2019;43:975–80. https://doi.org/10.1007/s00264-­018-­4255-­6. Hsieh MK, Chang CN, Hsiao MC, Chen WJ, Chen LH.  Conversion paralysis after surgery for lumbar disc herniation. Spine (Phila Pa 1976). 2010;35:E308–10. https://doi.org/10.1097/ BRS.0b013e3181c41bc3. Kienzler JC, Heidecke V, Assaker R, Fandino J, Barth M. Intraoperative findings, complications, and short-term results after lumbar microdiscectomy with or without implantation of annular closure device. Acta Neurochir. 2021;163:545–59. https://doi.org/10.1007/s00701-­ 020-­04612-­2. Konya D, Ozgen S, Pamir MN.  Cerebellar hemorrhage after spinal surgery: case report and review of the literature. Eur Spine J. 2006;15:95–9. https://doi.org/10.1007/s00586-­005-­0987-­2. Kraemer R, Wild A, Haak H, Herdmann J, Krauspe R, Kraemer J. Classification and management of early complications in open lumbar microdiscectomy. Eur Spine J. 2003;12:239–46. https://doi. org/10.1007/s00586-­002-­0466-­y.

216 Lewandrowski KU, Hellinger S, De Carvalho PST, Freitas Ramos MR, Soriano-Sánchez JA, Xifeng Z, et  al. Dural tears during lumbar spinal endoscopy: surgeon skill, training, incidence, risk factors, and management. Int J Spine Surg. 2021;15:280–94. https://doi. org/10.14444/8038. Pan M, Li Q, Li S, Mao H, Meng B, Zhou F, et al. Percutaneous endoscopic lumbar discectomy: indications and complications. Pain Physician. 2020;23:49–56. Pechlivanis I, Kuebler M, Harders A, Schmieder K.  Perioperative complication rate of lumbar disc microsurgery depending on the surgeon’s level of training. Cent Eur Neurosurg. 2009;70:137–42. https://doi.org/10.1055/s-­0029-­1216361. Phan K, Xu J, Schultz K, Alvi MA, Lu VM, Kerezoudis P, et al. Full-­ endoscopic versus micro-endoscopic and open discectomy: a systematic review and meta-analysis of outcomes and complications. Clin Neurol Neurosurg. 2017;154:1–12. https://doi.org/10.1016/j. clineuro.2017.01.003. Rajpal K, Singh J, Bahadur R, Bansal K, Shyam R, Khatri K.  Postoperative epidural fibrosis prevention: which is better-­autologous fat versus gelfoam. Asian Spine J. 2022;16:343–51. https://doi. org/10.31616/asj.2020.0268. Ramirez LF, Thisted R. Complications and demographic characteristics of patients undergoing lumbar discectomy in community hospitals. Neurosurgery. 1989;25:226–30. https://doi.org/10.1097/00006123-­ 198908000-­00012. Sebaaly A, Lahoud MJ, Rizkallah M, Kreichati G, Kharrat K.  Etiology, evaluation, and treatment of failed back surgery syndrome. Asian Spine J. 2018;12:574–85. https://doi.org/10.4184/ asj.2018.12.3.574. Shi JG, Xu XM, Sun JC, Wang Y, Kong QJ, Shi GD. Theory of Bowstring disease: diagnosis and treatment Bowstring disease. Orthop Surg. 2019;11:3–9. https://doi.org/10.1111/os.12417. Shriver MF, Xie JJ, Tye EY, Rosenbaum BP, Kshettry VR, Benzel EC, et  al. Lumbar microdiscectomy complication rates: a systematic review and meta-analysis. Neurosurg Focus. 2015;39:E6. https:// doi.org/10.3171/2015.7.FOCUS15281.

13  Surgical Complications of Discogenic Sciatica Slipman CW, Shin CH, Patel RK, Isaac Z, Huston CW, Lipetz JS, et al. Etiologies of failed back surgery syndrome. Pain Med. 2002;3:200– 14. https://doi.org/10.1046/j.1526-­4637.2002.02033.x. Stadler JA III, Wong AP, Graham RB, Liu JC. Complications associated with posterior approaches in minimally invasive spine decompression. Neurosurg Clin N Am. 2014;25:233–45. https://doi. org/10.1016/j.nec.2013.12.003. Takai K, Matsumoto T, Yabusaki H, Yokosuka J, Hatanaka R, Taniguchi M.  Surgical complications associated with spinal decompression surgery in a Japanese cohort. J Clin Neurosci. 2016;26:110–5. https://doi.org/10.1016/j.jocn.2015.06.029. Turgut M, Akhaddar A, Turgut AT. Retention of nonabsorbable hemostatic materials (retained surgical sponge, gossypiboma, textiloma, gauzoma, muslinoma) after spinal surgery: a systematic review of cases reported during the last half-century. World Neurosurg. 2018;116:255–67. https://doi.org/10.1016/j.wneu.2018.05.119. Turgut M, Turgut AT, Dogra VS. Iatrogenic ureteral injury as a complication of posterior or lateral lumbar spine surgery: a systematic review of the literature. World Neurosurg. 2020;135:280–96. https://doi.org/10.1016/j.wneu.2019.12.107. Vangen-Lønne V, Madsbu MA, Salvesen Ø, Nygaard ØP, Solberg TK, Gulati S.  Microdiscectomy for lumbar disc herniation: a single-­ center observational study. World Neurosurg. 2020;137:e577–83. https://doi.org/10.1016/j.wneu.2020.02.056. Vinas-Rios JM, Sanchez-Aguilar M, Medina Govea FA, Von Beeg-­ Moreno V, Meyer F, DWG Registry-group. Incidence of early postoperative complications requiring surgical revision for recurrent lumbar disc herniation after spinal surgery: a retrospective observational study of 9,310 patients from the German Spine Register. Patient Saf Surg. 2018;12:9. https://doi.org/10.1186/s13037-­018-­ 0157-­1. Willson MC, Ross JS.  Postoperative spine complications. Neuroimaging Clin N Am. 2014;24:305–26. https://doi.org/10.1016/j. nic.2014.01.002. Yoshihara H, Yoneoka D. Incidental dural tear in spine surgery: analysis of a nationwide database. Eur Spine J. 2014;23:389–94. https://doi. org/10.1007/s00586-­013-­3091-­z.

14

Surgical Outcomes of Discogenic Sciatica

14.1 Generalities and Relevance Adequate management of sciatica needs to include enough listening to patients’ stories, offering an adequate physical assessment, ample information about their complaints, and timely accurate diagnosis of the disorder. Explaining the choice of the type of treatment, its efficacy, complications, and limits are seen as positively contributing to the partnership between patients and clinicians, especially following a surgical procedure. In addition, caregivers need to consider psychological and psychosocial factors. Indeed, numerous studies indicate that the results of surgical treatment and pain-related outcomes are influenced by the patient’s personality and psychosocial factors. Surgical outcomes of discogenic sciatica have improved with the advancement of imaging diagnosis and an enhancement of surgical techniques. It is clear that the presence of severe neurological deficit, advanced age, underlying medical condition, and delay in the diagnosis have an important impact on the prognosis. Factors associated with excellent and poor prognosis in discogenic sciatica are given in Table 14.1. Unfortunately, even today, some neurologists, radiologists, rheumatologists, orthopedists, physical therapists, and even neurosurgeons still make errors regarding the proper diagnosis and treatment of sciatica, perhaps due to underlying misconceptions.

Table 14.1  Factors associated with good/excellent and poor prognoses in discogenic sciatica Factors associated with a good/excellent prognosis • Young age of the patient • Timely diagnosis • Acute pain (6 months) • Predominant low back pain • Severe neurological deficit including cauda equina syndrome (CES) • Poor general condition • Severe comorbid factors • Upper LDH • Multiple LDH • Contained LDH • Central LDH • Foraminal and extraforaminal LDH • Postoperative chronic intractable pain • Important psychological and psychosocial disorders • Kinesiophobia

14.2 Postoperative Management In the postoperative period, surgeons should check for strength of lower extremities (especially muscles controlled by the affected nerve root(s)), signs of cauda equina

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_14

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syndrome, postoperative pain out of the ordinary by their location or intensity, and appearance of dressing (especially signs of unusual bleeding or CSF leak). Any unusual symptoms or signs should be taken seriously and rapidly assessed to rule out potential complications. Most surgeons advise their patients to mobilize on the same day or the day after the surgery. Patients may be discharged (usually before the third postoperative day) when pain is sufficiently controlled and when they are able to eat, void, and move around without assistance. The majority of surgeons recommend returning to work and daily activities 4–6 weeks later. Adequate physical therapy or rehabilitation program initiated 3–4 weeks postoperatively increases general functional status before the patient’s full recovery. Postoperatively, patients should be assisted, reassured, and encouraged by their clinicians and nurses. Physical therapy, psychotherapy, and even cogno-behavioral therapy can be considered as well. Indeed, some patients with important psychological and psychosocial disorders influence negatively treatment outcomes. Recognition of all contributing

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factors, whether physical or non-physical, allows the clinician to adopt the best global approach that can lead to better patient outcomes. Sometimes, faced with an unsatisfactory postoperative result, the clinician must explain to the patient the possible limitations of the treatment. Planned follow-up after surgery is necessary to decrease complication occurrence. One-month, then 2- or 3-month, and 6-month follow-up intervals appear to be appropriate to monitor the evolution of the patient recovery. The utility of postoperative spinal imaging remains controversial, especially in pauci or asymptomatic patients. It seems reasonable to perform a postoperative spinal magnetic resonance imaging (MRI) only in case of persistence or reappearance of sciatica or any neurological disorders (Figs. 14.1, 14.2, 14.3, 14.4, 14.5, 14.6, and 14.7). However, MRI must be interpreted with caution in order to differentiate residual or recurrence from epidural fibrosis. For example, MRI performed at a 12-month follow-up in patients who had been treated for sciatic pain and LDH did not distinguish between those with a favorable outcome and those with an unfavorable outcome.

c

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Fig. 14.1  Case 1. Preoperative (a, c) and postoperative (b, d) spinal magnetic resonance imaging in a patient with a paramedian L5–S1 lumbar disk herniation (arrows)

14.2 Postoperative Management Fig. 14.2  Case 2. Preoperative (a, c) and postoperative (b, d) axial spinal magnetic resonance imaging in a patient with a foraminal L4–L5 lumbar disk herniation (arrows)

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Fig. 14.3  Case 3. Preoperative sagittal MRI in a patient with giant migrated and sequestrated L5–S1 disk herniation (arrows) (a–c)

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14  Surgical Outcomes of Discogenic Sciatica

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Fig. 14.4  Case 3. Preoperative axial MRI in the same patient with massive/giant and sequestrated L5–S1 disk herniation (arrows) (a–c)

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Fig. 14.5  Case 3. Postoperative sagittal (a, b) and axial (c) MRI following laminectomy and herniectomy

14.2 Postoperative Management

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Fig. 14.6  Case 4. Preoperative (a, b) and postoperative (c) sagittal MRI in a patient with L4–L5 disk herniation (arrows) combined with lumbar canal stenosis Fig. 14.7  Case 4. Preoperative (a, b) and postoperative (c, d) axial MRI in the same patient. Note the L4–L5 disk herniation (arrow) combined with lumbar canal stenosis (arrowheads)

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14  Surgical Outcomes of Discogenic Sciatica

14.3 Postoperative Complications (c.f. Chap. 13 About Surgical Complications of Discogenic Sciatica)

Some selective patients who present chronic intractable sciatic pain can be managed using some specific techniques such as:

Learning to identify and manage surgical complications is an essential part of spinal surgery and LDH has its own lessons. It has been expected that about 10–20% of patients undergoing surgery for lumbar disk herniation (LDH) may develop complications. These complications can be classified into general and specific. General complications are those, often medical, unrelated to the surgery strictly speaking, while specific complications include those directly related to the anatomic site, surgery, or the surgical procedure used. In a recent meta-analysis of lumbar discectomy complications performed by Shriver et al., the overall complication rates for open microdiscectomy, microendoscopic discectomy, and percutaneous microdiscectomy are 12.5%, 13.3%, and 10.8%, respectively. All complications can negatively affect the morbidity and mortality of patients as well as hospital and societal resources. In addition, some complications can even pose medicolegal problems to the surgeon. Once the etiology of the complication has been recognized, rapid action should be engaged by the surgeon to manage the situation and offer the patient the best chance of clinical recovery. Recurrence of LDH, epidural fibrosis, and failed back surgery syndrome are among the most frequent complications following surgery for discogenic sciatica. Great care and attention should be taken at every stage of the treatment: before, during, and following the surgical procedures to prevent and reduce these complications. Unfortunately, some complications can occur due to misdiagnosis or negligent surgery, called medical malpractice.

• Implanted Spinal Fluid Pumps. The idea is to inject medications directly into the cerebrospinal fluid surrounding the spinal cord and spinal nerves in order to significantly increase drug effectiveness with fewer side effects and risks. • Nerve and Spinal Cord Stimulation. The technique is based on electrical stimulation of nerves or the spinal cord, particularly for treating neuropathic pain. • Ablative Procedures. Different ablative procedures were developed to block pain signals at different levels within the peripheral and central nervous systems. There are two main types of ablative procedures: Peripheral (e.g., rhizotomy and dorsal root ganglia ablation using chemical agents, hot, cold, or radiofrequency probes) and central (e.g., commissurotomy, thalamotomy, and cingulotomy). After a preliminary wave of fervor for ablative procedures, it became clear that they were grafted with important complications and long-term results were poor, especially for chronic sciatic pain.

14.4 Sequels Recovery from neurological and sphincter dysfunction is variable. Unfortunately, permanent chronic pain and neurological damage can occur, especially in some patients who had preoperative CES or those with a delay in their management.

14.5 Surgical Results Recent studies showed that surgery accelerates recovery and leads to a greater reduction in leg pain on long-term follow­up compared with conservative management for sciatica. In addition, surgical treatment produces better outcomes than percutaneous treatments. Ultimately, the therapeutic decision is based on the discussion between the doctor and his/ her patient in light of the clinical and imaging evaluation, duration of symptoms, and patient’s desires. About 80–85% of surgically treated patients had a good improvement to excellent recovery from their sciatic pain, inferior extremities weakness, and/or sphincter disorders (Figs. 14.8, 14.9, 14.10, and 14.11). The postoperative results of central LDH are somewhat poorer than those of subarticular disk herniation. It seems that central LDH had a relatively high recurrence rate (up to 14%), persistent low back pain, and greater segmental instability in comparison with subarticular ones. In addition,

14.5 Surgical Results

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Fig. 14.8  Case 5. Preoperative patient presentation. Left lateral shift (sciatic scoliotic list) with flatback and slight trunk flexion (arrows) away from the right (contralateral) side of sciatica (a–c)

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Fig. 14.9  Case 5. Postoperative patient presentation the next day after surgery. Significant improvement of the patient’s postural deformities (a–c)

224 Fig. 14.10  Case 6. Preoperative (a) and postoperative (b) posture in a patient with right L4–L5 discogenic sciatica. Significant improvement of the sciatic scoliotic list

14  Surgical Outcomes of Discogenic Sciatica

a

patients with extrusion of the disk had a tendency for a better functional outcome than those with contained disk herniation. Interestingly, some studies demonstrated that both sequestrectomy (removal of disk fragment alone) and standard microdiscectomy (removal of disk fragment and disk) were associated with similar effects on pain after surgery, recurrence rate, functional outcome, and complications. ­ However, more evidence is needed to confirm this result.

b

The relative improvement of radicular pain was significantly better as compared to the improvement of low back pain. There was no convincing evidence to suggest that surgical technique or size of LDH herniation has a significant impact on long-term outcomes. None of the various operative procedures (i.e., microdiscectomy, endoscopic microdiscectomy, or the classical operation (laminectomy/laminotomy with discectomy)) gave a clearly different outcome.

Further Reading Fig. 14.11  Case 7. Preoperative (a) and postoperative (b) posture in a patient with left L5–S1 discogenic sciatica. Significant improvement of the sciatic scoliotic list

225

a

Further Reading Aono H, Iwasaki M, Ohwada T, Okuda S, Hosono N, Fuji T, et al. Surgical outcome of drop foot caused by degenerative lumbar diseases. Spine (Phila Pa 1976). 2007;32:E262–6. https://doi.org/10.1097/01. brs.0000259922.82413.72. Azarhomayoun A, Chou R, Shirdel S, Lakeh MM, Vaccaro AR, Rahimi-­ Movaghar V. Sequestrectomy versus conventional microdiscectomy for the treatment of a lumbar disc herniation: a systematic review. Spine (Phila Pa 1976). 2015;40:E1330–9. https://doi.org/10.1097/ BRS.0000000000001174. Bailey CS, Rasoulinejad P, Taylor D, Sequeira K, Miller T, Watson J, et  al. Surgery versus conservative care for persistent sciatica lasting 4 to 12 months. N Engl J Med. 2020;382:1093–102. https://doi. org/10.1056/NEJMoa1912658. BenDebba M, Augustus van Alphen H, Long DM. Association between peridural scar and activity-related pain after lumbar discectomy. Neurol Res. 1999;21S1:S37–42. https://doi.org/10.1080/01616412 .1999.11741025. Brouwer PA, Brand R, van den Akker-van Marle ME, Jacobs WC, Schenk B, van den Berg-Huijsmans AA, et  al. Percutaneous laser disc decompression versus conventional microdiscectomy for patients with sciatica: two-year results of a randomised controlled trial. Interv Neuroradiol. 2017;23(3):313–24. https://doi. org/10.1177/1591019917699981.

b

Dewing CB, Provencher MT, Riffenburgh RH, Kerr S, Manos RE. The outcomes of lumbar microdiscectomy in a young, active population: correlation by herniation type and level. Spine (Phila Pa 1976). 2008;33:33–8. https://doi.org/10.1097/BRS.0b013e31815e3a42. Dohrmann GJ, Mansour N. Long-term results of various operations for lumbar disc herniation: analysis of over 39,000 patients. Med Princ Pract. 2015;24:285–90. https://doi.org/10.1159/000375499. el Barzouhi A, Vleggeert-Lankamp CL, Lycklama à Nijeholt GJ, Van der Kallen BF, van den Hout WB, Jacobs WC, et al. Magnetic resonance imaging in follow-up assessment of sciatica. N Engl J Med. 2013;368:999–1007. https://doi.org/10.1056/NEJMoa1209250. Gadjradj PS, Rubinstein SM, Peul WC, Depauw PR, Vleggeert-­ Lankamp CL, Seiger A, et al. Full endoscopic versus open discectomy for sciatica: randomised controlled non-inferiority trial. BMJ. 2022;376:e065846. https://doi.org/10.1136/bmj-­2021-­065846. Iwasaki M, Akiyama M, Koyanagi I, Niiya Y, Ihara T, Houkin K. Double crush of L5 spinal nerve root due to L4/5 lateral recess stenosis and bony spur formation of lumbosacral transitional vertebra pseudoarticulation: a case report and review. NMC Case Rep J. 2017;4:121–5. https://doi.org/10.2176/nmccrj.cr.2016-­0308. Jensdottir M, Gudmundsson K, Hannesson B, Gudmundsson G. 20 years follow-up after the first microsurgical lumbar discectomies in Iceland. Acta Neurochir. 2007;149:51–8. https://doi.org/10.1007/ s00701-­006-­1068-­y. Jia H, Lubetkin EI, Barile JP, Horner-Johnson W, DeMichele K, Stark DS, et al. Quality-adjusted life years (QALY) for 15 chronic con-

226 ditions and combinations of conditions among US adults aged 65 and older. Med Care. 2018;56:740–6. https://doi.org/10.1097/ MLR.0000000000000943. Kerr D, Zhao W, Lurie JD. What are long-term predictors of outcomes for lumbar disc herniation? A randomized and observational study. Clin Orthop Relat Res. 2015;473:1920–30. https://doi.org/10.1007/ s11999-­014-­3803-­7. Kim MS, Park KW, Hwang C, Lee YK, Koo KH, Chang BS, et  al. Recurrence rate of lumbar disc herniation after open discectomy in active young men. Spine (Phila Pa 1976). 2009;34:24–9. https://doi. org/10.1097/BRS.0b013e31818f9116. Kulkarni AG, Tapashetti S.  Outcomes of discectomy in young adults with large central lumbar disc herniations presenting with ­predominant leg pain. Global Spine J. 2020;10:412–8. https://doi. org/10.1177/2192568219856871. Lassere MN, Johnson KR, Thom J, Pickard G, Smerdely P.  Protocol of the randomised placebo controlled pilot trial of the management of acute sciatica (SCIATICA): a feasibility study. BMJ Open. 2018;8:e020435. https://doi.org/10.1136/bmjopen-­2017-­020435. Lewandrowski KU, Ransom NA, Yeung A. Return to work and recovery time analysis after outpatient endoscopic lumbar transforaminal decompression surgery. J Spine Surg. 2020;6:S100–15. https://doi. org/10.21037/jss.2019.10.01. Liu C, Ferreira GE, Abdel Shaheed C, Chen Q, Harris IA, Bailey CS, et  al. Surgical versus non-surgical treatment for sciatica: systematic review and meta-analysis of randomised controlled trials. BMJ. 2023;381:e070730. https://doi.org/10.1136/bmj-­2022-­070730. Machado GC, Witzleb AJ, Fritsch C, Maher CG, Ferreira PH, Ferreira ML. Patients with sciatica still experience pain and disability 5 years after surgery: a systematic review with meta-analysis of cohort studies. Eur J Pain. 2016;20:1700–9. https://doi.org/10.1002/ejp.893. Mehendiratta D, Patel P, Bhambhu V, Chaudhary K, Dalvie S. Effect of preoperative parameters on outcomes of lumbar microdiscectomy: a retrospective analysis. Asian J Neurosurg. 2022;17:248–54. https:// doi.org/10.1055/s-­0042-­1750839. Ostelo RW.  Physiotherapy management of sciatica. J Physiother. 2020;66:83–8. https://doi.org/10.1016/j.jphys.2020.03.005. Ozgen S, Naderi S, Ozek MM, Pamir MN. Findings and outcome of revision lumbar disc surgery. J Spinal Disord. 1999;12:287–92. Peul WC, van Houwelingen HC, van den Hout WB, Brand R, Eekhof JA, Tans JT, et al. Surgery versus prolonged conservative treatment for sciatica. N Engl J Med. 2007;356:2245–56. https://doi. org/10.1056/NEJMoa064039.

14  Surgical Outcomes of Discogenic Sciatica Ran J, Hu Y, Zheng Z, Zhu T, Zheng H, Jing Y, et al. Comparison of discectomy versus sequestrectomy in lumbar disc herniation: a meta-­ analysis of comparative studies. PLoS One. 2015;10:e0121816. https://doi.org/10.1371/journal.pone.0121816. Samuel AM, Morse K, Lovecchio F, Maza N, Vaishnav AS, Katsuura Y, et al. Early failures after lumbar discectomy surgery: an analysis of 62 690 patients. Global Spine J. 2021;11:1025–31. https://doi. org/10.1177/2192568220935404. Sarma P, Thirupathi RT, Srinivas D, Somanna S. Adolescent prolapsed lumbar intervertebral disc: management strategies and outcome. J Pediatr Neurosci. 2016;11:20–4. https://doi.org/10.4103/1817­1745.181259. Sebaaly A, Lahoud MJ, Rizkallah M, Kreichati G, Kharrat K.  Etiology, evaluation, and treatment of failed back surgery syndrome. Asian Spine J. 2018;12:574–85. https://doi.org/10.4184/ asj.2018.12.3.574. Singh S, Ailon T, McIntosh G, Dea N, Paquet J, Abraham E, et al. Time to return to work after elective lumbar spine surgery. J Neurosurg Spine. 2021:1–9. https://doi.org/10.3171/2021.2.SPINE202051. Tutoglu A, Boyaci A, Karababa IF, Koca I, Kaya E, Kucuk A, et  al. Psychological defensive profile of sciatica patients with neuropathic pain and its relationship to quality of life. Z Rheumatol. 2015;74:646–51. https://doi.org/10.1007/s00393-­014-­1527-­4. Yen HK, Ogink PT, Huang CC, Groot OQ, Su CC, Chen SF, et al. A machine learning algorithm for predicting prolonged postoperative opioid prescription after lumbar disc herniation surgery. An external validation study using 1,316 patients from a Taiwanese cohort. Spine J. 2022;22:1119–30. https://doi.org/10.1016/j.spinee.2022.02.009. Valat JP, Genevay S, Marty M, Rozenberg S, Koes B. Sciatica. Best Pract Res Clin Rheumatol. 2010;24:241–52. https://doi.org/10.1016/j. berh.2009.11.005. Vinas-Rios JM, Sanchez-Aguilar M, Medina Govea FA, Von Beeg-­ Moreno V, Meyer F, DWG Registry-group. Incidence of early postoperative complications requiring surgical revision for recurrent lumbar disc herniation after spinal surgery: a retrospective observational study of 9,310 patients from the German Spine Register. Patient Saf Surg. 2018;12:9. https://doi.org/10.1186/s13037-­018-­ 0157-­1. Wera GD, Marcus RE, Ghanayem AJ, Bohlman HH. Failure within one year following subtotal lumbar discectomy. J Bone Joint Surg Am. 2008;90:10–5. https://doi.org/10.2106/JBJS.F.01569.

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“In most popular thoughts, any pain along the lower limb can be attributed to sciatica!” A. Akhaddar [The author] “Understanding cultural and traditional diversity allows the treating practitioner to adopt a comprehensive approach with the greatest chance of successful care.” A. Akhaddar [The author] “Pain shared is pain divided, joy shared is joy multiplied.” Lt-Col David Allen Grossman [1956—American author and trainer]

15.1 Traditional Therapeutic Practices Since the biblical period and the first reference to neurological pain in the lower extremity more than 35 centuries ago (c.f. Chap. 2 about Historical Aspects of Sciatica), different civilizations and cultures have tried to cure sciatica. Several treatments have been attempted. Some were successful, and others were not. However, until today and despite the availability of formal medical treatment, many patients try, rightly or wrongly, to use old remedies and old practices, sometimes inherited from ancient times, to relieve their pain. Indeed, several traditional therapeutic practices are still used in some parts of the world by non-health-related professionals (AKA traditional healers) to treat sciatica. Sometimes, patients’ suffering greatly benefits the healing sorcerers. These methods include but are not limited to the following: • Herbs and plants. • Ironing (iron therapy) (Figs.  15.1, 15.2, 15.3, 15.4, and 15.5). • Cautery scars (Figs. 15.6 and 15.7). • Scarification (Figs. 15.8, 15.9, and 15.10). • Cupping (hijama) (Fig. 15.11). • Cold and heat application. • Sand bath (psammotherapy, arenotherapy, sand therapy, or sand hammam).

Fig. 15.1  Sciatica self-treated repeatedly at the patient’s home using a red hot iron applied “on the path of pain,” as the patient said, causing local burns. This 76-year-old patient had a degenerative lumbar spinal stenosis

• • • • • • • •

Perspiration (excessive sweat). Massage. Spinal manipulation. Acupuncture. Auriculotherapy. Moxibustion. Bloodletting therapy. Leech therapy.

Also, clinicians should be aware of many potential complications inherent to each of these ancestral procedures.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_15

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228 Fig. 15.2  “Fire points” (arrows) (a, b) along the path of sciatic pain in a man

Fig. 15.3  Ironing for sciatic pain in a woman

15  Sciatica in Popular Cultures

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15.1 Traditional Therapeutic Practices

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Fig. 15.4  Recent use of ironing for sciatica in a man

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Fig. 15.5  The patient in Fig. 15.4 had a migrated L5–S1 disk herniation as seen on magnetic resonance imaging (a–d) (arrows)

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Fig. 15.7 Both “cautery scars” (dotted frame) and “fire points” (arrows) in a man suffering from sciatica Fig. 15.6  Cautery scars (a, b). This patient said that he wanted to cut the path of the sciatic pain

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Fig. 15.8  Scarification scars (arrows) (a, b) in a young man with L5–S1 migrated lumbar disk herniation as seen in sagittal (c) and axial (d) T2-weighted magnetic resonance imaging (arrows)

15.1 Traditional Therapeutic Practices

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Fig. 15.9  Scarification scars (arrows) (a) in a man with an L4–L5 lumbar disk herniation combined with lumbar spinal stenosis as seen in sagittal (b) and axial (c, d) T2-weighted magnetic resonance imaging (arrows)

Many societies are linked to their culture and the traditions and customs they hold. Culture still greatly influences defining the concepts of health and disease and the different treatment methods. In addition, it is well known that cultural identity can affect pain experience, beginning with pain perception and ending with expectation and treatment outcome satisfaction. This cultural determinism itself is influenced by various factors whether they are emotional, psychological, social, and/or spiritual. Faced with the great cultural and traditional diversity of our patients, it is difficult but necessary for clinicians to integrate the cultural understanding of pain into the management of any sciatic patient. Good and simple communication and mutual appreciation between the practitioner and his/her patient are the keys to ensuring effective treatment. Fig. 15.10  Recent use of scarification in a man with lumbosacral radicular pain

232 Fig. 15.11 Cupping (Hijama). This method uses heated glass cups to create local suction on the patient’s skin, causing circular bruises (a, b). It would seem that the fluid and blood are drawn away from the inflamed areas

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15.2 Sciatica in Nonmedical Literature Some days are like my sciatica, you know where it starts but you don’t know where, when, and how it ends. A.  Akhaddar [The author]

Unlike other types of pains, discussion of sciatica appears less frequently in nonmedical literature such as theater, movies, fiction, essays, autobiographies, and poetry. During many years of preparation for this book, the author came across some anecdotal stories, personal experiences, and quotes about sciatica, which he would like to share in this chapter. Usually, sciatic pain is correlated with a negative experience, suffering from sciatica is an unforgettable event. Anyone who has experienced it will never forget it. In the Arabic language, sciatica is known as “Irq An-Nasa” literally meaning that “The effect of sciatic pain makes people forget (Nasa) any other pain or forgets everything else.” Sciatica influences mood in daily life and even social behavior: • “I am not man or beast; I am bibliosexual1, and a seedy bibliosexual who haunts the streets, laden with carrier bags held by blistered fingers, stooping under the weight of the rucksack that has brought on sciatica and a Dickensian demeanour.” [Robin Ince, English comedian, actor, and writer. (1969–)]

A bibliosexual means a “bookworm.” Someone who is so fascinated by books and literature that they have no time for socialization and a life. Also, a person who is so intensely passionate about books that they discuss them with a level of enthusiasm that most people reserve for sex. 1 

• “I’m on the verge of a total breakdown. Sciatica. Taxes. Cars. Fleas, possibly. It’s an absurd existence.” [Jonathan Ames, American author. (1964–)] Others see sciatica as one of life’s terrors: • “My pain (namely lumboradicular pain) feels like a busy roundabout in my lower back, then the pain spreads in all directions, mostly down, less frequently to the sides but rarely up.” [One of my patients] • “Sciatic pain is worse than childbirth.” [Unknown] Sciatica is habitually a very severe pain. For many women who have experienced sciatica, labor pain is shorter than sciatic pain, and… unlike sciatica, you get a child at the end of it. Some other authors are more sympathetic in their presentation of sciatic pain. • “When you see a swallow for the first time in the spring, you have to let your back down so as not to have sciatica or toothache.” [French Proverb] • “Some days are like sciatica, you know where and when it starts but you don’t know where and when it ends.” [The author] • “Well, if you insist on a second opinion…Then it isn’t Sciatica.” (Joke quote) [Edgar Argo. American cartoonist (1941–2009)] • “I may have sciatica … But sciatica not have me.” [Unknown] • “Some people think that being strong means never feeling pain. In reality, the strongest people are those who feel it, understand it, and accept it” [Unknown]

15.2 Sciatica in Nonmedical Literature

• “Pain is inevitable, suffering is optional.” [Haruki Murakami, Japanese writer (1949–)] • “To a gentleman, a gentleman-someone who dies without ever pronouncing the word-is a man who climbs Everest, never mentions it to a soul, and listens politely to Pochet’s account of how in 1937  in spite of his sciatica, he ­conquered the Puy de Dome.” [Pierre Daninos, French writer and humorist (1913–2005)] • “There is one topic peremptorily forbidden to all well-­­ bred, to all rational mortals, namely, their distempers. If you have not slept or if you have slept or if you have headache or sciatica or leprosy or thunder-­stroke, I beseech you, by all angels, to hold your peace and not pollute the morning.” [Ralph Waldo Emerson, American philosopher, and essayist (1803–1882)] Sciatic pain can sometimes seem devastating; however, with a positive attitude toward this pain, some patients encourage themselves to succeed and recover. Sciatica should not disrupt a patient’s daily life in depth. • “Movie music is noise. It’s even more painful than my sciatica.” [Thomas Beecham, British conductor and impresario (1879–1961)] Some people have had brilliant careers because of or thanks to their sciatica: • “In the business world, I did fairly well but wasn’t happy. A bout of sciatica put me flat on my back. All I could do was read, listen to my mother’s stories about the Sandovals, and daydream: a return to self. My writing career had begun.” [Sandra Cisneros, American writer (1954–)] • “A sciatica sufferer only feels relief when he is moving. To get rid of our difficulties, we must constantly look for solutions.” [Thomas Gatabazi, Rwandan economist] Sciatica came early to the theater: • “How Now, which of your Hips has the most profound Sciatica?” (Measure to Measure, Act I, Scene 2) [William

233

Shakespeare English playwright, poet, and actor. (1565–1616)] • “Thou Cold Sciatica, cripple our Senators, that their Limbs may halt as lamely as their Manners” (Timon of Athens (Act IV, Scene 1)) [William Shakespeare English playwright, poet, and actor. (1565–1616)]

• TO MY GREAT SCIATICA In anger my nerve squirms What pain, what suffering! Sciatica, oh my goddess Your power is unmatched The impossible is your motto Move, sit, walk, sleep Nah, no cure Perlimpinpin powder! Invisible disability What am I saying, invincible A false gesture, my very big fault? And your fury is unleashed In front of you I flatten myself Time is solution Patience, your sweet clemency For peace to finally reign In my exhausted body. Author: Patient with sciatic pain, father of Ms. Giang-­­ Tien Patricia Clolus (French poem translated into English) Accessed on May 12, 2022. Work published under Creative Commons by-nc-nd 3.0 license (CC BY-NC-ND 3.0). Reproduced from Giang-Tien Patricia Clolus. A ma grande sciatique. www.atramenta.net/ lire/a-­ma-­grande-­sciatique/71871. Accessed on May 12, 2022. Under the terms of the Creative Commons Attribution Licence. • “Every pain gives a lesson, and every lesson changes a person.” [Unknown] Finally, our own beliefs change over time (Fig. 15.12).

234 Fig. 15.12  Adidas tattoo but Nike shoes (a, b)! Create new beliefs to change our life

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Further Reading Ansari R, Dadbakhsh A, Hasani F, Hosseinzadeh F, Abolhassanzadeh Z, Zarshenas MM. Traditional aspects of sciatic pain management and allied therapies from Persian medical reports. Curr Drug Discov Technol. 2021;18:194–206. https://doi.org/10.2174/157016381766 6200316112120. Briët MC, Haan J, Kaptein AA. Hermann Hesse and L: two narratives of sciatica. Clin Neurol Neurosurg. 2012;114:9–11. https://doi. org/10.1016/j.clineuro.2011.07.011. Burton AK, Waddell G, Tillotson KM, Summerton N.  Information and advice to patients with back pain can have a positive effect. A randomized controlled trial of a novel educational booklet in primary care. Spine (Phila Pa 1976). 1999;24:2484–91. https://doi. org/10.1097/00007632-­199912010-­00010. Patricia Clolus G-T. A ma grande sciatique. www.atramenta.net/lire/a-­ma-­grande-­sciatique/71871. Accessed 12 May 2022. Goldsmith R, Williams NH, Wood F.  Understanding sciatica: illness and treatment beliefs in a lumbar radicular pain population. A qualitative interview study. BJGP Open. 2019;3:bjgpopen19X101654. https://doi.org/10.3399/bjgpopen19X101654. Hashem M, AlMohaini RA, AlMedemgh NI, AlHarbi SA, Alsaleem LS. Knowledge and attitude of sciatica pain and treatment methods among adults in Saudi Arabia. Adv Orthop. 2022;2022:7122643. https://doi.org/10.1155/2022/7122643. Hohmann CD, Stange R, Steckhan N, Robens S, Ostermann T, Paetow A, et al. The effectiveness of leech therapy in chronic low back pain. Dtsch Arztebl Int. 2018;115:785–92. https://doi.org/10.3238/ arztebl.2018.0785. Hopayian K, Notley C. A systematic review of low back pain and sciatica patients’ expectations and experiences of health care. Spine J. 2014;14:1769–80. https://doi.org/10.1016/j.spinee.2014.02.029. Khan B, Alam I, Haqqani U, Ullah S, Hamayun S, Khanzada K, et al. Unusual local therapies used for the treatment of low back pain and

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sciatica: concepts and approaches. Cureus. 2021;13:e17080. https:// doi.org/10.7759/cureus.17080. Lo T, Tindall A. Acute lower back pain mapped by dermatomal scarification in urban Malawi. BMJ Case Rep. 2012;2012:bcr1120103529. https://doi.org/10.1136/bcr-­11-­2010-­3529. Löfman S, Räsänen P, Hakko H, Mainio A.  Suicide among persons with back pain: a population-based study of 2310 suicide victims in Northern Finland. Spine (Phila Pa 1976). 2011;36:541–8. https:// doi.org/10.1097/BRS.0b013e3181f2f08a. Lurie JD, Berven SH, Gibson-Chambers J, Tosteson T, Tosteson A, Hu SS, et al. Patient preferences and expectations for care: determinants in patients with lumbar intervertebral disc herniation. Spine (Phila Pa 1976). 2008;33:2663–8. https://doi.org/10.1097/ BRS.0b013e31818cb0db. Mancuso-Marcello M, Demetriades AK.  What is the quality of the information available on the internet for patients suffering with sciatica? J Neurosurg Sci. 2020;67:355. https://doi.org/10.23736/ S0390-­5616.20.05243-­1. Martinelli AM.  Pain and ethnicity. How people of different cultures experience pain. AORN J. 1987;46:273–4, 276, 278. https://doi. org/10.1016/s0001-­2092(07)66423-­0. Miller ET, Abu-Alhaija DM.  Cultural influences on pain perception and management. Pain Manag Nurs. 2019;20:183–4. https://doi. org/10.1016/j.pmn.2019.04.006. Nogier PFM.  Traité d’auriculothérapie. Moulins-lès-Metz: Maisonneuve; 1969. Nouri M, Rasouli MR, Rahimi-Movaghar V. Deliberate burns in patients with sciatica. Surg Neurol. 2008;70:223. https://doi.org/10.1016/j. surneu.2007.10.033. Ong BN, Konstantinou K, Corbett M, Hay E. Patients’ own accounts of sciatica: a qualitative study. Spine (Phila Pa 1976). 2011;36:1251–6. https://doi.org/10.1097/BRS.0b013e318204f7a2. Peacock S, Patel S. Cultural influences on pain. Rev Pain. 2008;1:6–9. https://doi.org/10.1177/204946370800100203.

Further Reading Rogers L.  Sciatica, with particular reference to its causes and treatment. Postgrad Med J. 1947;23:517–21. https://doi.org/10.1136/ pgmj.23.265.517. Romoli M, Greco F, Giommi A.  Auricular acupuncture diagnosis in patients with lumbar hernia. Complement Ther Med. 2016;26:61–5. https://doi.org/10.1016/j.ctim.2016.02.006. Ryan C, Pope CJ, Roberts L.  Why managing sciatica is difficult: patients’ experiences of an NHS sciatica pathway. A qualitative, interpretative study. BMJ Open. 2020;10:e037157. https://doi. org/10.1136/bmjopen-­2020-­037157.

235 Walsh K.  Should we stop teaching and just tell stories? Age Ageing. 2007;36:480. https://doi.org/10.1093/ageing/afm030. www.azquotes.com/quotes/topics/sciatica.html. Accessed 12 Aug 2022. Zargaran A, Daneshamouz S, Kordafshari G, Mohagheghzadeh A.  Report—Renovation of a traditional Ergh-al-Nassa pill (Hab) to a standard pharmaceutical molded tablet. Pak J Pharm Sci. 2016;29:1703–9.

Part II Lumbosacral Discogenic Sciatica

16

Central and Subarticular Lumbar Disk Herniations

16.1 Definition and Relevance Lumbar disk herniation (LDH) (AKA herniated lumbar disk) is defined as localized or focal displacement of lumbar disk material (less than 25% or 90° of the global disk circumference) beyond the normal margin of the intervertebral disk space. Disk herniation commonly refers to a displacement of the nucleus pulposus through a disruption in the annulus fibrosis; however, disk material may include not only “nucleus pulposus” but also cartilaginous endplate, fragmented apophyseal bone, or annulus fibrosus tissue itself. LDH has been recognized as a cause of sciatic pain (AKA discogenic sciatica) since only the 1930s (c.f. Chap. 2 about Historical Aspects of Sciatica). There are two subcategories of disk herniation: “protrusion” and “extrusion” (Fig. 16.1). –– Protrusion (AKA protruded disk): The fragment does not have a neck that is narrower than the fragment in any dimension. –– Extrusion (AKA extruded disk): The fragment has a neck (pedicled aspect) that is narrower than the fragment in at least one dimension. There are two subtypes of disk extrusion: “sequestration” and “migration”. Fig. 16.1  Classification of the lumbar disk herniations related to their morphologies. Intervertebral disks are in green and disk herniations are in red. Budge (a), protrusion (b), extrusion (c), and sequestration (d)

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–– Sequestration (AKA sequestrated disk): The fragment is completely separated from the disk of origin. –– Migration (AKA migrated disk): The disk material is displaced away from the site of extrusion, but it is still in continuity with the disk of origin. In addition, it is important to evaluate whether the LDH is contained or not (AKA uncontained) by the outer annulus fibrosus and/or the posterior longitudinal ligament (PLL). On spinal imaging, contained herniations usually have a smooth margin, whereas uncontained LDHs most frequently have irregular margins because the outer annulus fibrosus and/or the PLL have been penetrated by the disk material. Classically, there are four anatomic zones of LDH: central, subarticular, foraminal, or extraforaminal. This classification relates to various clinical syndromes of presentation (Figs. 16.2 and 16.3). –– Central Zone: It is the limited area between the sagittal planes through the medial edges of each facet. The center of the central zone is a sagittal plane through the center of the vertebral body. For some authors, central zone can be divided into median and paramedian zones). –– Subarticular Zone: (AKA lateral recess) It is the area between the sagittal plane of the medial edges of the pedicles and the plane of the medial edges of the facets.

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Coronally, it is the zone between the planes of the posterior surfaces of the vertebral bodies and the anterior surfaces of the superior facets. –– Foraminal Zone: It is the limited area between planes passing through the medial and lateral borders of the pedicles. –– Extraforaminal Zone: It is the area outside the sagittal plane of the lateral borders of the pedicles. The extraforaminal zone has no precise lateral border.

Fig. 16.2  Classification of the lumbar disk herniations related to the axial plane on CT scan: central (median and paramedian) in blue, subarticular (lateral recess) in red, foraminal in yellow, extraforaminal in orange, and anterior retroperitoneal in green Fig. 16.3  Illustration of different anatomic zones of lumbar disk herniations in axial views of lumbar disk space: central (median and paramedian), subarticular, foraminal, extraforaminal, and anterior. Disk herniations are represented in red color

Although rare, a fifth zone can be added: the anterior retroperitoneal zone, which is too anterior to the extraforaminal zone in the retroperitoneal space. Central (including median and paramedian) and subarticular zones are within the vertebral canal. For some authors, “intraspinal” LDH includes both central and subarticular LDHs (Fig. 16.4). The foraminal zone is sometimes called the “lateral zone,” and the extraforaminal zone is also named the “far lateral zone.” For some authors, the extreme lateral zone includes both the foraminal and extraforaminal zones. Seize of LDH may vary between a few millimeters to a few centimeters in length. Massive or giant LDH is an

16.1 Definition and Relevance

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Fig. 16.4  Illustration of intraspinal lumbar disk herniations in the median (a), paramedian (b), and subarticular zones (c) in both axial and coronal views of lumbar disk space. Disk herniations are represented in red color

unusual condition defined as herniated disk material occupying more than 50% of the antero-posterior diameter of the lumbar spinal canal (Figs. 16.5 and 16.6). About 85–90% of LDHs occur within the spinal canal (namely central and subarticular LDH) at L4–L5 or L5–S1 vertebral level and less than 15% are within the foramen or extraforaminal zones. The lateral recess (subarticular zone) is the commonest site of nerve root compression by herniated lumbar disk material. The preponderance of subarticular LDH is mainly due to the anatomic vulnerability of both the lateral portion of the annulus fibrosus and the posterior longitudinal ligament in the lateral recess area. Most patients with symptomatic LDH complain of traditional low back and lumbar radicular pain with or without motor deficit. Cauda equina syndrome is a more unusual but serious condition. Neurological symptoms can be explained by various mechanisms such as mechanic compression theory, ischemic theory, and inflammatory and immune ­ theories. The majority of symptomatic intraspinal LDHs impinge the traversing (inferior) nerve to the level below. Therefore,

at the L4–L5 intervertebral disk space, it is the L5 superior nerve that is most likely to be affected. This is in distinction to foraminal and extra-foraminal LDH (lateral LDH), which can affect nerves exiting (superior) at the corresponding disk level itself. LDHs can migrate upward or downward, anterior or posteriorly relative to the original lumbar disk. Sometimes disk material can be found intradural within the thecal sac or even into the dural sheath of the nerve root itself (namely intraradicular LDH). LDH is a relatively common disease, with 5–20 cases per 1000 adults annually. Most patients are male (about 65%) in the third to fifth decade of life. Pediatric (children and adolescents) LDHs are relatively rare representing less than 5% of all LDHs (c.f. Chap. 24 about Pediatric Lumbar Disc Herniations). The prevalence of herniated disks increases with increasing age, but unlike lumbar spinal stenosis, LDHs are significantly less common in the elderly population (only 5–7% of patients are over the age of 70). LDH is the main cause of sciatic pain; however, the herniated disk can be associated with other spinal disorders, mainly degenerative.

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Fig. 16.5  Sagittal and axial T2-weighted MRIs showing LDHs related to their size: small (a, b), medium (c, d), and massive (AKA giant) (e, f) (arrows)

16.2 Clinical Presentations

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Fig. 16.6  Sagittal T1-weighted (a), T2-weighted (b), axial T2-weighted (c–e) MRI, and axial CT scan (f–h) of the lumbar spine showing three different LDHs in the same patient

16.2 Clinical Presentations As with other forms of spinal degenerative diseases, the initial evaluation of patients should include a sufficient and detailed history and a neurologic, spinal, and somatic examination. Classically, there are no distinctive clinical features allowing clear differentiation between patients with intraspinal LDH and those with lateral LDH. Indeed, most cases present with both lower back and lumbar radicular pain. Pain exacerbates with straining, coughing, sneezing, and being in a seated position. Neurological deficits and cauda equina syndrome (CES) are unusual. However, extreme lateral zones LDHs are more likely associated with unilateral L4 radiculopathy, minimal low back pain, negative straight leg raising, more painful radicular pain, higher incidence of sensory dysesthesia and quadriceps weakness, and decreased or absent knee jerk reflex. For many authors, there is no real correlation between the size of the disk fragment on spinal imaging and the degree of clinical symptomatology except that massive LDHs are more

likely to be hyperalgic with a mean duration of symptoms shorter than the population with smaller LDHs, have bilateral sciatica, lower-extremity motor weakness, and above all a predominance of CES. Patients with central LDH had greater low back pain than those with subarticular disk herniations. In addition, bilateral lumbar radicular pain is more likely correlated with central and massive LDH.  Classic straight leg raising test (AKA Lasègue’s sign) will be positive for both central and subarticular LDHs; however, crossed straight leg raising test (AKA Fajersztajn’s sign or contralateral SLR test) may correlate with a more central LDH. Patients with extrusion and sequestration (non-contained type) had higher pain intensity and shorter duration of symptoms compared with patients with protrusions (contained type). Regarding migrated LDHs, radiculopathy is significantly more frequent in patients with caudal migrations than in those with rostral migrations. When a sciatic scoliotic list co-exists (AKA sciatic scoliosis or nonstructural scoliosis secondary to nerve root irritation), the curve convexity is often identical to the symptomatic

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side for subarticular LDH. When a sciatic scoliotic list co-­ exists (AKA sciatic scoliosis, nonstructural scoliosis secondary to nerve root irritation), the curve convexity is often identical to the symptomatic side for subarticular LDH. When the LDH is located laterally to the emerging nerve root, the lumbar spine inclines laterally toward the opposite side of the painful lesion (Fig.  16.7). The concavity of the sciatic scoliosis is on the same side of the LDH when the disk frag-

Fig. 16.7  When the LDH (in red color) is located laterally to the emerging nerve root, then the concavity of the sciatic scoliosis is on the opposite side of the herniation

16  Central and Subarticular Lumbar Disk Herniations

ment is located medially to the emerging nerve root (Fig. 16.8). Central LDH will rather present with a flexed antalgic list (Fig. 16.9). According to some surgeons, the side of sciatic scoliosis is primarily related to hand or leg dominance rather than the side of the sciatic pain or the topographic position of the LDH.

16.2 Clinical Presentations

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Fig. 16.8  Concavity of the sciatic scoliosis is on the same side of the LDH when the disk fragment is located medially (in red color) to the emerging nerve root

The majority of the patients with pediatric LDHs are male adolescents. Clinical presentations of LDH in the pediatric age group are normally comparable to those encountered in the adults except that most pediatric patients have the following: –– A mild truncated sciatic pain (sometimes confused with hamstring pain). –– A positive straight leg raising test (up to 90%). –– Predominant mechanical signs including low back pain, scoliosis, paravertebral muscle spasm, and lumbosacral radicular pain. –– Few neurological symptoms such as numbness and motor weakness.

–– Exceptionally a CES (only one previous presentation in a 13-year-old child). In contrast to the adult population, where the main etiology of LDH is degenerative, many factors have been recognized as the possible causes of pediatric LDH, especially trauma and intensive sport activity. On the opposite, there is no major clinical particularity in the elderly, apart from the rarity of scoliotic lists, which are difficult to distinguish from some degenerative spine deformities at this age (e.g., lumbar spondylosis). Neurophysiological explorations can assess the relative severity of neurological damage and predict the prognosis or follow-up course of recovery.

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Fig. 16.9  A patient with central L4–L5 disk herniation (arrows) showing a flexed antalgic list as seen on posterior (a) and lateral (b) views. Lumbosacral spinal reconstruction (c) and axial (d) CT scan

16.3 Imaging Features As with the majority of other forms of LDHs, diagnosis of central and subarticular disk herniations should correlate with the patient’s history, clinical examination, and imaging investigations. The best imaging technique should show and evaluate the size of the herniated disk, its morphology, its exact location, whether it is contained or non-contained, and migration of disk fragment (c.f. Chap. 9 about Paraclinic Evaluations of Sciatica). Plain radiography is sometimes the first-line imaging test performed. Limited intervertebral space, traction osteophytes, and compensatory scoliosis are findings that usually suggest LDH (Fig.  16.10). Lateral flexion and extension (dynamic) views are useful in evaluating lumbosacral spinal instability.

In myelography (saccoradiculography), the lesion presents as an extradural filling defect at the level of the intervertebral disk. Sometimes, there is a cutoff of the filling of the nerve root sleeve in comparison with the contralateral normal nerve. Massive (giant) LDH may produce a total or subtotal block. However, this old method does not provide any information about the origin of the lesion although the diagnosis of LDH is most common. Computed tomography (CT) scan can usually demonstrate and localize the herniated mass, which has a similar density as the disk material. The correct diagnosis is helped by careful examination of the surrounding epidural fat (Figs. 16.10 and 16.11). A bony CT scan may be useful for identifying possible concomitant secondary degenerative vertebral–articular disorders. CT scan is useful for diagnosing associated posterior ring apophysis separation of a vertebral endplate (Fig.  16.12). However, this diagnosis tool is

16.3 Imaging Features Fig. 16.10 Antero-posterior plain film radiography of the lumbosacral spine showing compensatory scoliosis (a). The concavity of the sciatic scoliosis is on the opposite side (right) of the paramedian L4–L5 disk herniation (left) as seen on axial CT scan views (arrows) (b, c)

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Fig. 16.11  L4–L5 subarticular disk herniation (arrows) on the right side as seen on sagittal reconstruction (a) and axial (b, c) CT scan in one patient. Axial CT scan showing an L4–L5 paramedian/subarticular disk herniation on the left side (arrows) in another patient (d–f)

248 Fig. 16.12  L5–S1 central disk herniation with concomitant posterior ring apophysis separation (arrows) as seen on axial (a, b) and sagittal reconstruction (c, d) CT scan. Note the border defect of the postero-superior vertebral body of S1 combined with a bony fragment near the posterior edge of the superior endplate of S1 (arrows)

16  Central and Subarticular Lumbar Disk Herniations

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poor for the visualization of intraspinal nerve roots, making it unsuitable in the diagnoses of radiculopathy. CT myelography may be helpful for visualizing herniated disks in patients who cannot undergo magnetic resonance imaging (MRI). With a diagnostic precision of more than 95%, MRI is superior to a CT scan in visualizing all constituents of the LDH in different planes and sequences (Figs. 16.12, 16.13, 16.14, and 16.15). Classically, post-gadolinium T1-weighted MRI is not required except for some atypical forms, which can be confused with other anterior epidural masses (often neoplasms). If this happens, migrated disk fragment is clearly displayed on axial and sagittal images, with or without discontinuity with the parent disk. The signal intensity of disk fragments is variable and unspecific, but in the majority of cases, the epidural lesions have low-to-isointense signal on T1-weighted and low or sometimes high signal intensity on T2-weighted MRI depending on the time of evolution.

More rarely, some cases may be accompanied by an intradural extension of the disk fragment or posterior epidural migration (c.f. Chap. 30 about Intradural Lumbar Disc Herniations and Chap. 21 about Posterior Epidural Migration of Lumbar Disc Herniation). Table 16.1 presents the main differential diagnoses of common LDH on MRI. A useful mnemonic for remembering these most frequent differential diagnoses is “CD INAPT TV” (Table  16.1). For more information, please refer to Chap. 10 about Neuroimaging Differential Diagnoses of Common Lumbar Disc Herniations. It is important to correlate CT scan and/or MRI features with preoperative and intraoperative radiographs (Figs. 16.16, 16.17, 16.18, 16.19, 16.20, 16.21, and 16.22). Effective communication between the surgeon and the radiologist is essential regarding the precise location of the compressive lesions in order to avoid the wrong diagnosis or the wrong level.

16.3 Imaging Features

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Fig. 16.13  L4–L5 subarticular disk herniation (arrows) on the left side as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted sequence (c, d)

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Fig. 16.14  L4–L5 central disk herniation (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted sequence (c, d)

16  Central and Subarticular Lumbar Disk Herniations

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Fig. 16.15  L4–L5 paramedian/subarticular disk herniation (arrows) on the left side with superior migration as seen on axial CT scan (a) and T2-weighted MRI (b) and on sagittal T2-weighted sequence (c, d)

Table 16.1  Differential diagnoses of common lumbar disk herniation on neuroimaging Cystic lesions Degenerative lesions Infectious lesions Nerve root lesions and anomalies Apophyseal ring fracture

Postoperative disorders

•  Synovial cyst (juxtafacet cyst) •  Discal cyst •  Epidural gas pseudocyst •  Osteophytes (vertebral body, endplate, facet joint) •  Ossifications of the posterior longitudinal ligament • Discitis •  Epidural abscess •  Conjoined nerve root anomalies •  Enlarged nerve roots Also known as:  •  “Posterior ring apophysis separation”  •  “Limbus vertebral fracture”  •  “Posterior retroextramarginal disk hernia”  •  “Slipped vertebral epiphysis”  •  “Posterior Schmorl node” •  Postoperative scar and fibrosis •  Recurrent disk material

16.3 Imaging Features

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Table 16.1 (continued) Tumors and pseudotumors (epidural non-vertebral) Tumors (nerve root tumors) Vascular lesions Rare etiologies

•  Metastases (secondary tumors) •  Primary tumors (e.g., lipoma, angiolipoma, and ganglioneuroma) •  Extramedullary hematopoiesis (e.g., lymphoma and myeloma) •  Schwannoma (neurinoma) • Neurofibromatosis • Metastasis •  Epidural hematoma •  Epidural varices (venous plexus engorgement) •  Cavernous hemangioma Ganglionitis, pigmented villonodular synovitis, rheumatoid nodules, eosinophilic granuloma, sarcoidosis, gouty tophus, posterior longitudinal ligament cyst, and vascular malformations

“CD INAPT TV” can be used as an acronym

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Fig. 16.16  Paramedian/subarticular L5–S1 disk herniation (arrows) on the left as seen on sagittal T1-weighted (a), T2-weighted MRI (b), and on STIR sequence (c) and on axial T2-weighted sequence (d–f)

252 Fig. 16.17  Case A. L4–L5 paramedian disk herniation on the right side with concomitant posterior ring apophysis separation (arrows) as seen on axial T2-weighted MRI (a, b) and CT scan (c, d). Note the secondary central canal stenosis

16  Central and Subarticular Lumbar Disk Herniations

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Fig. 16.18  Case A.  L4–L5 paramedian disk herniation on the right side with concomitant posterior ring apophysis separation (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on sag-

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254 Fig. 16.19 Case B. Unsuspected small subarticular disk herniation on axial CT scan (arrow) (a). This L5–S1 herniated disk (arrows) was more obvious on axial (b, c) and sagittal (d) T2-weighted MRI. Note the appearance of the left S1 nerve root (arrowheads)

16  Central and Subarticular Lumbar Disk Herniations

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Fig. 16.20  Case B. Photograph showing the small disk fragment that was removed via an L5–S1 interlaminar approach on the right side

16.4 Treatment Options

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Fig. 16.21  Case C. A small paramedian L5–S1 disk herniation (arrows) on the left side hardly detected on CT scan. Lumbosacral sagittal (a, b) and axial (c, d) T2-weighted MRI

16.4 Treatment Options

Fig. 16.22  Case C. Photograph showing the small disk fragment that was removed via an L5–S1 interlaminar approach on the left side

Conservative management is typically the primary therapeutic intervention in patients with intraspinal LDH as long as they have no red flag symptoms including neurological weakness, sphincter disturbances, or uncontrolled pain. Conservative measures consist of bed rest, pharmacological therapy (analgesic, anti-inflammatory medications, and muscle relaxants), physical therapy interventions, lumbar bracing (rarely), and limitation of physical activities. Posture-modifying exercises can improve symptoms by improving muscle strength, coordination, and flexibility. When symptoms persist beyond 4–6 weeks, transforaminal or interlaminar epidural steroid injections may be considered for a short term.

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If the previous measures are unsuccessful or persistent radicular pain unfavorably compromises the patient’s daily activities, regardless of existing neurological deficits, the need for surgical decompression is highlighted. Surgical strategy requests neurological decompression and herniated disk removal with or without discectomy. There are several methods of performing surgical intervention, including an open approach and a minimally invasive approach. The surgeon can perform an interlaminar approach, a hemilaminectomy, or even a complete laminectomy depending on the size and the location of the lumbar disk fragment. The majority of subarticular LDH requires a unilateral approach (Figs.  16.23, 16.24, 16.25, and 16.26), but some Fig. 16.23 Axial lumbosacral CT scan (a, b) and T2-weighted MRI (c, d) views. There is a median L5– S1 disk herniation (extruded disk material) (arrows) unsuspected on CT scan examination

voluminous central LDH may need a bilateral approach (bilateral fenestration). In the presence of a central LDH with a bilateral radicular syndrome, surgery can commonly be restricted to the side where radicular signs and symptoms are more severe. The disk fragment should be removed carefully to avoid a dural tear and/or a further spinal root injury. More recently, a variety of minimally invasive surgical techniques for the treatment of LDH has been increased utilization using more small incisions, tube access, and endoscopy. These methods show great promise because they are less invasive, give better recovery, and provide good results and successful outcomes.

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Fig. 16.24  Case D. L4–L5 paramedian disk herniation (arrows) on the right side as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted sequence (c–e)

Fig. 16.25  Case D. Intraoperative views of the right L4–L5 interlaminar approach (a–d). Following retraction of the nerve root (arrow), the disk fragment was exposed (star) (a, b) and removed (herniectomy) with discectomy (c). The appearance of the nerve root at the end of the procedure (d)

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Fig. 16.26 Case D. Photograph showing the disk fragment and the disk material that were removed (herniectomy and discectomy, respectively)

16.5 Outcome and Prognosis Between 80 and 90% of patients with acute symptomatic LDH report relief of their symptoms including sciatic pain within 6–12 weeks with or without conservative treatments. Regarding the treatment type of non-emergent intraspinal LDH, many authors believe that both conservative and surgical treatment have the same outcomes in the medium and long term. However, surgically treated groups may result in faster relief of symptoms and improvement in life quality. Ultimately, the therapeutic decision is based on the discussion between the doctor and his/her patient in light of the clinical and imaging evaluation, duration of symptoms, and patient’s desires. Factors expecting positive outcomes after surgery for intraspinal LDH include severe preoperative leg and lower back pain, shorter symptom duration, younger age, better mental health status, and increased preoperative physical activity. About 80–85% of surgically treated patients had a good improvement to excellent recovery from their sciatic pain, inferior extremities weakness, and/or sphincter disorders. However, as with any surgery, there are risks related to its invasive nature: infection, treatment failure, recurrence, or postoperative fibrosis. More specific complications include direct nerve root injury, unintended durotomy (AKA dural tear), retroperitoneal vascular injury, iatrogenic spinal instability, and complications of positioning. The postoperative results of central LDH are somewhat poorer than those of subarticular disk herniation. It seems that central LDH had a relatively high recurrence rate (up to 14%), persistent low back pain, and greater segmental instability in comparison with subarticular ones. In addition, patients with extrusion of the disk had a tendency for a better functional outcome than those with contained disk herniation.

Persistent neurological deficits, chronic sciatica, or continuing neuropathic pains are mainly observed in some patients who had preoperative CES or those with a delay in their management.

Further Reading Ahn SH, Ahn MW, Byun WM. Effect of the transligamentous extension of lumbar disc herniations on their regression and the clinical outcome of sciatica. Spine (Phila Pa 1976). 2000;25:475–80. https:// doi.org/10.1097/00007632-­200002150-­00014. Ahn Y, Yoo BR, Jung JM. The irony of the transforaminal approach: a comparative cohort study of transforaminal endoscopic lumbar discectomy for foraminal versus paramedian lumbar disc herniation. Medicine (Baltimore). 2021;100:e27412. https://doi.org/10.1097/ MD.0000000000027412. Akhaddar A, Boulahroud O, Elasri A, Boucetta M. Radicular interdural lumbar disc herniation. Eur Spine J. 2010;19(Suppl 2):S149–52. https://doi.org/10.1007/s00586-­009-­1200-­9. Akhaddar A, Belfquih H, Oukabli M, Boucetta M. Posterior ring apophysis separation combined with lumbar disc herniation in adults: a 10-year experience in the surgical management of 87 cases. J Neurosurg Spine. 2011a;14:475–83. https://doi.org/10.3171/2010.11. SPINE10392. Akhaddar A, El-Asri A, Boucetta M.  Posterior epidural migration of a lumbar disc fragment: a series of 6 cases. J Neurosurg Spine. 2011b;15:117–28. https://doi.org/10.3171/2011.3.SPINE10832. Akhaddar A, Belfquih H, Salami M, Boucetta M.  Surgical management of giant lumbar disc herniation: analysis of 154 patients over a decade. Neurochirurgie. 2014;60:244–8. https://doi.org/10.1016/j. neuchi.2014.02.012. Amoretti N, Huwart L, Marcy PY, Foti P, Hauger O, Boileau P.  CTand fluoroscopy-guided percutaneous discectomy for lumbar radiculopathy related to disc herniation: a comparative prospective study comparing lateral to medial herniated discs. Skeletal Radiol. 2013;42:49–53. https://doi.org/10.1007/s00256-­012-­1422-­5. Bärlocher CB, Krauss JK, Seiler RW. Central lumbar disc herniation. Acta Neurochir (Wien). 2000;142:1369–74. https://doi.org/10.1007/ s007010070007. Compte R, Granville Smith I, Isaac A, Danckert N, McSweeney T, Liantis P, et al. Are current machine learning applications comparable to radiologist classification of degenerate and herniated discs

Further Reading and Modic change? A systematic review and meta-analysis. Eur Spine J. 2023:1–24. https://doi.org/10.1007/s00586-­023-­07718-­0. Deyo RA, Mirza SK. Clinical Practice. Herniated lumbar intervertebral disk. N Engl J Med. 2016;374:1763–72. https://doi.org/10.1056/ NEJMcp1512658. Diehn FE, Maus TP, Morris JM, Carr CM, Kotsenas AL, Luetmer PH, et al. Uncommon manifestations of intervertebral disk pathologic conditions. Radiographics. 2016;36:801–23. https://doi. org/10.1148/rg.2016150223. Fardon DF, Williams AL, Dohring EJ, Murtagh FR, Gabriel Rothman SL, Sze GK.  Lumbar disc nomenclature: version 2.0: recommendations of the combined task forces of the North American Spine Society, the American Society of Spine Radiology and the American Society of Neuroradiology. Spine J. 2014;14:2525–45. https:// doi.org/10.1016/j.spinee.2014.04.022. Halldin K, Lind B, Rönnberg K, Göthlin J, Gadeholt-Göthlin G, Zoëga B, et al. Three-dimensional radiological classification of lumbar disc herniation in relation to surgical outcome. Int Orthop. 2009;33:725– 30. https://doi.org/10.1007/s00264-­008-­0519-­x. Kang Q, Li X, Cheng Z, Liu C. Effects of release and decompression techniques on nerve roots through percutaneous transforaminal endoscopic discectomy on patients with central lumbar disc herniation. Exp Ther Med. 2017;13:2927–33. https://doi.org/10.3892/ etm.2017.4293. Khan JM, McKinney D, Basques BA, Louie PK, Carroll D, Paul J, et al. Clinical presentation and outcomes of patients with a lumbar far lateral herniated nucleus pulposus as compared to those with a central or paracentral herniation. Global Spine J. 2019;9:480–6. https://doi. org/10.1177/2192568218800055. Kondo M, Oshima Y, Inoue H, Takano Y, Inanami H, Koga H. Significance and pitfalls of percutaneous endoscopic lumbar discectomy for large central lumbar disc herniation. J Spine Surg. 2018;4:79– 85. https://doi.org/10.21037/jss.2018.03.06. Konieczny MR, Reinhardt J, Prost M, Schleich C, Krauspe R. Signal intensity of lumbar disc herniations: correlation with age of herniation for extrusion, protrusion, and sequestration. Int J Spine Surg. 2020;14:102–7. https://doi.org/10.14444/7014.

259 Kulkarni AG, Tapashetti S.  Outcomes of discectomy in young adults with large central lumbar disc herniations presenting with predominant leg pain. Global Spine J. 2020;10:412–8. https://doi. org/10.1177/2192568219856871. Lee JH, Lee SH.  Clinical and radiological characteristics of lumbosacral lateral disc herniation in comparison with those of medial disc herniation. Medicine (Baltimore). 2016;95:e2733. https://doi. org/10.1097/MD.0000000000002733. Mérot OA, Maugars YM, Berthelot JM.  Similar outcome despite slight clinical differences between lumbar radiculopathy induced by lateral versus medial disc herniations in patients without ­previous foraminal stenosis: a prospective cohort study with 1-year follow-up. Spine J. 2014;14:1526–31. https://doi.org/10.1016/j. spinee.2013.09.020. Pearson AM, Blood EA, Frymoyer JW, Herkowitz H, Abdu WA, Woodward R, et  al. SPORT lumbar intervertebral disk herniation and back pain: does treatment, location, or morphology matter? Spine (Phila Pa 1976). 2008;33:428–35. https://doi.org/10.1097/ BRS.0b013e31816469de. Porter RW, Miller CG.  Back pain and trunk list. Spine (Phila Pa 1976). 1986;11:596–600. https://doi.org/10.1097/00007632-­ 198607000-­00011. Schick U, Döhnert J.  Technique of microendoscopy in medial lumbar disc herniation. Minim Invasive Neurosurg. 2002;45:139–41. https://doi.org/10.1055/s-­2002-­34345. Słomkowski Z, Gołebiowski J, Dreczka J, Sarna R, Michaluk A, Erdenberger M. Clinical picture of medial prolapse of a lumbar intervertebral disk. Neurol Neurochir Pol. 1997;31:915–26. Yue JJ, Scott DL, Han X, Yacob A.  The surgical treatment of single level multi-focal subarticular and paracentral and/or far-lateral lumbar disc herniations: the single incision full endoscopic approach. Int J Spine Surg. 2014;8:16. https://doi.org/10.14444/1016. Zhang AS, Xu A, Ansari K, Hardacker K, Anderson G, Alsoof D, Daniels AH.  Lumbar disc herniation: diagnosis and management. Am J Med. 2023;136:645–51. https://doi.org/10.1016/j. amjmed.2023.03.024.

Foraminal and Extraforaminal (Far Lateral) Lumbar Disk Herniations

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17.1 Generalities and Relevance The foraminal zone is the limited area between planes passing through the medial and lateral borders of the pedicles. While the extraforaminal zone is the area outside the sagittal plane of the lateral borders of the pedicles, the extraforaminal zone has no precise lateral border but is certainly posterior to anterior zone (AKA anterior retroperitoneal zone. (c.f. Chap. 23 about Anterior Retroperitoneal Lumbar Disk Herniation). The foraminal zone is sometimes called the “lateral zone,” and the extraforaminal zone is also named the “far lateral zone.” For some authors, the extreme lateral zone includes both the foraminal and extraforaminal zones. The majority of lumbar disk herniations (LDHs) occur within the spinal canal (AKA intraspinal) and less than 15% are within the foramen or extraforaminal zones (Figs. 17.1 and 17.2). The age and sex distribution of patients with symptomatic foraminal and extraforaminal LDH (FELDH) is the same as those found with more traditional lumbar intraspinal ones except that the age is somewhat older. Most patients are male subjects with a peak incidence in their 60s. Foraminal LDH has been recognized as a cause of sciatic pain shortly after the description of the first cases of discogenic sciatica in the 1930s. On the other hand, extraforaminal LDH was first described by the Swedish radiologist Knut Lindblom (1905–1963) in 1944 on cadaveric studies, and it was only in 1974 that Adel Abdullah and his team reported the first clinical descriptions of this entity. FELDHs differ from routine intraspinal canal LDHs by some important distinctions (see below). Clinicians should be aware that the association of both foraminal and extraforaminal LDH is not rare. Some patients may be asymptomatic and the lesion incidentally discovered, but can still be confused with a wide variety of differential diagnoses.

Fig. 17.1  Classification of the lumbar disk herniations related to the axial plane: central (median and paramedian) in blue, subarticular (lateral recess) in red, foraminal in yellow, extraforaminal in orange, and anterior retroperitoneal in green

As with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as compression theory, ischemic theory, and chemical irritative theories. However, compressive neurological structures do not concern only lumbar or sacral radicular nerves but also their corresponding nerve root ganglions, part of the proximal lumbosacral plexus, and even lumbar sympathetic structure. Neurophysiological explorations can assess the relative severity of neurological damage and predict the prognosis or follow-up course of recovery.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_17

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262 Fig. 17.2  Illustration of the lumbosacral spine on axial and coronal views showing the foraminal (a) and extraforaminal (b) location of the lumbar disk herniations. The herniated disk is represented in red color

Fig. 17.3  Case A. Right-­ sided foraminal/ extraforaminal L4–L5 disk herniation (arrows) as seen on axial CT scan (a, b)

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17.2 Main Particularities of Foraminal and Extraforaminal Lumbar Disk Herniations Foraminal and extraforaminal lumbar disk herniations (FELDH) differ from the more common intraspinal LDH (c.f. Chap. 16 about Central and Subarticular Lumbar Disk Herniations) by the main following points: • The nerve root involved is often the one exiting at that corresponding level also known as the upper nerve root (e.g., at the L4–L5 intervertebral disk space, it is the L4 superior nerve that is most likely to be affected). • L4 is the most common nerve involved followed by L3.

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• Most patients complain of anterior thigh and knee, and sometimes proximal hip pain. • Low back pain is minimal or even absent (Fig. 17.3). • Lasègue’s test (AKA straight leg raising) is often negative but the femoral stretch test (AKA reverse straight leg raising) may be positive. • Radicular pain is reproduced by lateral flexion to the ipsilateral side of the herniated disk. • Radicular pain is likely to be more painful by direct compression of both nerve root and spinal ganglion. • Higher incidence of sensory dysesthesia. • Quadriceps weakness, decreased or absent knee jerk reflex (AKA patellar tendon reflex), and hypoesthesia in the dermatome L3 or L4.

17.3 Imaging Features

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• Higher incidence of motor deficits: minor or moderate lower limb paresis in up to 70% without significant gait impairment. However, cauda equina syndrome is rare. • Extrusions and sequestrations are the most common types of FELDH. • More frequent occurrence of spinal “crush syndrome” (e.g., double herniated disk on the same side same level) (c.f. Chap. 32 about Sciatic Double Crush Syndrome at the Same Root Site). • Myelography (saccoradiculography) is rarely decisive. • Often misdiagnosed or overlooked on spine computed tomography or magnetic resonance imaging. • Decompressive surgery is usually required because conservative treatment is less successful. • More difficult surgical procedure as the traditional posterior midline interlaminar approach requires extension into the neural foramen and may need destruction of pars interarticularis and facet joint, which could give rise to spinal lumbar instability. • Overall, such disorder can lead to worse postoperative course and outcomes after treatment and a higher frequency of failed back surgery syndrome, especially following a midline surgical approach.

Fig. 17.4  Foraminal L3–L4 posterior ring apophysis separation on the left side (arrows) as seen on axial CT scan, parenchymal (a, b), and bone windows (c, d)

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17.3 Imaging Features Diagnosis of FELDH should correlate with the patient’s history, clinical examination, and spinal imaging investigations. In addition, preoperative spinal imaging should permit the planning of the surgery and, therefore, select the most appropriate procedure. Some symptomatic patients may have mild-to-moderate degenerative lumbar scoliosis on plain radiography. The curve convexity is identical to the symptomatic side. Disk height loss is a common finding at the L5–S1 intervertebral level, and the L5 vertebral body inclines laterally toward the opposite side of the painful lesion. Myelography (saccoradiculography) fails to identify the lesion because the nerve root compression occurs away from the nerve root sleeve. Computed tomography (CT) scan can usually demonstrate the herniated mass, which has a similar density as the disk material. The intraforaminal and extraforaminal disk fragments appear isodense, while the contralateral normal root ganglion is surrounded by normal fat (Figs. 17.3, 17.4, and 17.5). Axial, parasagittal, and even coronal CT scan on bone and parenchymatous windows can assess certain asso-

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264 Fig. 17.5  Case B. Foraminal L5–S1 disk herniation on the right side (arrows) as seen on axial CT scan (a, b) and on T2-weighted MRI (c, d)

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ciated spinal lesions such as facet joint arthrosis, spinal canal and foraminal stenosis, osteophytosis, spondylolysis or spondylolisthesis, pseudoarticulation between the L5 transverse process and the sacrum and possible sacroiliac joint disorders. Magnetic resonance imaging (MRI) with a standard axial and parasagittal view is the key diagnosis method for identifying FELDH.  It is important to look beyond the foramen and the immediately adjacent extraforaminal zone (Figs. 17.5, 17.6, 17.7, 17.8, 17.9, 17.10, and 17.11). Four MRI findings are particularly useful for the diagnosis: –– –– –– ––

Occlusion of the affected neural foramen. Focal eccentric contour of the disk in this zone. A change in the diameter of the exiting nerve root. Displacement of the nerve root.

Sometimes, it is difficult to determine whether the location of the herniated disk is in or outside the foramen or both in and outside. In addition, it is challenging in some cases to define which degenerative lesions are responsible for the nerve entrapment based only on MRI results.

Following gadolinium administration, peripheral ring-­ type enhancement is characteristic. More rarely, solid homogeneous post-gadolinium enhancement may be encountered and can be confused with other diseases, especially neoplasms. It is important to correlate CT scan and/or MRI features with preoperative and intraoperative radiographs (Fig. 17.12). Effective communication between the surgeon and the radiologist is essential regarding the precise location of the compressive lesions in order to avoid wrong the level. More rarely, some cases may be accompanied by an intradural extension of the disk fragment [c.f. Chap. 30 about Intradural LDHs]. Overall, the detection of FELDH is often difficult on imaging. For some radiologists, up to 30% of extraforaminal LDH are misdiagnosed or overlooked on initial spinal imaging. There is no real correlation between the size of the disk herniation on spinal imaging and the degree of clinical symptomatology. In some cases, major compression induces few neurological symptoms, whereas in other cases, mild compression may cause severe paralysis. This divergence is

17.3 Imaging Features Fig. 17.6  Case B. Sagittal T2-weighted MRI showing the appearance of the L5–S1 foramen on the left side (normal) (a) versus the right side (disk herniation) (b)

Fig. 17.7  Foraminal L4–L5 disk herniation on the left side (arrows) as seen on sagittal (a, b) and axial (c, d) T2-weighted MRI. Note the vertebral scalloping caused by the disk herniation (double arrows) (d)

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266 Fig. 17.8 Extraforaminal L4–L5 disk herniation on the right side. Axial (a) and sagittal (b) T2-weighted MRI

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Fig. 17.9  Foraminal/extraforaminal L4–L5 disk herniation on the left side (arrows) as seen on axial CT scan (a) and T2-weighted MRI (b) and on sagittal T1-weighted (c) and T2-weighted MRI (d)

17.3 Imaging Features Fig. 17.10 Lateral/foraminal sequestrated disk fragment (arrows) behind the posterior wall of L4 vertebral body as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted (c, d) MRI

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explained by the existence of other factors besides pure mechanical compression such as inflammatory and vascular phenomena. Imaging features are sometimes unspecific and can be confused with other lesions in the foraminal or extraforaminal lumbar area such as follows: –– –– –– ––

Schwannoma and neurofibroma. Malignant peripheral nerve sheath tumor. Metastasis. Lymphoma.

–– –– –– –– –– ––

Vertebral osteophytes (bone spurs). Lateral recess stenosis. Articular facet hypertrophy. Spondylolysis with or without listhesis. Conjoined nerve roots. Prominent foraminal or paraspinal venous plexus (AKA enlarged foraminal veins). –– Paraspinal abscesses. –– Discitis. –– Fibrosis.

268 Fig. 17.11  L4–L5 disk herniation migrating cranially and toward the right foramen (arrows) as seen on sagittal (a, b), axial (c), and coronal (d) T2-weighted MRI

Fig. 17.12  Axial CT scan (a) and T2-weighted MRI (b) showing a right-sided enlarged nerve root (arrows) mimicking a foraminal L4–L5 disk herniation

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17.4 Treatment Options and Prognosis

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17.4 Treatment Options and Prognosis

tional complications. Various approaches are used including classic midline interlaminar approach (Figs.  17.13, 17.14, Conservative management is typically the primary therapeu- 17.15, 17.16, and 17.17) and posterolateral paraspinal tic intervention in patients with FELDH as long as they have approach. Some FELDH may need to be approached from a no neurological deficit. Conservative measures consist of combined midline and posterolateral approach. bed rest, pharmacological therapy (analgesic, anti-­ In the past, the most common procedure was partial or inflammatory medications, and muscle relaxants), physical complete facetectomy with or without fusion through the therapy interventions, lumbar bracing (rarely), and limitation medial standard approach. Via this technique, it is important of physical activities. Posture-modifying exercises can to expose and repair the exiting (upper) nerve root axilla and improve symptoms by improving muscle strength, coordina- then to follow the nerve laterally in or outside the neural tion, and flexibility. If conservative therapy is unsuccessful foramen until to identify the LDH.  This procedure might or persistent radicular pain unfavorably compromises the develop iatrogenic spinal instability due to facet resection patient’s daily activities, regardless of existing neurological and concomitant discectomy. Wiltse and coworkers in the mid-1970s recommended a deficits, the need for surgical decompression is highlighted. unilateral posterolateral (extracanal) approach via intra- or at Direct local anesthetic and corticosteroid injection in the foraminal or extraforaminal area under CT scan guidance best inter-muscular route (via a paramedian muscle-splitting may produce successful relief of pain for a more or less long technique), highlighting the great importance to decompress the nerve far enough laterally (Fig.  17.18). Typically, the period of time. The surgical strategy for FELDH requests neurological nerve root is displaced cranially by the herniated disk decompression and herniated disk removal without addi- (Figs. 17.19, 17.20, 17.21, 17.22, 17.23, 17.24, and 17.25).

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Fig. 17.13  Case C. Left-sided foraminal L5–S1 herniated disk (arrows) as seen on sagittal (a, b) and axial T2-weighted MRI (c, d)

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Fig. 17.14 Case C. Photograph showing the disk fragment and the disk material that were removed (herniectomy and discectomy, respectively, via a lateral interlaminar approach)

Fig. 17.15  Case D. Clinical pictures of a patient with L4–L5 right foraminal LDH (a, b) showing ipsilateral sciatic scoliosis. Note the left lateral shift away from the right (contralateral) side of sciatica

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Fig. 17.16  Case D. Right-sided L4–L5 foraminal disk herniation (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted MRI (c). Note the normal appearance of the L3–L4 disk level (d) Fig. 17.17 Case D. Intraoperative views of the surgical procedure via an L4– L5 interlaminar approach on the right side (a–d). Right L5 nerve root (stars) and disk herniation (arrows). Operative appearance before (a, b) and after (c) herniectomy and discectomy. Disk fragment removed (d)

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Fig. 17.18  Illustration of the axial lumbar spinal area at the L4–L5 disk level showing unilateral posterolateral (extracanal) approach via paramedian muscle-splitting technique (transmusclar Wiltse approach) for extraforaminal disk herniation

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Fig. 17.19  Case A. Right-sided foraminal/extraforaminal L4–L5 disk herniation (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted sequence (c, d)

17.4 Treatment Options and Prognosis Fig. 17.20 Case A. Intraoperative views of the right L4–L5 paraspinal approach (a, b). Exposure of the intertransverse ligament (a). Following dissection of the L4 nerve root (arrow), the disk fragment was exposed (star) (b) and removed without discectomy

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Fig. 17.21  Lumbosacral MRI showing mild vertebral slippage but an L4–L5 foraminal disk herniation (arrows). Sagittal (a, b) and axial (c) T2-weighted MRI. Note the defect of the pars interarticularis (isthmolysis) (arrowheads)

274 Fig. 17.22 Intraoperative views of the left L4–L5 paraspinal approach (a–d) under fluoroscopic guidance (a). Exposure of the intertransverse ligament (b). Following retraction of the nerve root (arrow), the disk fragment was exposed (star) (c) and removed without discectomy (d)

Fig. 17.23  Case E. Axial CT scan (a, b) and T2-weighted MRI (c, d) showing a left foraminal L4–L5 disk herniation (arrows) migrating cranially into the foramen

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Fig. 17.24  Case E. This left foraminal L4–L5 herniated disk migrates superiorly (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b, c)

However, surgical access to L5–S1 (lumbosacral junction) extraforaminal area is often difficult mainly due to the depth operating field, inclination of sacral ala, and bleeding from the vessels around the L5 radicular nerve. Fusion is often not required with Wiltse’s approach because the medial part of the facet joint is often conserved. The posterolateral approach demonstrated significantly better results in comparison with medial procedures. In addition, surgical complications are apparently more than twice as with the midline approach. Currently, microendoscopic technique and minimally invasive tubular-based procedures are increasingly used and show great promise because they are less invasive, give better recovery, and provide gratifying results and successful

outcomes. However, patients with concomitant spinal stenosis require more extended spinal decompressions. FELDHs are deemed to have less good postsurgical results than intraspinal LDH.  However, with the development of minimally invasive procedures, posterolateral ­(extracanal) approach, and microendoscopic technique, the outcome is not so different from that of more frequent central and subarticular LDH.  About 90% of surgically treated patients had good to excellent results with less than 10% of the recurrent rate. Dysesthesias have been reported to be among the most important postoperative patient complaint. Nevertheless, undiagnosed forms are usually responsible for poor outcomes including a high rate of failed back surgery syndrome.

276 Fig. 17.25 Case E. Preoperative (a, b) and postoperative (c, d) axial T2-weighted MRI showing complete decompression of the left herniated disk

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Further Reading

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logic conditions. Radiographics. 2016;36:801–23. https://doi. org/10.1148/rg.2016150223. Dogu H, Ozdemir NG, Yilmaz H, Atci IB. Long-term follow-up results Abdullah AF, Ditto EW 3rd, Byrd EB, Williams R.  Extreme-lateral of surgically treated patients with foraminal and far lateral disc herlumbar disc herniations. Clinical syndrome and special problems of niations. Br J Neurosurg. 2023;37:49–52. https://doi.org/10.1080/0 diagnosis. J Neurosurg. 1974;41:229–34. https://doi.org/10.3171/ 2688697.2021.1874293. jns.1974.41.2.0229. Doi T, Harimaya K, Matsumoto Y, Tono O, Tarukado K, Iwamoto Ahn Y, Yoo BR, Jung JM. The irony of the transforaminal approach: a Y. Endoscopic decompression for intraforaminal and extraforaminal comparative cohort study of transforaminal endoscopic lumbar disnerve root compression. J Orthop Surg Res. 2011;6:16. https://doi. cectomy for foraminal versus paramedian lumbar disc herniation. org/10.1186/1749-­799X-­6-­16. Medicine (Baltimore). 2021;100:e27412. https://doi.org/10.1097/ Epstein NE. Foraminal and far lateral lumbar disc herniations: surgical MD.0000000000027412. alternatives and outcome measures. Spinal Cord. 2002;40:491–500. Ashkenazi E, Pomeranz S, Floman Y. Foraminal herniation of a lumbar https://doi.org/10.1038/sj.sc.3101319. disc mimicking neurinoma on CT and MR imaging. J Spinal DisFardon DF, Williams AL, Dohring EJ, Murtagh FR, Gabriel Rothman ord. 1997;10:448–50. SL, Sze GK.  Lumbar disc nomenclature: version 2.0: recommenBerra LV, Di Rita A, Longhitano F, Mailland E, Reganati P, Frati A, dations of the combined task forces of the North American Spine et al. Far lateral lumbar disc herniation part 1: imaging, neurophysiSociety, the American Society of Spine Radiology and the Ameriology and clinical features. World J Orthop. 2021;12:961–9. https:// can Society of Neuroradiology. Spine J. 2014;14:2525–45. https:// doi.org/10.5312/wjo.v12.i12.961. doi.org/10.1016/j.spinee.2014.04.022. Cusimano MD, Bukala BP, Bilbao J.  Extreme lateral disc herniaFiorenza V, Ascanio F. Percutaneous endoscopic transforaminal outsidetion manifesting as nerve sheath tumor. Case report. J Neurosurg. ­in outside technique for foraminal and extraforaminal lumbar disc 1995;82:654–6. https://doi.org/10.3171/jns.1995.82.4.0654. herniations-operative technique. World Neurosurg. 2019;130:244– Bonis PDE, Musio A, Mongardi L, Marca FLA, Lofrese G, Visani 53. https://doi.org/10.1016/j.wneu.2019.07.005. J, et  al. Transpars approach for L5-S1 foraminal and extra-­ Haines CM, Samtani RG, Bernatz JT, Abugideiri M, O’Brien JR. Far-­ foraminal lumbar disc herniations: technical note. J Neurosurg Sci. lateral disc herniation treated by lateral lumbar interbody fusion 2023;67:213–8. https://doi.org/10.23736/S0390-­5616.20.05165-­6. without complete fragment excision: a case report and review of Di Lorenzo N, Porta F, Onnis G, Cannas A, Arbau G, Maleci A. Pars the literature. Cureus. 2018;10:e3404. https://doi.org/10.7759/ interarticularis fenestration in the treatment of foraminal lumbar disc cureus.3404. herniation: a further surgical approach. Neurosurgery. 1998;42:87– Jang JS, An SH, Lee SH. Transforaminal percutaneous endoscopic dis9. https://doi.org/10.1097/00006123-­199801000-­00018. cectomy in the treatment of foraminal and extraforaminal lumbar Diehn FE, Maus TP, Morris JM, Carr CM, Kotsenas AL, Luetmer disc herniations. J Spinal Disord Tech. 2006;19:338–43. https://doi. PH, et al. Uncommon manifestations of intervertebral disk pathoorg/10.1097/01.bsd.0000204500.14719.2e.

Further Reading Khan JM, McKinney D, Basques BA, Louie PK, Carroll D, Paul J, et al. Clinical presentation and outcomes of patients with a lumbar far lateral herniated nucleus pulposus as compared to those with a central or paracentral herniation. Global Spine J. 2019;9:480–6. https://doi. org/10.1177/2192568218800055. Kim JY, Heo DH.  Contralateral sublaminar approach for decompression of the combined lateral recess, foraminal, and extraforaminal lesions using biportal endoscopy: a technical report. Acta Neurochir (Wien). 2021;163:2783–7. https://doi.org/10.1007/s00701-­021-­ 04978-­x. Kim KS, Chin DK, Park JY.  Herniated nucleus pulposus in isthmic spondylolisthesis: higher incidence of foraminal and extraforaminal types. Acta Neurochir (Wien). 2009;151:1445–50. https://doi. org/10.1007/s00701-­009-­0411-­5. Kotil K, Akcetin M, Bilge T.  A minimally invasive transmuscular approach to far-lateral L5-S1 level disc herniations: a prospective study. J Spinal Disord Tech. 2007;20:132–8. https://doi. org/10.1097/01.bsd.0000211268.43744.2a. Lee DY, Lee SH. Microdecompression for extraforaminal L5-S1 disc herniation; the significance of concomitant foraminal disc herniation for postoperative leg pain. J Korean Neurosurg Soc. 2008;44:19–25. https://doi.org/10.3340/jkns.2008.44.1.19. Lee JH, Lee SH.  Clinical and radiological characteristics of lumbosacral lateral disc herniation in comparison with those of medial disc herniation. Medicine (Baltimore). 2016;95:e2733. https://doi. org/10.1097/MD.0000000000002733. Lejeune JP, Hladky JP, Cotten A, Vinchon M, Christiaens JL. Foraminal lumbar disc herniation. Experience with 83 patients. Spine (Phila Pa 1976). 1994;19:1905–8. https://doi.org/10.1097/00007632-­ 199409000-­00007. Lindblom K. Protrusions of disks and nerve compression in the lumbar region. Acta Radiol. 1944;25:195–212. Mérot OA, Maugars YM, Berthelot JM.  Similar outcome despite slight clinical differences between lumbar radiculopathy induced by lateral versus medial disc herniations in patients without previous foraminal stenosis: a prospective cohort study with 1-year follow-up. Spine J. 2014;14:1526–31. https://doi.org/10.1016/j. spinee.2013.09.020. Moon KP, Suh KT, Lee JS. Reliability of MRI findings for symptomatic extraforaminal disc herniation in lumbar spine. Asian Spine J. 2009;3:16–20. https://doi.org/10.4184/asj.2009.3.1.16. Ohmori K, Kanamori M, Kawaguchi Y, Ishihara H, Kimura T. Clinical features of extraforaminal lumbar disc herniation based on the radiographic location of the dorsal root ganglion. Spine (Phila

277 Pa 1976). 2001;26:662–6. https://doi.org/10.1097/00007632-­ 200103150-­00022. Ozpeynirci Y, Braun M, Lubotzki I, Schmitz B, Antoniadis G. Extra-­ foraminal Intraneural L5-S1 disc herniation mimicking a retroperitoneal peripheral nerve sheath tumour: case report and review of the literature. Cureus. 2019;11:e4956. https://doi.org/10.7759/ cureus.4956. Perno JR, Rossitch E Jr. Extreme lateral lumbar disc herniation. Diagnosis and management. N C Med J. 1993;54:224–6. Sharma MS, Morris JM, Pichelmann MA, Spinner RJ. L5-S1 extraforaminal intraneural disc herniation mimicking a malignant peripheral nerve sheath tumor. Spine J. 2012;12:e7–e12. https://doi. org/10.1016/j.spinee.2012.10.033. Siu TLT, Lin K. Direct tubular lumbar microdiscectomy for far lateral disc herniation: a modified approach. Orthop Surg. 2016;8:301–8. https://doi.org/10.1111/os.12263. Tschugg A, Tschugg S, Hartmann S, Rhomberg P, Thomé C. Far caudally migrated extraforaminal lumbosacral disc herniation treated by a microsurgical lateral extraforaminal transmuscular approach: case report. J Neurosurg Spine. 2016;24:385–8. https://doi.org/10.3 171/2015.7.SPINE15342. Ünsal ÜÜ Sr, Senturk S.  Minimally invasive far-lateral microdiscectomy: a new retractor for far-lateral lumbar disc surgery. Cureus. 2021;13:e12625. https://doi.org/10.7759/cureus.12625. Verla T, Goethe E, Srinivasan VM, Winnegan L, Omeis I.  The minimally invasive paramedian approach for foraminal disc herniation. J Clin Neurosci. 2020;75:62–5. https://doi.org/10.1016/j. jocn.2020.03.029. Wang C, Zhang Y, Tang X, Cao H, Song Q, Tan J, et al. Microscopic extra-laminar sequestrectomy (MELS) for the treatment of hidden zone lumbar disc herniation: report of the surgical technique, patient selection, and clinical outcomes. BMC Surg. 2021;21:255. https:// doi.org/10.1186/s12893-­021-­01255-­7. Wiltse LL.  The paraspinal sacrospinalis-splitting approach to the lumbar spine. Clin Orthop Relat Res. 1973;91:48–57. https://doi. org/10.1097/00003086-­197303000-­00009. Wong KW, Ho CH, Yu TC, Wu CD, Tsang YS.  Clinical outcome of minimally invasive decompression without discectomy in contained foraminal disc herniation: a single-center study. World Neurosurg. 2018;118:e367–74. https://doi.org/10.1016/j.wneu.2018.06.192. Yue JJ, Scott DL, Han X, Yacob A. The surgical treatment of single level multi-focal subarticular and paracentral and/or far-lateral l­umbar disc herniations: the single incision full endoscopic approach. Int J Spine Surg. 2014;8:16. https://doi.org/10.14444/1016.

Migrated Lumbar Disk Herniations

18.1 Generalities and Relevance Migrated disk fragment is a form of extruded disk herniation (AKA disk extrusion) in which a portion of disk material is displaced away from the site of extrusion in either the sagittal or axial plane. An extruded disk is a type of disk herniation that is distinguished from a protruded disk (AKA disk protrusion) by in at least one anatomic plane, and disk extrusion has a neck that is narrower than the dome. Because the distinction between “protrusion” and “extrusion” is not always possible by advanced spinal imaging, some radiologists describe “disk extrusion” as “uncontained disk” where ligamentous structures surrounding the disk are interrupted (broken). There are two subtypes of extruded disk: “sequestration” and “migration.” –– Migrated disk: The disk material is displaced away from the site of extrusion, but it is still in continuity with the disk of origin. –– Sequestrated disk: The fragment is completely separated from the disk of origin. Fig. 18.1  Illustration of the lumbosacral spine on coronal views showing the migrated lumbar disk herniations. The disk fragment (in red) can be migrated upward/cranially (a) or downward/caudally (b) from the L4–L5 parent disk (arrows)

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Only “migrated lumbar disk herniation” (MigLDH) will be detailed in the present chapter. For “Sequestrated lumbar disk herniations,” please refer to Chap. 19. Migrated-type disk herniation is a usual phenomenon that can involve all lumbar spine levels; however, the majority of cases are located in the lower lumbar spine. About 35–70% of all lumbar disk herniation (LDH) are migrated and the majority of patients complain of traditional low back and lumbar radicular pain with or without motor deficit. As seen with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as mechanic compression theory, ischemic theory, and chemical irritative theories. The migrated lumbar disk size may vary between a few millimeters to a few centimeters in length. Often, it can be localized medially or laterally and can be migrated upward or downward, anterior or posteriorly relative to the original lumbar disk (Fig.  18.1). The number of downward migrations seems to be twice as common as the upward migration of the herniated disk fragments. Moreover, subarticular migration is more frequent than central and lateral migration of LDH. On the other part, subarticular herniations are

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displaced more significantly downward, whereas foraminal herniations always migrate upward. Interestingly, the number of upward migrations increased considerably with increasing age and in higher-level locations of LDH. In the same way, the incidence of foraminal migrations increased with aging. The majority of MigLDH is fragmented into small pieces, and it is not easy to predict them in preoperative imaging studies. In addition, migrated disk fragments may be a source of failed back surgery syndrome because of the high occurrence of operative missing disk fragments. Although the etiopathogenic mechanism of migrated LDH is unknown, some predisposing conditions have been suggested such as unusual movements of the patient (e.g., torsional movements), heavy physical activities and loading forces to the intervertebral disk, adjacent intervertebral disk instability (e.g., spondylolisthesis), prior spinal surgery, or specific anatomy of the posterior longitudinal ligament itself. Sometimes this form of LDH can be found in rare locations such as intradural, posterior epidural, and even extraforaminal far away from the original intervertebral space. Occasionally, some MigLDH will be also sequestrated (c.f. Chap. 19 about Sequestrated Lumbar Disk Herniations).

18.2 Clinical Presentations The higher incidence of patients with MigLDH is seen in patients in their fifth and sixth decades of life. There is no significant association between gender, body mass index, disk herniation laterality, and the level of MigLDH. The initial clinical evaluation of these patients should include a sufficient and detailed history and a neurological and spinal examination. Classically, there are no distinctive clinical features allowing clear differentiation between patients with MigLDH and those with traditional protruded LDH.  Indeed, most cases present with both lower back and lumbar radicular pain. Neurological deficits and cauda equina syndrome are unusual. For many authors, there is no real correlation between the size of the disk fragment on spinal imaging and the degree of clinical symptomatology. Regarding neurological pain, radiculopathy is significantly more frequent in patients with caudal migrations than in those with rostral migrations. On the other hand, there is a high incidence of radiculopathy in subarticular and foraminal migrated LDH in comparison with central and extraforaminal migrations. The straight leg raising test (Lasègue sign) result is often positive with associated lumbosacral spinal root stretching. Sometimes, the Lasègue sign is positive in the contralateral side (AKA crossed over the Lasègue sign) and this is ­considered more specific for the diagnosis of MigLDH but not sensitive.

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Any related signs of spinal stenosis or spondylolisthesis should be considered in order to exclude other mimicking or associated pathologies. Neurophysiological explorations can assess the relative severity of neurological damage and predict the prognosis or follow-up course of recovery.

18.3 Paraclinic Features The majority of MigLDH are located at lower lumbar disk levels. In addition, the disk fragment may migrate in different directions, medially or laterally, upward (cranially/rostral) or downward (caudal), and anterior or posteriorly relative to the original lumbar disk. The ability to identify an LDH that has migrated is crucial for the correct management and surgical planning. Various classifications had been suggested to determine the exact location of the MigLDH compared to the horizontal or vertical plane (Table 18.1). In myelography (saccoradiculography), the spinal lesion presents as an atypical subtotal or total block. However, this old technique does not deliver any information about the origin of the lesion. On computed tomography (CT), the extradural lesion has often similar density as the disk material. Bony CT scan may be useful for identifying possible adjacent degenerative osteoarticular changes and potential isthmic defects. However, magnetic resonance imaging (MRI) remains the best imaging procedure for visualizing all constituents of the LDH including local adhesion, inflammatory tissue, and associated spinal lesions. The migrated fragment is clearly displayed on axial and sagittal images, with or without discontinuity in the parent disk (Figs.  18.2, 18.3, 18.4, 18.5, 18.6, 18.7, 18.8, 18.9, 18.10, 18.11, 18.12, 18.13, 18.14, 18.15, 18.16, and 18.17). The “lava flow” sign is quite charTable 18.1  Differential diagnosis of migrated disk fragment Tumors

Infections Degenerative diseases Trauma and Hematological disorders Metabolic disorders Iatrogenic disorders Conjoined nerve roots Enlarged nerve root

Chordoma, chondrosarcoma, lipoma, lymphoma, cystic schwannoma, neurofibroma, neuroblastoma, metastasis (mainly breast and prostate cancer) Abscess, cysticercosis, echinococcosis, fungal Synovial cyst, Tarlov’s cyst, ligamentum cyst, osteophyte of the facet joint, hypertrophy of unilateral ligamentum flavum, pigmented villonodular synovitis Hematoma

Gout disease Postoperative scar, fibrosis, and granuloma (e.g., textiloma) C.f. Chap. 59 Fig. 18.17

18.3 Paraclinic Features Fig. 18.2  Case A. L4–L5 disk herniation (arrows) migrating posterolaterally on the right side. Sagittal reconstruction (a) and axial (b, c) CT scan on parenchymal windows

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acteristic: It represents the migrated extruded material into the epidural space in a sagittal plane (Figs. 18.3, 18.4, 18.5, 18.7, 18.8, 18.9, 18.11, 18.15, and 18.16). The signal intensity of disk fragments is variable and unspecific, but in the majority of cases, the epidural lesions have low-to-isointense signal intensity on T1-weighted and low or sometimes high signal intensity on T2-weighted MRI depending on the time of evolution. Following gadolinium injection, some fragments may present peripheral ring enhancement (Figs. 18.11, 18.12, and 18.15). Solid homogeneous post-gadolinium enhancement is rare and can be confused with other diseases, especially neoplasms. To differentiate between subligamentous and extraligamentous LDH, the following five criteria have been suggested by Oh et  al. in favor of an extraligamentous herniation:

(a) Spinal canal stenosis for more than half its dimension. (b) Heterogeneous internal signal in the LDH. (c) Unclear border of the LDH. (d) Disruption of the continuous low signal intensity line covering the LDH. (e) Presence of an internal dark line in the LDH. Concerning other rare locations of LDH namely intradural, intraradicular, extraforaminal, or posterior epidural, please refer to the relevant chapters of this book. Even with the wide use of high-resolution MRI, some MigLDH can be still confused with many neoplastic or nonneoplastic lesions, especially when there is a large size sequestrated disk fragment, conservation of intervertebral space height and form, and central contrast enhancement on imaging.

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Fig. 18.3  Case A. L4–L5 disk herniation migrating cranially and posterolaterally on the right side. Sagittal (a, b) and axial (c, d) T2-weighted MRI

18.3 Paraclinic Features Fig. 18.4  L5–S1 disk herniation migrating caudally and posterolaterally on the left side (arrows). Axial CT scan (a) and T2-weighted MRI (b) and sagittal T1-weighted (c) and T2-weighted MRI (d)

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Fig. 18.5  L4–L5 disk herniation migrating cranially (arrows) behind the posterior wall of the L4 vertebral body. Sagittal T1-weighted (a, b) and T2-weighted MRI (c–e)

18.3 Paraclinic Features Fig. 18.6  L4–L5 disk herniation migrating cranially and toward the right foramen (arrows) as seen on sagittal (a, b), axial (c), and coronal (d) T2-weighted MRI

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Fig. 18.7  L5–S1 disk herniation migrating caudally and laterally on the left side (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial (c, d) T2-weighted MRI

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Fig. 18.8  L4–L5 disk herniation migrating cranially behind the posterior wall of the L4 vertebral body (arrows) as seen on sagittal T1-weighted (a), T2-weighted MRI (b), and on STIR sequence (c)

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Fig. 18.9  L4–L5 disk herniation migrating caudally (arrows) with concomitant L3–L5 spinal canal stenosis as seen on axial (a) CT scan and T2-weighted MRI (b) as well as on sagittal T1-weighted (c) and T2-weighted MRI (d)

Fig. 18.10  Operative view of the L4–L5 migrated disk herniation on the right side (stars) following L3–L5 bilateral laminectomy

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Fig. 18.11  Case B. L5–S1 disk herniation migrating cranially (arrows) as seen on sagittal T1-weighted MRI before (a) and after gadolinium injection (b) and on STIR sequence (c)

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Fig. 18.12  Case B. The L4–L5 disk fragment migrated cranially and posterolaterally on the right side (arrows) as seen on axial T2-weighted (a, b) and post-gadolinium T1-weighted MRI (c)

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Fig. 18.13  Case B. Operative view of the disk fragment removed

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Fig. 18.14  Case B. Postoperative sagittal T1-weighted (a) and T2-weighted MRI (b) and axial T2-weighted MRI (c) showing complete removal of the migrated disk herniation

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Fig. 18.15  L5–S1 disk fragment migrated inferiorly and laterally on post-gadolinium T1-weighted MRI (d). Note the peripheral ring the right side (arrows) as seen on sagittal T2-weighted (a) and post-­ enhancement of the disk fragment (b, d) gadolinium T1-weighted MRI (b) and on axial T2-weighted (c) and

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Fig. 18.16  L4–L5 disk fragment migrated superiorly and posterolaterally on the right side (arrows) as seen on sagittal T1-weighted (a, b) and T2-weighted MRI (c, d) and on axial T2-weighted MRI (e, f)

18.4 Treatment Options and Prognosis

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Fig. 18.17  Right L5 enlarged nerve root (arrows) mimicking an L4–L5 disk herniation migrating superiorly as seen on sagittal (a, b) and axial (c, d) T2-weighted MRI

18.4 Treatment Options and Prognosis Conservative management is typically the primary therapeutic intervention in patients with MigLDH as long as they have no neurological deficit or uncontrolled pain. Conservative measures consist of bed rest, pharmacological therapy (analgesic, anti-inflammatory medications, and muscle relaxants), physical therapy interventions, lumbar bracing (rarely), and limitation of physical activities. Posture-modifying exercises can improve symptoms by improving muscle strength, coordination, and flexibility. If conservative therapy is unsuccessful or persistent radicular pain unfavorably compromises the patient’s daily activities, regardless of existing neurological deficits, the need for surgical decompression is highlighted. Surgical technique may vary according to the exact localization of the MigLDH.  However, proper removal of migrated disk material remains somewhat complicated owing to many anatomic difficulties and its potential for

being fragmented. The surgical procedure can require extensive vertebral bone removal including laminas, pars ­interarticularis, and facet joints, which might be responsible for potential spinal instability and associated complications. Globally, surgery is indicated in cauda equina syndrome or in the presence of symptoms such as motor weakness or pain refractory to conservative treatment. The majority of operated patients underwent an interlaminar approach to ensure full exposure of the disk fragment and easier removal of the lesion with minimum complications such as dural weakness (CSF leak), root damage, or spinal instability. It is preferable to explore the nerve root and the dura using microsurgical techniques to avoid iatrogenic neurological injuries. More recently, some surgeons experienced a variety of minimally invasive surgical techniques via different approaches for the treatment of MigLDH such as percutaneous endoscopic lumbar discectomy. This last method shows great promise because it is less invasive, gives better recovery, and provides good results and successful outcomes.

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Some surgeons recommend removing only the compressing fragment(s), whereas the healthy disk should be preserved. For others, this procedure would be the source of a high rate of recurrences. Patients with associated lumbar spinal stenosis require more extended spinal decompressions. Overall, there are no distinctive postoperative results between patients with MigLDH and those with more traditional protruded LDH. Clinically, the majority of cases (up to 90%) are associated with clinical improvement with less than 10% of the recurrent rate. However, it seems that migrated disk fragments may be a source of failed back surgery syndrome due to the high existence of operative missing disk fragment(s).

Further Reading Abdelrahman H, Seyed-Emadaldin S, Krajnovic B, Ezzati A, Abdelgawaad AS. Trans-tubular translaminar microscopic-­assisted nucleotomy for lumbar disc herniations in the hidden zone. Global Spine J. 2022;12:1420–7. https://doi.org/10.1177/2192568221990421. Ahn Y, Kim JE, Yoo BR, Jeong YM. A new grading system for migrated lumbar disc herniation on sagittal magnetic resonance imaging: an agreement study. J Clin Med. 2022;11:1750. https://doi. org/10.3390/jcm11071750. Akhaddar A, Boulahroud O, Elasri A, Boucetta M. Radicular interdural lumbar disc herniation. Eur Spine J. 2010;19(Suppl 2):S149–52. https://doi.org/10.1007/s00586-­009-­1200-­9. Akhaddar A, El-Asri A, Boucetta M.  Posterior epidural migration of a lumbar disc fragment: a series of 6 cases. J Neurosurg Spine. 2011;15:117–28. https://doi.org/10.3171/2011.3.SPINE10832. Cai H, Liu C, Lin H, Wu Z, Chen X, Zhang H. Full-endoscopic foraminoplasty for highly down-migrated lumbar disc herniation. BMC Musculoskelet Disord. 2022;23:303. https://doi.org/10.1186/ s12891-­022-­05254-­4. Chen C, Sun X, Liu J, Ma X, Zhao D, Yang H, et  al. Targeted fully endoscopic visualized laminar trepanning approach under local anaesthesia for resection of highly migrated lumbar disc herniation. Int Orthop. 2022;46:1627–36. https://doi.org/10.1007/s00264-­022-­ 05401-­5. Choi KC, Lee DC, Shim HK, Shin SH, Park CK.  A strategy of percutaneous endoscopic lumbar discectomy for migrated disc herniation. World Neurosurg. 2017;99:259–66. https://doi.org/10.1016/j. wneu.2016.12.052. Choi YS, Ifthekar S, Bae J, Lee SH.  Full endoscopic transpedicular technique in the treatment of high grade down migrated herniated disc: an evaluation of clinical outcomes at 12  months follow-up. World Neurosurg. 2023;173:e408–14. https://doi.org/10.1016/j. wneu.2023.02.065. Daghighi MH, Pouriesa M, Maleki M, Fouladi DF, Pezeshki MZ, Mazaheri Khameneh R, et al. Migration patterns of herniated disc fragments: a study on 1,020 patients with extruded lumbar disc herniation. Spine J. 2014;14:1970–7. https://doi.org/10.1016/j. spinee.2013.11.056. Fardon DF, Williams AL, Dohring EJ, Murtagh FR, Gabriel Rothman SL, Sze GK.  Lumbar disc nomenclature: version 2.0: recommendations of the combined task forces of the North American Spine Society, the American Society of Spine Radiology and the American Society of Neuroradiology. Spine J. 2014;14:2525–45. https:// doi.org/10.1016/j.spinee.2014.04.022.

18  Migrated Lumbar Disk Herniations Gao W, Zhang W, Pan H, Wang D. Independent reliability and availability analyses of modified classification for migrated lumbar disc herniation. J Orthop Surg Res. 2023;18:201. https://doi.org/10.1186/ s13018-­023-­03688-­7. Huang H, Hu H, Lin X, Wu C, Tan L. Percutaneous endoscopic interlaminar discectomy via inner border of inferior pedicle approach for downmigrated disc herniation: a retrospective study. J Orthop Surg Res. 2022;17:359. https://doi.org/10.1186/s13018-­022-­03245-­8. Huang K, Chen G, Lu S, Lin C, Wu S, Chen B, et  al. Early clinical outcomes of percutaneous endoscopic lumbar discectomy for L4-5 highly down-migrated disc herniation: interlaminar approach versus transforaminal approach. World Neurosurg. 2021;146:e413–8. https://doi.org/10.1016/j.wneu.2020.10.105. Hussein M. Minimal incision, multifidus-sparing microendoscopic diskectomy versus conventional microdiskectomy for highly migrated intracanal lumbar disk herniations. J Am Acad Orthop Surg. 2016;24:805–13. https://doi.org/10.5435/JAAOS-­D-­15-­00588. Jiang Y, Zuo R, Yuan S, Li J, Liu C, Zhang J, Ma M. A novel trajectory for a transpedicular approach in the treatment of a highly downward-­ migrated lumbar herniation with a full endoscopic technique. Front Surg. 2022;9:915052. https://doi.org/10.3389/fsurg.2022.915052. Kang T, Park SY, Park GW, Lee SH, Park JH, Suh SW. Biportal endoscopic discectomy for high-grade migrated lumbar disc herniation. J Neurosurg Spine. 2020:1–6. https://doi.org/10.3171/2020.2.SP INE191452. Kim HS, Ju CI, Kim SW, Kim JG. Endoscopic transforaminal suprapedicular approach in high grade inferior migrated lumbar disc herniation. J Korean Neurosurg Soc. 2009;45:67–73. https://doi. org/10.3340/jkns.2009.45.2.67. Lee S, Kim SK, Lee SH, Kim WJ, Choi WC, Choi G, et al. Percutaneous endoscopic lumbar discectomy for migrated disc herniation: classification of disc migration and surgical approaches. Eur Spine J. 2007;16:431–7. https://doi.org/10.1007/s00586-­006-­0219-­4. Lin ET, Hsiao PH, Lin CY, Chang CC, Lo YS, Lai CY, et al. Computed tomography-guided endoscopic surgery in lumbar disc herniation with high-grade migration: a retrospective, comparative study. Pain Physician. 2022;25:E777–85. Lin GX, Park CW, Suen TK, Kotheeranurak V, Jun SG, Kim JS. Full endoscopic technique for high-grade up-migrated lumbar disk herniation via a translaminar keyhole approach: preliminary series and technical note. J Neurol Surg A Cent Eur Neurosurg. 2020;81:379– 86. https://doi.org/10.1055/s-­0039-­1700574. Liu C, Chu L, Yong HC, Chen L, Deng ZL. Percutaneous endoscopic lumbar discectomy for highly migrated lumbar disc herniation. Pain Physician. 2017;20:E75–84. Mallepally AR, Gantaguru A, Marathe N, Meena SK, Tandon V. Missing disc fragment: a rare surgical experience. Asian J Neurosurg. 2020;15:674–7. https://doi.org/10.4103/ajns.AJNS_79_20. Oh J, Jo D. Epiduroscopic laser neural decompression as a treatment for migrated lumbar disc herniation: case series. Medicine (Baltimore). 2018;97:e0291. https://doi.org/10.1097/MD.0000000000010291. Oh KJ, Lee JW, Yun BL, Kwon ST, Park KW, Yeom JS, et al. Comparison of MR imaging findings between extraligamentous and subligamentous disk herniations in the lumbar spine. AJNR Am J Neuroradiol. 2013;34:683–7. https://doi.org/10.3174/ajnr.A3258. Ozturk S, Cakin H, Demir F, Albayrak S, Akgun B, Turan Y, et al. Cranially migrated lumbar intervertebral disc herniations: a m ­ ulticenter analysis with long-term outcome. J Craniovertebr Junction Spine. 2019;10:57–63. https://doi.org/10.4103/jcvjs.JCVJS_15_19. Pearson AM, Blood EA, Frymoyer JW, Herkowitz H, Abdu WA, Woodward R, et  al. SPORT lumbar intervertebral disk herniation and back pain: does treatment, location, or morphology matter? Spine (Phila Pa 1976). 2008;33:428–35. https://doi.org/10.1097/ BRS.0b013e31816469de. Qiao L, Liu JY, Tang XB, Liu HT, Wei D, Zhu ZQ, et al. The trans-­ superior articular process approach utilizing visual trephine: a more

Further Reading time-saving and effective percutaneous endoscopic Transforaminal lumbar discectomy for migrated lumbar disc herniation. Turk Neurosurg. 2022;32:612–7. https://doi.org/10.5137/1019-­5149. JTN.34049-­21.3. Schellinger D, Manz HJ, Vidic B, Patronas NJ, Deveikis JP, Muraki AS, et al. Disk fragment migration. Radiology. 1990;175:831–6. https:// doi.org/10.1148/radiology.175.3.2343133. Son ES, Kim DH, Jung JW, Lee D.  Analysis of migration patterns of disk fragments and contributing factors in extruded lumbar disk herniation. PM R. 2017;9:15–20. https://doi.org/10.1016/j. pmrj.2016.06.007. Yang F, Ren L, Ye Q, Qi J, Xu K, Chen R, et al. Endoscopic and microscopic interlaminar discectomy for the treatment of far-migrated

295 lumbar disc herniation: a retrospective study with a 24-month follow-up. J Pain Res. 2021;14:1593–600. https://doi.org/10.2147/ JPR.S302717. Yao Y, Qin R, Feng Q, Jiang X, Zhou P, Guo Z, et  al. Percutaneous endoscopic transforaminal decompression in the treatment of patients with migrated lumbar disc herniation: a retrospective study. World Neurosurg. 2019;128:e562–9. https://doi.org/10.1016/j. wneu.2019.04.195. Ying J, Huang K, Zhu M, Zhou B, Wang Y, Chen B, et al. The effect and feasibility study of transforaminal percutaneous endoscopic lumbar discectomy via superior border of inferior pedicle approach for down-migrated intracanal disc herniations. Medicine (Baltimore). 2016;95:e2899. https://doi.org/10.1097/MD.0000000000002899.

Sequestrated Lumbar Disk Herniations

19.1 Generalities and Relevance Sequestrated disk fragment, also known as free disk fragment or sequestered disk fragment, is a form of extruded disk herniation (AKA disk extrusion). An extruded disk is a type of disk herniation and is distinguished from a protruded disk (AKA disk protrusion) by at least one anatomic plane; disk extrusion has a neck that is narrower than the dome. Because the distinction between protrusion and extrusion is not always possible by advanced spinal imaging, some radiologists describe “disk extrusion” as an “uncontained disk” where ligamentous structures surrounding the disk are interrupted (broken). There are two subtypes of extruded disk: “sequestration” and “migration.” –– Sequestrated disk: The fragment is completely separated from the disk of origin. –– Migrated disk: The disk material is displaced away from the site of extrusion, but it is still in continuity with the disk of origin. Fig. 19.1  Illustration of the lumbosacral spine on coronal views showing the sequestrated lumbar disk herniations. The sequestrated free disk fragment (in red) can be migrated upwards (a) or downwards (b) from the L4–L5 disk of origin (arrows)

19

Only “sequestrated lumbar disk herniation” (SeqLDH) will be detailed in the present chapter. For “migrated lumbar disk herniations,” refer to Chap. 18. Sequestrated-type disk herniation is an unusual phenomenon that can involve all lumbar spine levels; however, the majority of cases are located in the lower lumbar segments. About 0.3–3% of all lumbar disk herniations (LDHs) are sequestrated, and the majority of patients complain of traditional low back and lumbosacral radicular pain with or without motor deficit. As seen with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as mechanical compression theory, ischemic theory, and chemical irritative theories. The free fragment sizes may vary between a few millimeters and nine centimeters in length. Often, it can be localized medially or laterally and can be migrated upwards or downwards relative to the parent disk (Fig.  19.1). There is also more or less adherence of the disk fragment to the dura matter depending on the degree of inflammatory and vascular reaction. The material can be hard, elastic, or fat-like in appearance, but adjacent vertebral bony erosions are rare.

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© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_19

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One of the first cases of sequestered LDH was reported in 1973 as a posterior epidural migration of a lumbar disk fragment into the spinal canal. As mentioned in migrated LDH, some predisposing conditions have been suggested in the occurrence of SeqLDH including unusual movements of the patient (heavy physical activities, spinal manipulation, and conditions of hypermobility), adjacent intervertebral disk instability (e.g., spondylolisthesis), or prior spinal surgery. Sometimes, this atypical form of LDH can be found in rare locations (i.e., intradural, posterior epidural, and extraforaminal) and even migrated far away from the parent disk. Therefore, the free fragment can be easily confused with many neoplastic or nonneoplastic lesions, especially when there is a large size of disk fragment, conservation of intervertebral space height and form, and central contrast enhancement on imaging. Indeed, many cases with this condition are diagnosed intraoperatively because imaging features may lack specificities. Sequestration is among the most forms of LDH that are likely to regress or resorb spontaneously.

19.2 Clinical Presentations The higher incidence of patients with SeqLDH is seen in patients in their fifth decade with a relative male predominance (55–60%). The initial evaluation should include a sufficient and detailed history and a neurological and spinal examination. Classically, there are no distinctive clinical features allowing clear differentiation between patients with SeqLDH and those with traditional protruded LDH.  Indeed, most cases (two-thirds) presented with both lower back pain and lumbosacral radicular pain. However, it seems that the incidence of neurological deficit (up to 66%) and cauda equina syndrome (CES) is much higher (up to 40%) perhaps due to the large size of the disk fragment and/or the narrowness of the spinal canal. For other authors, there is no real correlation between the size of the disk fragment on spinal imaging and the degree of clinical symptomatology. In some cases, major compression induces few neurological symptoms, whereas in other cases, mild compression may cause a complete CES. This divergence is explained by the existence of other factors besides pure mechanical compression such as inflammatory and vascular phenomena. According to several series, it appears that the sequestrated lesions produce neurological deficits within the first 3  months (relatively early) after the onset of symptoms. However, isolated back pain is unusual (5%).

19  Sequestrated Lumbar Disk Herniations

The straight leg raising test result is often positive with associated lumbosacral spinal root stretching. Any related signs of spinal stenosis or spondylolisthesis should be considered to exclude other mimicking or associated pathologies. Generally, the diagnosis of SeqLDH is not suspected preoperatively, before spinal imaging evaluation. Neurophysiological explorations can assess the relative severity of neurological damage and predict the prognosis or follow-up course of recovery.

19.3 Paraclinical Features The majority of sequestrated disk herniations are at the level of L4–L5 and L5–S1. In addition, the free fragment may migrate in different directions, intraspinal and even extraspinal. Preoperative diagnosis of SeqLDH is often challenging. In myelography (saccoradiculography), the lesion presents as an atypical subtotal or total block. However, this old technique does not deliver any information about the origin of the lesion. Traditional discography is useless. Computed tomography (CT) scan with intrathecal contrast (myelo-CT) can suspect an extradural mass, but they usually fail to indicate its precise nature. Generally, the pathological tissue has a similar density as the disk material (Figs.  19.2 and 19.3). Like in other more usual forms of LDH, if the extruded mass contains gas, this will suggest the correct diagnosis. A bony CT scan may be useful for identifying possible secondary degenerative osteoarticular changes and potential isthmic defects. Adjacent vertebral bony erosions are possible but rare. Magnetic resonance imaging (MRI) is superior to myelography, discography, and CT scan in visualizing all constituents of the LDH including local adhesion, inflammatory tissue, and associated disk herniation/protrusion. The migrated fragment is displayed on sagittal images, with obvious discontinuity in the diseased disk. The signal intensity of disk fragments is variable and unspecific, but in the majority of cases, the epidural lesions have low-to-isointense signal on T1-weighted MRI and low or sometimes high signal on T2-weighted MRI depending on the time of evolution (Figs. 19.4, 19.5, 19.6, 19.7, 19.8, 19.9, 19.10, 19.11, 19.12, 19.13, 19.14, 19.15, 19.16, and 19.17). In short-T1 inversion recovery (STIR) sequences, the fragment is often hyperintense (Figs.  19.7 and 19.13). Following gadolinium injection, peripheral ring enhancement is characteristic (known as “bull’s eye sign”) (Figs.  19.7, 19.9, and 19.12). However, solid homogeneous post-gadolinium enhancement is rare and can be confused with other diseases, especially neo-

19.3 Paraclinical Features Fig. 19.2 Large posterolateral epidural sequestrated disk fragment (arrows) on S1 vertebral level as seen on axial CT scan (a, b)

Fig. 19.3  A large anterior epidural disk fragment (star) migrated to the posterior S1–S2 sacral hole on the left side. Note the compression of both S1 and S2 nerve roots (arrows). Axial sacral CT scan (a–c)

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plasms. Regarding other rare locations of SeqLDH namely intradural, intraradicular, extraforaminal, or posterior epidural, refer to the relevant chapters of this book. MRI is still limited in assessing free disk fragments between the nerve root and dural sac and the relationship of the posterior disk fragment with the thecal sac (Figs. 19.5, 19.11, 19.15, and 19.16).

Even with the wide use of the high resolution of MRI, SeqLDHs are often still misinterpreted as intraspinal mass-­ occupying lesions, and many cases were previously only identified in surgery (Table 19.1). Occasionally, even intraoperative findings are doubtful. Therefore, the final diagnosis may depend on the results of the histopathological study.

300 Fig. 19.4  Case A. Plain film radiography of the lumbosacral spine: antero-­ posterior (a) and lateral (b) views showing a limited L4– L5 intervertebral space (arrows) (b)

19  Sequestrated Lumbar Disk Herniations

a

Sometimes, further imaging and/or biological investigations are needed to reach the correct preoperative diagnosis; however, unnecessary examinations for malignancy might

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delay final diagnosis and appropriate treatment, increase medical costs, and may result in considerable anxiety for patients “misdiagnosed” with spinal tumors.

19.3 Paraclinical Features

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Fig. 19.5  Case A. Extensive anterior epidural sequestered disk fragment (arrows) behind the posterior wall of L4 vertebral body as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted MRI (c)

Fig. 19.6  Case A. Operative view of the sequestered disk fragment removed

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19  Sequestrated Lumbar Disk Herniations

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Fig. 19.7  Extensive anterior epidural sequestered L4–L5 disk fragment (arrowheads) as seen on post-gadolinium T1-weighted MRI (a) and on STIR sequence (b), and on axial post-gadolinium T1-weighted MRI (c) and on STIR sequence (d)

19.3 Paraclinical Features

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Fig. 19.8  Case B. This 61-year-old man suffered from right-sided hyperalgesic sciatica. Sagittal T1-weighted (a) and T2-weighted MRI (b) and axial T2-weighted MRI (c) revealed a small anterolateral epidural lesion completely separated from the L5–S1 space (arrows)

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Fig. 19.9  Case B. Following gadolinium injection, there was a peripheral ring enhancement (known as “bull’s eye sign”) (arrows) as seen on sagittal (a, b) and axial (c, d) views

Fig. 19.10  Case B. Operative view of the free disk fragment involved

19.3 Paraclinical Features Fig. 19.11  Case C. Posterior epidural mass at the level of L5–S1 disk space (arrows) in a 28-year-old man as seen on sagittal T1-weighted (a) and T2-weighted MRI (b)

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306 Fig. 19.12  Case C. There is a peripheral ring enhancement around this epidural mass (arrows) as seen on sagittal (a) and axial (b) post-­ gadolinium T1-weighted MRI. The appearance of the posterior epidural mass on axial T2-weighted MRI (c)

19  Sequestrated Lumbar Disk Herniations

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Fig. 19.13  Case D. Lateral sequestrated disk fragment (arrows) behind the posterior wall of L5 vertebral body with concomitant disk herniation as seen on sagittal T1-weighted (a) and T2-weighted MRI (b, c) and on STIR sequence (d)

19.3 Paraclinical Features Fig. 19.14  Case D. Lateral sequestrated disk fragment (arrows) on the right side with concomitant central L4–L5 disk herniation as seen on axial T2-weighted MRI (a–d)

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308 Fig. 19.15 Lateral/foraminal sequestrated disk fragment (arrows) behind the posterior wall of L4 vertebral body as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted (c, d) MRI

19  Sequestrated Lumbar Disk Herniations

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19.3 Paraclinical Features

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Fig. 19.16  Sagittal T1-weighted (a) and T2-weighted MRI (b) and axial T2-weighted (c, d) MRI showing a lateral sequestrated disk fragment (arrows) behind the posterior wall of the vertebral body of L4. (Courtesy of Dr. Achraf Moussa)

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Fig. 19.17  Lateral sequestrated disk fragment (arrows) behind the posterior wall of S1 vertebral body as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted (c) MRI Table 19.1  Differential diagnosis of epidural free lumbar disk fragment reported in the literature Tumors

Infections Degenerative diseases

Trauma and hematological disorders Metabolic disorders Iatrogenic disorders Conjoined nerve roots Enlarged nerve root

Chordoma, chondrosarcoma, lipoma, lymphoma, cystic schwannoma, neurofibroma, neuroblastoma, and metastasis (mainly breast or prostate cancer) Abscess, cysticercosis, echinococcosis, and fungal Synovial cyst, Tarlov’s cyst, ligamentum cyst, osteophyte of the facet joint, hypertrophy of unilateral ligamentum flavum, and pigmented villonodular synovitis Hematoma

Gout disease Postoperative scar, fibrosis, and granuloma (e.g., textiloma)

19.4 Treatment Options and Prognosis For many clinicians, treatment of SeqLDH should be conservative for all cases as long as they have no motor deficit, CES, or uncontrollable pain because it was observed that a significant proportion of patients with free disk fragments might regress spontaneously following conservative therapy. The greater the disk fragment, the easier it is to decrease. According to some authors, up to 80% of cases with SeqLDH will have regression or complete resorption of their LDH and improvement of their clinical symptoms under conservative treatment alone. However, this complete regression may require several months and therefore does not protect the patient from potential neurological complications. Among predictive factors for spontaneous regression of SeqLDH: (a) Herniation with contrast enhancement known as “bull’s eye sign.” (b) High signal intensity of the disk fragment on T2-weighted MRI.

Further Reading

Many conservative treatment modalities are available including bed rest, pain control medications, direct epidural injection, physiotherapy, and even acupuncture. Globally, surgery is indicated in CES or in the presence of symptoms such as motor weakness or pain refractory to conservative treatment. The majority of operated patients underwent laminectomy to ensure full exposure of the disk fragment(s) and easier removal of the lesion with minimum complications such as dural weakness (CSF leak), root damage, or spinal instability. It is preferable to explore the nerve root and the dura using microsurgical techniques to avoid iatrogenic neurological injuries. Hemilaminectomy, laminotomy, and endoscopic interlaminar approach were previously used in many cases with successful outcomes. More recently, some surgeons experienced a variety of minimally invasive surgical techniques for the treatment of SeqLDH such as percutaneous endoscopic lumbar discectomy. This last method shows great promise because it is less invasive, gives better recovery, and provides good results and successful outcomes. Some authors recommend removing only the compressing-­ free fragment(s), whereas the healthy disk should be preserved. For others, this procedure would be the source of a high rate of recurrences. Several authors reported regression (size reduction) of lumbar disk sequestration in 89–100% of cases and complete resolution in 44–64% of cases after an average follow-up period between 4 and 9 months. Clinically, the majority of cases are associated with clinical improvement. There is no difference in terms of clinical recovery between partial regression and complete resolution. However, all non-operated patients should be followed up closely to avoid potentially more severe and complicated neurological outcomes. Comparing surgical and conservative treatment in SeqLDH treatment, it was shown that pain reduced faster in the short term with surgery, but in medium- and long-term follow-ups (after approximately 6 months), both treatments have similar benefits. Overall, the outcome of SeqLDH is better than other more classic forms of LDH.

Further Reading Abdelrahman H, Seyed-Emadaldin S, Krajnovic B, Ezzati A, Abdelgawaad AS. Trans-tubular translaminar microscopic-­assisted nucleotomy for lumbar disc herniations in the hidden zone. Global Spine J. 2022;12:1420–7. https://doi.org/10.1177/2192568221990421. Ahn SH, Ahn MW, Byun WM. Effect of the transligamentous extension of lumbar disc herniations on their regression and the clinical outcome of sciatica. Spine (Phila Pa 1976). 2000;25:475–80. https:// doi.org/10.1097/00007632-­200002150-­00014. Ahn Y, Kim JE, Yoo BR, Jeong YM. A new grading system for migrated lumbar disc herniation on sagittal magnetic resonance imag-

311 ing: an agreement study. J Clin Med. 2022;11:1750. https://doi. org/10.3390/jcm11071750. Akhaddar A, El-Asri A, Boucetta M.  Posterior epidural migration of a lumbar disc fragment: a series of 6 cases. J Neurosurg Spine. 2011;15:117–28. https://doi.org/10.3171/2011.3.SPINE10832. Briceno CE, Fazl M, Willinsky RA, Gertzbein S.  Sequestrated lumbar intervertebral disc associated with vertebral erosion. Spine (Phila Pa 1976). 1989;14:898–9. https://doi.org/10.1097/00007632-­ 198908000-­00026. Carvi y Nievas MN, Hoellerhage HG. Unusual sequestered disc fragments simulating spinal tumors and other space-occupying lesions. Clinical article. J Neurosurg Spine. 2009;11:42–8. https://doi.org/1 0.3171/2009.3.SPINE08161. Chen CY, Chuang YL, Yao MS, Chiu WT, Chen CL, Chan WP. Posterior epidural migration of a sequestrated lumbar disk fragment: MR imaging findings. AJNR Am J Neuroradiol. 2006;27:1592–4. Chiu CC, Chuang TY, Chang KH, Wu CH, Lin PW, Hsu WY.  The probability of spontaneous regression of lumbar herniated disc: a systematic review. Clin Rehabil. 2015;29:184–95. https://doi. org/10.1177/0269215514540919. Daghighi MH, Pouriesa M, Maleki M, Fouladi DF, Pezeshki MZ, Mazaheri Khameneh R, et al. Migration patterns of herniated disc fragments: a study on 1,020 patients with extruded lumbar disc herniation. Spine J. 2014;14:1970–7. https://doi.org/10.1016/j. spinee.2013.11.056. Deburge A, Benoist M, Boyer D.  The diagnosis of disc sequestration. Spine (Phila Pa 1976). 1984;9:496–9. https://doi. org/10.1097/00007632-­198407000-­00015. Dimogerontas G, Paidakakos NA, Konstantinidis E.  Voluminous free disk fragment mimicking an extradural tumor. Neurol Med Chir (Tokyo). 2012;52:656–8. https://doi.org/10.2176/nmc.52.656. Elsharkawy AE, Hagemann A, Klassen PD.  Posterior epidural migration of herniated lumbar disc fragment: a literature review. Neurosurg Rev. 2019;42:811–23. https://doi.org/10.1007/s10143-­ 018-­01065-­1. Fardon DF, Williams AL, Dohring EJ, Murtagh FR, Gabriel Rothman SL, Sze GK.  Lumbar disc nomenclature: version 2.0: recommendations of the combined task forces of the North American Spine Society, the American Society of Spine Radiology and the American Society of Neuroradiology. Spine J. 2014;14:2525–45. https:// doi.org/10.1016/j.spinee.2014.04.022. Frati A, Pesce A, Palmieri M, Vangelista T, Caruso R, Salvati M, et al. Anterior-to-posterior migration of a lumbar disc sequestration: surgical remarks and technical notes about a tailored microsurgical discectomy. Case Rep Surg. 2017;2017:1762047. https://doi. org/10.1155/2017/1762047. Ge CY, Hao DJ, Yan L, Shan LQ, Zhao QP, He BR, et al. Intradural lumbar disc herniation: a case report and literature review. Clin Interv Aging. 2019;14:2295–9. https://doi.org/10.2147/CIA.S228717. Ito T, Yamada M, Ikuta F, Fukuda T, Hoshi SI, Kawaji Y, et al. Histologic evidence of absorption of sequestration-type herniated disc. Spine (Phila Pa 1976). 1996;21:230–4. https://doi.org/10.1097/00007632-­ 199601150-­00014. Jia J, Wei Q, Wu T, He D, Cheng X. Two cases in which 3D MRI was used to differentiate between a disc mass that mimics a tumor and neurinoma. BMC Musculoskelet Disord. 2018;19:154. https://doi. org/10.1186/s12891-­018-­2070-­2. Kachramanoglou C, Farmer SF, Choi D.  Sequestered disc fragment mimicking a psoas abscess. Spine J. 2012;12:e1–4. https://doi. org/10.1016/j.spinee.2012.08.022. Kim HS, Eun JP, Park JS. Intradural migration of a sequestrated lumbar disc fragment masquerading as a spinal intradural tumor. J Korean Neurosurg Soc. 2012;52:156–8. https://doi.org/10.3340/ jkns.2012.52.2.156. Kim JH, Kim SW. Preliminary report of combined microscopic fragmentectomy and nucleoplasty for sequestrated lumbar disc hernia-

312 tion. Korean J Neurotrauma. 2014;10:6–9. https://doi.org/10.13004/ kjnt.2014.10.1.6. Kim YY, Lee JH, Kwon YE, Gim TJ.  Spinal nerve root swelling mimicking intervertebral disc herniation in magnetic resonance imaging—a case report. Korean J Pain. 2010;23:51–4. https://doi. org/10.3344/kjp.2010.23.1.51. Konbaz F, Aleissa SI, Al Helal F, Abaalkhail M, Alrogy W, Bin Dohaim A, et  al. Sequestrated lumbar disc herniation mimicking spinal neoplasm. Cureus. 2021;13:e18529. https://doi.org/10.7759/ cureus.18529. Li ST, Zhang T, Shi XW, Liu H, Yang CW, Zhen P, et al. Lumbar disc sequestration mimicking a tumor: report of four cases and a literature review. World J Clin Cases. 2022;10:2883–94. https://doi. org/10.12998/wjcc.v10.i9.2883. Lombardi V.  Lumbar spinal block by posterior rotation of anulus fibrosus. Case report. J Neurosurg. 1973;39:642–7. https://doi. org/10.3171/jns.1973.39.5.0642. Macki M, Hernandez-Hermann M, Bydon M, Gokaslan A, McGovern K, Bydon A.  Spontaneous regression of sequestrated lumbar disc herniations: literature review. Clin Neurol Neurosurg. 2014;120:136–41. https://doi.org/10.1016/j.clineuro.2014.02.013. Masaryk TJ, Ross JS, Modic MT, Boumphrey F, Bohlman H, Wilber G. High-resolution MR imaging of sequestered lumbar intervertebral disks. AJR Am J Roentgenol. 1988;150:1155–62. https://doi. org/10.2214/ajr.150.5.1155. Montalvo Afonso A, Mateo Sierra O, de Sagredo G, Del Corral OL, Vargas López AJ, González-Quarante LH, Sola Vendrell E, et  al. Misdiagnosis of posterior sequestered lumbar disc herniation: report of three cases and review of the literature. Spinal Cord Ser Cases. 2018;4:61. https://doi.org/10.1038/s41394-­018-­0100-­9. Nakagawa H, Saito K, Mitsugi T.  Surgical strategies in the management of sequestrated disc herniations in the lumbar and cervical spines. World Neurosurg. 2012;77:67–8. https://doi.org/10.1016/j. wneu.2011.06.021. Orief T, Orz Y, Attia W, Almusrea K.  Spontaneous resorption of sequestrated intervertebral disc herniation. World Neurosurg. 2012;77:146–52. https://doi.org/10.1016/j.wneu.2011.04.021.

19  Sequestrated Lumbar Disk Herniations Parmar G, Soin P, Sharma P, French C, Han B, Kochar PS.  Sequestered disc herniation mimicking psoas abscess: a rare case report. Radiol Case Rep. 2021;17:223–6. https://doi.org/10.1016/j. radcr.2021.10.024. Passanisi M, Scalia G, Palmisciano P, Franceschini D, Crea A, Capone C, et al. Difficulty differentiating between a posterior extradural lumbar tumor versus sequestered disc even with gadolinum-enhanced MRI.  Surg Neurol Int. 2021;12:267. https://doi.org/10.25259/ SNI_504_2021. Schellinger D, Manz HJ, Vidic B, Patronas NJ, Deveikis JP, Muraki AS, et al. Disk fragment migration. Radiology. 1990;175:831–6. https:// doi.org/10.1148/radiology.175.3.2343133. Sucuoğlu H, Barut AY.  Clinical and radiological follow-up results of patients with sequestered lumbar disc herniation: a prospective cohort study. Med Princ Pract. 2021;30:244–52. https://doi. org/10.1159/000515308. Tempel Z, Zhu X, McDowell MM, Agarwal N, Monaco EA 3rd. Severe Intradural lumbar disc herniation with cranially oriented free fragment migration. World Neurosurg. 2016;92:582.e1–4. https://doi. org/10.1016/j.wneu.2016.06.024. Ward TRW, Sahemey R, Sneath R, Solanki S.  Lumbar disc sequestration through the dura into the intrathecal space presenting as acute cauda equina. BMJ Case Rep. 2021;14:e241983. https://doi. org/10.1136/bcr-­2021-­241983. Weinstein JN, Lurie JD, Tosteson TD, Skinner JS, Hanscom B, Tosteson AN, et al. Surgical vs nonoperative treatment for lumbar disk herniation: the spine patient outcomes research trial (SPORT) observational cohort. JAMA. 2006;296:2451–9. https://doi. ­ org/10.1001/jama.296.20.2451. Witzmann A, Hammer B, Fischer J.  Free sequestered disc herniation at the S2 level misdiagnosed as neuroma. Neuroradiology. 1991;33:92–3. https://doi.org/10.1007/BF00593349. Xu BS, Xia Q, Ma XL, Yang Q, Ji N, Shah S, et al. The usefulness of magnetic resonance imaging for sequestered lumbar disc herniation treated with endoscopic surgery. J Xray Sci Technol. 2012;20:373– 81. https://doi.org/10.3233/XST-­2012-­0336.

Massive (Giant) Lumbar Disk Herniations

20

20.1 Generalities and Relevance Massive lumbar disk herniation (LDH) is an unusual condition defined as herniated disk occupying more than 50% of the antero-posterior diameter of the lumbar spinal canal (Figs. 20.1 and 20.2). Also recognized as “giant” or “large” disk herniation, they represent 8–22% of all LDHs. The majority of these lesions involve low lumbar intervertebral levels, particularly L5–S1 and L4–L5 disks. Patients with massive lumbar disk herniation (MALDH) are renowned to present severe unilateral or bilateral sciatica with or without neurological deficits. More seriously, up to 20% of cases have symptoms of cauda equina syndrome (CES). Likewise, in a series of patients with CES, 45–60% of cases are secondary to giant LDH. In the era of computed tomography (CT) scan, some voluminous LDHs were undiagnosed due to low CT scan resolution. Nowadays, magnetic resonance imaging (MRI) remains the key examination of MALDH. As seen with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as compression theory, ischemic theory, and chemical inflammatory theory. Although the etiopathogenic mechanism of MALDH is unknown, some conditions have been suspected such as unusual movements of the patient (heavy physical activities, spinal manipulation, and conditions of hypermobility) and adjacent intervertebral disk instability (e.g., spondylolysis or spondylolisthesis). Based on their exact anatomical localization, some MALDHs are central, while others are lateral into the spinal canal. The migrated herniations are often in continuity with the parent intervertebral disk anteriorly. There is usually more or less adherence of the disk fragment to the dura matter depending on the degree of inflammatory and vascular

Fig. 20.1  Illustration in an axial view of a giant lumbar disk herniation (in red color)

reaction. The material can be hard or elastic in appearance. In some rare cases, the voluminous disk fragment may skirt the thecal sac laterally presenting as a postero-epidural migration of LDH or even migrating intradurally (c.f. Chaps. 21 and 30, respectively).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_20

313

314 Fig. 20.2  Measuring disk herniation in the spinal canal (a, b). Maximum antero-­ posterior diameter of the disk herniation (α) divided by the maximum antero-posterior diameter of the spinal canal (β) = α/β. Massive LDHs have a ratio greater than 50% (1/2)

20  Massive (Giant) Lumbar Disk Herniations

a

20.2 Clinical Presentations As with other forms of spinal degenerative diseases, the initial evaluation should include a sufficient and detailed history and a neurologic, spinal, and somatic examination. The majority of the patients with MALDH are aged between 40 and 50 years (a mean of about 42 years), which is the same as the overall population with a traditional simple herniated disk in the lower spine. However, there are varying results in the literature regarding gender predominance. Signs and symptoms of MALDHs do not differ from those related to smaller LDHs. Clinical presentation can vary from acute to chronic low back pain with or without neurological deficit. However, patients with MALDH are likely to be hyperalgesic with a mean duration of symptoms shorter than the population with smaller LDHs, have bilateral sciatica, lower-extremity motor weakness, and above all a predominance of CES.  However, MALDH does not always induce CES because less than 20% of cases present partial or complete CES. Indeed, most authors reported that lumbosacral radicular pain and neurological findings are worse in patients with MALDH than in those with traditional smaller LDH. For others, the severity of neurological symptoms did not have a strong correlation with the size of the herniated disk. Let us remember that CES may associate with various degrees of severity the following symptoms and signs: –– Sphincter disturbance (urinary and/or anal). –– Saddle anesthesia. –– Motor weakness.

b

–– Sciatic pain with or without back pain. –– Absence of Achilles reflex (AKA ankle jerk reflex). –– Sexual dysfunction. Any related signs of chronic spinal stenosis or spondylolisthesis should be considered to exclude other mimicking or associated diseases. Neurophysiological explorations (e.g., can assess the relative severity of neurological damage and predict the prognosis or follow-up course of recovery.

20.3 Imaging Features As with the majority of other forms of LDH, diagnosis of MALDH should correlate with the patient’s history, clinical examination, and imaging investigations. In myelography (saccoradiculography), the lesion presents as an atypical total or subtotal block. However, this old method does not provide any information about the origin of the lesion although the diagnosis of LDH is most common. Computed tomography (CT) scan can usually demonstrate the herniated mass, which has a similar density as the disk material (Figs.  20.3, 20.4, 20.5, 20.6, and 20.7). However, the analysis of some central larger lesions may sometimes be challenging and may be confused with the normal dural sac (Figs. 20.3 and 20.6). The correct diagnosis is helped by careful examination of the surrounding epidural fat. A bony CT scan may be useful for identifying possible secondary degenerative osteoarticular changes.

20.3 Imaging Features

a

315

b

c

Fig. 20.3  Giant central L4–L5 disk herniation (arrows) as seen on axial CT scan (a–c)

a

b

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Fig. 20.4  Giant left-sided paramedian L4–L5 disk herniation (arrows) as seen on axial CT scan (a–c)

MRI is superior to a CT scan in visualizing all constituents of the LDH in different planes and sequences. Sometimes, post-gadolinium T1-weighted MRI may be needed if the lesion is confused with other anterior epidural masses (often neoplasms) (Figs.  20.8, 20.9, 20.10, 20.11, 20.12, 20.13, 20.14, 20.15, 20.16, and 20.17). The diagnosis of MALDH is even more difficult to make preoperatively, especially when the disk fragment is not in continuity with the parent intervertebral disk, when he migrated very high or very low, or when there is no disk degeneration (Figs. 20.9, 20.10, 20.14, 20.15, and 20.16).

There is no real correlation between the size of the disk herniation on spinal imaging and the degree of clinical symptomatology. In some cases, major compression induces few neurological symptoms, whereas in other cases, mild compression may cause a complete cauda equina syndrome. This divergence is explained by the existence of other factors besides pure mechanical compression such as inflammatory and vascular phenomena. More rarely, some cases may be accompanied by an intradural extension of the disk fragment (c.f. Chap. 30 about Intradural Lumbar Disk Herniations).

316 Fig. 20.5  Giant subarticular and lateral L5–S1 disk herniations (arrows) on the left (a, b) and right (c, d) sides as seen on axial CT scan (a–d)

a

20  Massive (Giant) Lumbar Disk Herniations

a

b

c

d

b

Fig. 20.6  Undiagnosed giant central L4–L5 disk herniation on axial CT scan (a, b). The herniated disk was confused with a normal dural sac. Note the asymmetry of the surrounding epidural fat (arrowheads).

c

This massive disk herniation was confirmed on sagittal T2-weighted MR imaging (c)

20.3 Imaging Features

a

317

b

c

Fig. 20.7  Case A. Lumbosacral axial (a, b) and sagittal reconstruction (c) CT scan showing a giant central L4–L5 disk herniation (arrows)

a

b

c

d

Fig. 20.8  Case A.  Giant central L4–L5 disk herniation (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted MRI (c, d)

318 Fig. 20.9  Case B. Giant lateral L5–S1 disk herniation (arrows) migrated up as seen on axial (a) and sagittal reconstruction (b) CT scan and on axial T1-weighted (c) and T2-weighted MRI (d)

a

20  Massive (Giant) Lumbar Disk Herniations

a

b

c

d

b

c

Fig. 20.10  Case B. The giant L5–S1 disk herniation (arrows) as seen on T1-weighted MRI before (a) and after (b) gadolinium injection and on T2-weighted sequence (c)

20.3 Imaging Features Fig. 20.11  Giant central L5–S1 herniated disk (arrows) as seen on sagittal T1-weighted (a), axial (b), and sagittal (c) T2-weighted MRI. Note the L4–L5 disk protrusion (arrowhead)

319

a

c

b

Fig. 20.12  Case C. Plain film radiography of the lumbosacral spine: antero-­ posterior (a) and lateral (b) views showing compensatory scoliosis (a), straightness of the lumbar lordosis, and limited L4–L5 intervertebral space (arrows) (b)

a

b

320

a

20  Massive (Giant) Lumbar Disk Herniations

b

c

d

Fig. 20.13  Case C. Giant central L4–L5 disk herniation (arrows) as seen on lumbosacral MRI. Sagittal T1-weighted (a) and T2-weighted (b) MR imaging and axial T2-weighted MRI (c, d)

20.3 Imaging Features Fig. 20.14  Large (giant) central migrated L4–L5 disk herniation with sequestrated disk fragment (arrows) as seen on sagittal (a) and axial (b) post-gadolinium T1-weighted and sagittal (c) and axial (d) T2-weighted MRI. Note the pars interarticularis defect of L4 (arrowheads) (b, d)

321

a

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c

d

322

20  Massive (Giant) Lumbar Disk Herniations

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Fig. 20.15  Case D. Massive L4–L5 disk herniation with sequestrated disk fragment migrated very high behind the posterior vertebral hall of L4 (arrows). Sagittal T1-weighted (a), T2-weighted MR imaging (b), and STIR sequence (c)

20.3 Imaging Features Fig. 20.16  Case D. This giant disk herniation was in continuity with the L4–L5 parent disk space (arrow), however, the sequestrated fragment (stars) had a different signal intensity. Note the compression of the right L5 nerve root (arrowheads). Axial T2-weighted MRI (a–d)

323

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20  Massive (Giant) Lumbar Disk Herniations

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Fig. 20.17  Giant central L4–L5 disk herniation (arrows) as seen on sagittal T1-weighted (a), T2-weighted (b), and on STIR sequence (c) and on axial T2-weighted MRI (d, e)

20.4 Treatment Options and Prognosis For many spinal surgeons, treatment of MALDH is mainly surgical due to the severity of back and radicular pain and the greater risk of CES. Such decompressive surgery also faces more risks and difficulties, such as intraoperative nerve root injury, cauda equina syndrome, CSF leakage, chronic lumbalgia, and iatrogenic postoperative spinal instability. For other clinicians, treatment should be conservative for all cases as long as they have no neurological deficit or CES because it was observed that disk fragments may regress following conservative therapy. The greater the disk herniation, the easier it is to decrease. Up to two-thirds of cases with MALDH will have resorption of their LDH and improvement of their clinical symptoms under conservative treatment alone. Many conservative treatment modalities are available including bed rest, pain control medications, direct epidural injection, physiotherapy, and even acupuncture. The surgical strategy requests neurological decompression and herniated disk removal with or without discectomy. This condition may require more extensive surgical exposure and dural sac traction without necessarily a supplementary spinal fusion (except if there is segmental instability). The surgeon can perform an interlaminar approach, a hemilaminectomy, or even a complete laminectomy depending on the

size and the location of the voluminous lumbar disk fragment. For some authors, a complete laminectomy is more advantageous for MALDH and for some migrated disk fragments to decompress. The majority of patients are operated on through a unilateral approach; however, a bilateral approach (via bilateral fenestrations or laminectomy) can be needed for cases with central LDH.  In all cases, the disk fragment should be removed carefully to avoid dural tears and/or further root injury. Although some authors had advocated the posterior trans-­ dural approach for central MALDH, this surgical method is highly invasive, requires prolonged operative time, and had the potential of postoperative CSF leakage and its subsequent infectious complications. More recently, some surgeons experienced a variety of minimally invasive surgical techniques for the treatment of MALDHs such as minimally invasive transforaminal lumbar interbody fusion and percutaneous endoscopic lumbar discectomy. These methods show great promise because they are less invasive, give better recovery, and provide good results and successful outcomes. The outcome after surgery is not so different from those with smaller LDHs. Generally, the occurrence of MALDH is not associated with poor results or a high rate of recurrence. Finally, MALDH may be more benign than previously thought.

Further Reading

About 90% of surgically treated patients had a good improvement to excellent recovery from their sciatic pain, inferior extremities weakness, and/or sphincter disorders. Another peculiarity of the voluminous LDH is that they were associated with relatively low surgical complications and a low recurrence rate (less than 15% of patients develop re-­ herniation). Patients with central MALDH tended a worst postoperative outcome than those with more lateral (namely subarticular) MALDH. Persistent neurological deficits, chronic sciatica, or prolonged neuropathic pains are mainly observed in some patients who had preoperative CES or those with a delay in their management.

Further Reading Akhaddar A, Belfquih H, Salami M, Boucetta M.  Surgical management of giant lumbar disc herniation: analysis of 154 patients over a decade. Neurochirurgie. 2014;60:244–8. https://doi.org/10.1016/j. neuchi.2014.02.012. Benson RT, Tavares SP, Robertson SC, Sharp R, Marshall RW. Conservatively treated massive prolapsed discs: a 7-year follow-­up. Ann R Coll Surg Engl. 2010;92:147–53. https://doi.org/10.1308/0035884 10X12518836438840. Choi KC, Kim JS, Park CK. Percutaneous endoscopic lumbar discectomy as an alternative to open lumbar microdiscectomy for large lumbar disc herniation. Pain Physician. 2016;19:E291–300. Cribb GL, Jaffray DC, Cassar-Pullicino VN. Observations on the natural history of massive lumbar disc herniation. J Bone Joint Surg Br. 2007;89:782–4. https://doi.org/10.1302/0301-­620X.89B6.18712. Davis A.  Massive L5/S1 disc protrusion: subtle CT signs. Australas Radiol. 2001;45:394–5. https://doi.org/10.1046/j.1440-­ 1673.2001.0945c.x. Diehn FE, Maus TP, Morris JM, Carr CM, Kotsenas AL, Luetmer PH, et al. Uncommon manifestations of intervertebral disk pathologic conditions. Radiographics. 2016;36:801–23. https://doi. org/10.1148/rg.2016150223. Epstein NE. Unnecessary multiple epidural steroid injections delay surgery for massive lumbar disc: case discussion and review. Surg Neurol Int. 2015;6:S383–7. https://doi.org/10.4103/2152-­7806.163958. Gupta A, Chhabra HS, Nagarjuna D, Arora M.  Comparison of functional outcomes between lumbar interbody fusion surgery and discectomy in massive lumbar disc herniation: a retrospective analysis. Global Spine J. 2021;11:690–6. https://doi. org/10.1177/2192568220921829. Hong SJ, Kim DY, Kim H, Kim S, Shin KM, Kang SS. Resorption of massive lumbar disc herniation on MRI treated with epidural steroid injection: a retrospective study of 28 cases. Pain Physician. 2016;19:381–8.

325 Jeon CH, Chung NS, Son KH, Lee HS. Massive lumbar disc herniation with complete dural sac stenosis. Indian J Orthop. 2013;47:244–9. https://doi.org/10.4103/0019-­5413.111505. Kondo M, Oshima Y, Inoue H, Takano Y, Inanami H, Koga H. Significance and pitfalls of percutaneous endoscopic lumbar discectomy for large central lumbar disc herniation. J Spine Surg. 2018;4:79– 85. https://doi.org/10.21037/jss.2018.03.06. Liu C, Zhou Y. Percutaneous endoscopic lumbar discectomy and minimally invasive transforaminal lumbar interbody fusion for massive lumbar disc herniation. Clin Neurol Neurosurg. 2019;176:19–24. https://doi.org/10.1016/j.clineuro.2018.10.017. Louison R, Barber JB. Massive herniation of lumbar discs with compression of the cauda equina—a surgical emergency; report of two cases. J Natl Med Assoc. 1968;60:188–90. Ma Z, Yu P, Jiang H, Li X, Qian X, Yu Z, et al. Conservative treatment for giant lumbar disc herniation: clinical study in 409 cases. Pain Physician. 2021;24:E639–48. Meng SW, Peng C, Zhou CL, Tao H, Wang C, Zhu K, et al. Massively prolapsed intervertebral disc herniation with interlaminar endoscopic spine system delta endoscope: a case series. World J Clin Cases. 2021;9:61–70. https://doi.org/10.12998/wjcc.v9.i1.61. Naidoo D. Spontaneous and rapid resolution of a massive lumbar disc herniation. Surg Neurol Int. 2021;12:352. https://doi.org/10.25259/ SNI_491_2021. Nishikawa H, Fujimoto M, Tanioka S, Ikezawa M, Nakatsuka Y, Araki T, et al. Novel transdural epiarachnoid approach for large central disk herniation in upper lumbar spine. Oper Neurosurg (Hagerstown). 2022;22:e58–61. https://doi.org/10.1227/ONS.0000000000000028. Peng B, Pang X.  Tumour-like lumbar disc herniation. BMJ Case Rep. 2013;2013:bcr2013009358. https://doi.org/10.1136/bcr-­ 2013-­009358. Sommer F, McGrath L, Kirnaz S, Goldberg J, Medary B, Schmidt FA, et al. Lumbar giant disk herniations treated with a unilateral approach for bilateral decompression. Oper Neurosurg (Hagerstown). 2022;23:60–6. https://doi.org/10.1227/ons.0000000000000198. Tascioglu T, Sahin O.  The relationship between pain and herniation radiology in giant lumbar disc herniation causing severe sciatica: 15 cases. Br J Neurosurg. 2022;36(4):483–6. https://doi.org/10.1080/0 2688697.2020.1866168. Tulloch I, Papadopoulos MC.  Giant central lumbar disc herniations: a case for the transdural approach. Ann R Coll Surg Engl. 2018;100:e53–6. https://doi.org/10.1308/rcsann.2017.0218. U ECY, Shetty A, Craig PRS, Chitgopkar SD. An observation of massive lumbar disc prolapse. J Spine Surg. 2018;4:583–7. https://doi. org/10.21037/jss.2018.07.12. Wang H, Yuan H, Yu H, Li C, Zhou Y, Xiang L.  Percutaneous endoscopic lumbar discectomy using a double-cannula guide tube for large lumbar disc herniation. Orthop Surg. 2022;14:1385. https:// doi.org/10.1111/os.13313. Zhao CQ, Ding W, Zhang K, Zhao J.  Transforaminal lumbar interbody fusion using one diagonal fusion cage with unilateral pedicle screw fixation for treatment of massive lumbar disc herniation. Indian J Orthop. 2016;50:473–8. https://doi.org/10.4103/0019­5413.189595.

Posterior Epidural Migration of Lumbar Disk Herniations

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21.1 Generalities and Relevance Epidural migration of a herniated intervertebral disk into the posterior space is a rare phenomenon with about 120 cases documented in the literature since the first description by Dandy in 1942 and Lombardi in 1973. The majority of posterior epidural migration of lumbar intervertebral disk fragments (PEMLIFs) is located in the lumbosacral spine, mainly in L3–L4 (about 40% of cases) and L4–L5 (about 30% of cases) levels. Approximately 1% of all lumbar disk herniations (LDHs) are migrated posteriorly in the epidural space (Fig.  21.1). When involving the lumbosacral area, most patients complain of traditional sciatic pain. Most cases with this condition are diagnosed intraoperatively because imaging features lack specificities. The potential of failure to distinguish this atypical variant of LDH can be high with subsequent complications and poor results. Some anatomic barriers prevent this posterior epidural migration including nerve root, sagittal midline septum (septum posticum), peridural or lateral membrane, epidural fat tissue, venous plexus, dura mater, and meningovertebral ligaments (AKA lateral Hoffman’s ligaments). As seen with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as compression theory, ischemic theory, and chemical irritative theories. Some predisposing conditions have been suspected in the development of a PEMLIF as follows:

Fig. 21.1  Illustration in an axial view of a posterior (dorsal) epidural migration of a lumbar disk herniation (in red color)

Previous surgery. Spinal trauma. Narrow spinal canal. Preexisting scoliosis in older patients. General predisposing factors as any classic LDH: heavy physical activities, elevated body mass index, previous family history of disk disease, absence of sports activities, and spinal manipulation.

Based on their exact anatomical localization, some disk fragments are completely posteromedial, while others are posterolateral. The lesion size may also vary between one to four centimeters in length. The migrated herniation may be in continuity or not with the mother’s intervertebral disk at that level anteriorly. There is usually more or less adherence of the disk fragment to the dura matter depending on the

• • • • •

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degree of inflammatory and vascular reaction. The material can be hard, elastic, or fat-like in appearance. In one previous case, the posterior epidural fragment was partially intradural (within the thecal sac itself).

21.2 Clinical Presentations The initial evaluation should include a sufficient and detailed history and a neurological and spinal examination. The majority of the patients with PEMLIF are male subjects (more than 70% of cases) aged between 50 and 60 years old (mean of about 54 years) which is somewhat older than the overall population with a classic herniated disk in the lower spine. Signs and symptoms do not differ from those related to classic lumbar diskogenic or even spinal lumbar stenosis. Clinical presentation can vary from acute low back pain (lumbago) without neurological deficit to complete cauda equina syndrome (CES). In more than 40% of cases, patients present with unilateral or bilateral sciatic pain. Indeed, most authors reported that lumbosacral radicular pain and neurological findings are worse than in patients with traditional epidural LDH. Interestingly, about one-third of patients presented with CES. Cases with cauda equina compression usually have a past history of chronic low back pain. Then, lumbago and sciatic pain occur over a period of a few days followed by progressive neurological and sphincter disturbances. The straight leg raising test result is often positive with associated lumbosacral spinal root stretching. Any related signs of spinal stenosis or spondylolisthesis should be considered in order to exclude other mimicking or associated pathologies. Generally, the diagnosis of PEMLIF is not suspected preoperatively, before spinal imaging assessment. Neurophysiological explorations can assess the relative severity of neurological damage and predict the prognosis or follow-up course of recovery.

21.3 Imaging Features Preoperative diagnosis of PEMLIF is challenging since almost 70% of cases are still confused with other posterior epidural lesions.

21  Posterior Epidural Migration of Lumbar Disk Herniations

In saccoradiculography (myelography), the lesion presents as an atypical total or subtotal block. However, this old technic does not deliver any information about the origin of the lesion. In some patients, the diagnosis was made using discography. Nevertheless, this last invasive procedure is known to be the source of some complications. Computed tomography (CT) scan with intrathecal contrast (myelo-CT) can suspect an extradural mass, but they usually fail to indicate its precise nature. Generally, the pathological tissue has a similar density as the disk material (Fig. 21.2). Like in other more usual forms of LDH, if the extruded mass contains gas, this will suggest the correct diagnosis. A bony CT scan may be useful for identifying possible secondary degenerative osteoarticular changes. Magnetic resonance imaging (MRI) is superior to myelography, discography, and CT scan in visualizing all constituents of the LDH including local adhesion, inflammatory tissue, and associated disk herniation/protrusion. The signal intensity of disk material is variable and unspecific, but in the majority of cases, the epidural lesions have high signal intensity T2-weighted and low signal intensity on T1-weighted MRI (Figs. 21.3, 21.4, 21.5, 21.6, 21.7, and 21.8). In short-­T1 inversion recovery sequences (STIR), the fragment is hyperintense. Following gadolinium injection, peripheral ring enhancement is characteristic (Fig.  21.4). Solid homogeneous post-gadolinium enhancement is rare and can be confused with other diseases, especially neoplasms. Also, unusual ring-enhancing lesion on T1-weighted post-gadolinium images, the appearance of communication with the intervertebral space, and disk degeneration are suggested for PEMLIF. In addition, adjacent involvement of the ipsilateral anterior and lateral epidural space may be indicative of the diagnosis of disk PEMLIF. As with other classic forms of LDHs, clinical symptoms did not correlate with the size of migrated disk fragment. One case with posterolateral intradural sequestered disk herniation has been previously reported. Imaging features are unspecific and can mimic other pathological conditions in the posterior epidural space in the lumbosacral area mainly neoplasms, abscesses, hematomas, synovial cysts, and other degenerative diseases (Table 21.1). Sometimes, intraoperative findings may be doubtful. Subsequently, the final diagnosis depends only on the results of the histopathological study (Fig. 21.6).

21.3 Imaging Features

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Fig. 21.2  Case 1. Posterior epidural migration of an L5–S1 lumbar lateral epidural space with thecal sac (in blue color) (d). The structure disk fragment (arrows) as seen on axial CT scan (a–d). Note the epi- in green color corresponds to the contralateral S1 nerve root (d) dural herniated intervertebral disk (in yellow color) into the postero-­

330 Fig. 21.3  Case 2. Posterior epidural mass at the level of L5–S1 disk space (arrows) in a 28-year-old man as seen on sagittal T1-weighted (a) and T2-weighted MRI (b)

21  Posterior Epidural Migration of Lumbar Disk Herniations

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21.3 Imaging Features Fig. 21.4  Case 2. There is a peripheral ring enhancement around this epidural mass (arrows) as seen on sagittal (a) and axial (b) post-­ gadolinium T1-weighted MRI. The appearance of the posterior epidural mass on axial T2-weighted MRI (c)

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Fig. 21.5  Case 2. Intraoperative view of the posterior epidural mass (dotted circle) following bilateral L5 laminectomy

Fig. 21.6  Case 2. Microscopic image of the posterior epidural mass showing liquefaction, degeneration, and granulation tissue corresponding to a disk material (hematoxylin–eosin stain, original magnification ×40). (Courtesy of Pr. Mohamed Amine Azami)

332 Fig. 21.7  Case 3. Posterior epidural disk fragment at the level of L4–L5 disk space (arrows) in a 44-year-old woman as seen on sagittal T1-weighted (a) and T2-weighted MRI (b)

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21.4 Treatment Options and Prognosis

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Fig. 21.8  Case 3. Intraoperative view of the posterior epidural disk fragment (dotted line) following bilateral L4 laminectomy (a). Operative view of the thecal sac after disk fragment removal (b). Disk fragment appearance (c)

Table 21.1  Differential diagnoses of posterior epidural migration of lumbar disk herniation reported in the literature Tumors Infections Degenerative diseases Trauma and Hematological disorders Metabolic disorders Iatrogenic disorders

Chordoma, chondrosarcoma, lipoma, lymphoma, cystic schwannoma, elastofibroma, metastasis Abscess, cysticercosis, echinococcosis Synovial cyst, Tarlov cyst, ligamentum cyst, hypertrophied facet joint osteophyte, hypertrophy of unilateral ligamentum flavum, pigmented villonodular synovitis Hematoma

Gout disease Postoperative scar and fibrosis

21.4 Treatment Options and Prognosis The treatment of PEMLIF is mainly surgical via posterior approaches. The surgical strategy requests disk fragment removal and neurological decompression without further complications such as dural weakness (CSF leak), root damage, or spinal instability. However, for some authors, treatment should be conservative for all cases as long as they have no neurological deficit or CES. Conservative treatment modalities include bed rest, pain control medications, and physiotherapy. About 4% of patients were managed conservatively with good clinical and imaging results (spontaneous regression of disk material). Surgically, the majority of patients underwent laminectomy to ensure full exposure of the disk fragment and easier

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removal of the lesion with minimum complications (see Figs. 21.5 and 21.8). It is preferable to explore the nerve root and the dura using microsurgical technics to avoid iatrogenic neurological injuries. Hemilaminectomy, laminotomy, and endoscopic interlaminar approach were previously used in a few cases with successful outcomes. Previous surgery at the same disk level is associated with the difficulty of anatomic dissection of the involved structures and subsequent complications due to fibrosis and scarring adhesions. All surgical patients had well to excellent results in 96% of reported cases without documented complications or postoperative recurrence. Persistent neurological deficits were mostly observed in some patients who had preoperative CES. Overall, postoperative outcomes are better than those encountered in cases with traditional anterior epidural LDHs.

Further Reading Akhaddar A, El-Asri A, Boucetta M.  Posterior epidural migration of a lumbar disc fragment: a series of 6 cases. J Neurosurg Spine. 2011;15:117–28. https://doi.org/10.3171/2011.3.SPINE10832. Akhaddar A, Boucetta M. Posterior epidural migration of lumbar intervertebral disc fragment. J Neurosurg Spine. 2015;23:135–6. https:// doi.org/10.3171/2011.2.SPINE1190. Ayyappan Unnithan AK. A review of the diagnostic features of posteriorly migrated lumbar discs with reports of two cases. Neurol India. 2022;70:1213–6. https://doi.org/10.4103/0028-­3886.349665. Bonaroti EA, Welch WC. Posterior epidural migration of an extruded lumbar disc fragment causing Cauda equina syndrome. Clinical and magnetic resonance imaging evaluation. Spine (Phila Pa 1976). 1998;23:378–81. https://doi.org/10.1097/00007632-­ 199802010-­00018. Chiapparini L, Opancina V, Erbetta A, Pollo B, Broggi M, Ciceri E.  Case 310: posterior epidural migration of a lumbar disk herniation. Radiology. 2023;306:e212607. https://doi.org/10.1148/ radiol.212607. Dandy WE.  Serious complications of ruptured intervertebral disks. J Am Med Assoc. 1942;119:474–7. Derincek A, Ozalay M, Sen O, Pourbagher A. Posterior epidural mass: can a posteriorly migrated lumbar disc fragment mimic tumour, haematoma or abscess? Acta Orthop Belg. 2009;75:423–7. Diehn FE, Maus TP, Morris JM, Carr CM, Kotsenas AL, Luetmer PH, et al. Uncommon manifestations of intervertebral disk pathologic conditions. Radiographics. 2016;36:801–23. https://doi. org/10.1148/rg.2016150223. Dösoğlu M, Is M, Gezen F, Ziyal MI. Posterior epidural migration of a lumbar disc fragment causing cauda equina syndrome: case report and review of the relevant literature. Eur Spine J. 2001;10:348–51. https://doi.org/10.1007/s005860100300. Elsharkawy AE, Hagemann A, Klassen PD.  Posterior epidural migration of herniated lumbar disc fragment: a literature review. Neurosurg Rev. 2019;42:811–23. https://doi.org/10.1007/s10143-­ 018-­01065-­1. Frati A, Pesce A, Palmieri M, Vangelista T, Caruso R, Salvati M, et al. Anterior-to-posterior migration of a lumbar disc sequestration: surgical remarks and technical notes about a tailored microsurgi-

21  Posterior Epidural Migration of Lumbar Disk Herniations cal discectomy. Case Rep Surg. 2017;2017:1762047. https://doi. org/10.1155/2017/1762047. Huang TY, Lee KS, Tsai TH, Su YF, Hwang SL.  Posterior epidural migration of sequestrated lumbar disc fragments into the bilateral facet joints: case report. Neurosurgery. 2011;69:E1148–51. https:// doi.org/10.1227/NEU.0b013e3182245b21. Kil JS, Park JT.  Posterior epidural herniation of a lumbar disk fragment at L2-3 that mimicked an epidural hematoma. Korean J Spine. 2017;14:115–7. https://doi.org/10.14245/kjs.2017.14.3.115. Konbaz F, Aleissa SI, Al Helal F, Abaalkhail M, Alrogy W, Bin Dohaim A, et  al. Sequestrated lumbar disc herniation mimicking spinal neoplasm. Cureus. 2021;13:e18529. https://doi.org/10.7759/ cureus.18529. Lombardi V.  Lumbar spinal block by posterior rotation of annulus fibrosus. Case report. J Neurosurg. 1973;39:642–7. https://doi. org/10.3171/jns.1973.39.5.0642. Montalvo Afonso A, Mateo Sierra O, de Sagredo G, Del Corral OL, Vargas López AJ, González-Quarante LH, Sola Vendrell E, et  al. Misdiagnosis of posterior sequestered lumbar disc herniation: report of three cases and review of the literature. Spinal Cord Ser Cases. 2018;4:61. https://doi.org/10.1038/s41394-­018-­0100-­9. Mugge L, Caras A, Miller W, Buehler M, Medhkour A. A successful outcome despite delayed intervention for Cauda equina syndrome in a young patient with a posterior epidural disc extrusion. Cureus. 2019;11:e4645. https://doi.org/10.7759/cureus.4645. Oh Y, Eun J.  Posterior epidural migration of lumbar disc fragment: case reports and literature review. Medicine (Baltimore). 2021;100:e28146. https://doi.org/10.1097/MD.0000000000028146. Park T, Lee HJ, Kim JS, Nam K.  Posterior epidural disc fragment masquerading as spinal tumor: review of the literature. J Back Musculoskelet Rehabil. 2018;31:685–91. https://doi.org/10.3233/ BMR-­170866. Palmisciano P, Balasubramanian K, Scalia G, Sagoo NS, Haider AS, Bin Alamer O, et  al. Posterior epidural intervertebral disc migration and sequestration: a systematic review. J Clin Neurosci. 2022;98:115–26. https://doi.org/10.1016/j.jocn.2022.01.039. Rai SS, Goulart CR, Lalezari S, Galgano MA, Krishnamurthy S. Dorsal migration of lumbar disc fragments causing cauda equina syndromes: a three case series and literature review. Surg Neurol Int. 2020;11:175. https://doi.org/10.25259/SNI_197_2020. Seok H, Lee SY, Shin DS, Kang JH, Im SB, Jeong JH. Sudden bilateral foot drop due to dorsally unilateral migration of the herniated lumbar disc: a case report. J Back Musculoskelet Rehabil. 2022;35:749–53. https://doi.org/10.3233/BMR-­210067. Takano M, Hikata T, Nishimura S, Kamata M.  Discography aids definitive diagnosis of posterior epidural migration of lumbar disc fragments: case report and literature review. BMC Musculoskelet Disord. 2017;18:151. https://doi.org/10.1186/s12891-­017-­1516-­2. Tarukado K, Ikuta K, Fukutoku Y, Tono O, Doi T.  Spontaneous regression of posterior epidural migrated lumbar disc fragments: case series. Spine J. 2015;15:e57–62. https://doi.org/10.1016/j. spinee.2013.07.430. Tatli M, Güzel A, Ceviz A, Karadağ O.  Posterior epidural migration of sequestered lumbar disc fragment causing cauda equina syndrome. Br J Neurosurg. 2005;19:257–9. https://doi. org/10.1080/02688690500208593. Teufack SG, Singh H, Harrop J, Ratliff J. Dorsal epidural intervertebral disk herniation with atypical radiographic findings: case report and literature review. J Spinal Cord Med. 2010;33:268–71. https://doi. org/10.1080/10790268.2010.11689706. Zarrabian MM, Diehn FE, Kotsenas AL, Wald JT, Yu E, Nassr A. Dorsal lumbar disc migrations with lateral and ventral epidural extension on axial MRI: a case series and review of the literature. AJNR Am J Neuroradiol. 2016;37:2171–7. https://doi.org/10.3174/ajnr.A4875.

Sciatica Due to High Lumbar Disk Herniations and Spinal Stenosis

22.1 Generalities and Relevance Classically, the term “sciatica” is known to be specific to the pain, and/or paresthesia, which is a direct consequence of sciatic nerve root (L4–S3) or sciatic nerve compression/irritation. Most cases of sciatica result from an inflammatory or a mechanical disorder. Spinal sciatica may result from a variety of degenerative problems dominated by low lumbar disk herniation (LDH) and lower lumbar spinal stenosis. Regarding intervertebral LDH, the hernia affects the nerve root exiting under the pedicle of the vertebral body, one level caudal. Nevertheless, in rare cases, clinical findings do not match radiological results. Sometimes, a disk herniation or spinal stenosis can cause isolated, remote, lumbosacral radicular symptoms or sciatic pain not related to the direct level of nerve root compression. This false localizing presentation may lead to missed or delayed diagnosis and a possible risk of unnecessary lumbosacral spinal surgery. According to the British neurologist Andrew Larner, a “false localizing sign” can be defined as a confusing clinical condition in which the anatomical situation of the lesion causing neurological symptoms is distant or remote from the anatomical site predicted by neurological examination. However, sciatica related to high spinal lesion should be distinguished from “funicular sciatica,” which is a tract pain mainly due to irritation of the ascending spinothalamic tract (c.f. Chap. 44 about Intraspinal Funicular Sciatica). The first report of such an instance was described by Osamu Shirado in 1996, involving L5 radiculopathy second-

22

ary to L1–L2 disk herniation. Since then, less than 20 cases have been published in the literature mainly in patients with high lumbar disk herniation and upper lumbar spinal stenosis (with or without spondylolisthesis). This rare phenomenon most often develops among mature adult men between their fourth and sixth decades without specific risk factors. The exact pathophysiology of sciatica due to high lumbar spinal lesions is poorly understood. Classically, the pain is attributed to three main mechanisms: (a) Compression of the low radicular nerves (mainly L5 and S1 roots) at a high spinal lumbar vertebral level below the conus medullaris and the epiconus, between L1 and L4 vertebral levels as part of the cauda equina. Inside the dural sac, the more distal sacral nerve roots are positioned dorsally, whereas the lumbar nerve roots are sited ventrally within the dural sac before leaving the spinal canal via the corresponding intervertebral foramina (Fig. 22.1). (b) Venous congestion of the cauda equina. Engorgement of the blood vessels with blood by upper-level compression may damage the lower nerve roots including the dorsal root ganglia and cause radiculopathy at a lower level. (c) Nerve root anomalies such as the “furcal nerve” give branches to L4 and L5 roots and may cause atypical neurological findings. The furcal nerve is an independent nerve found in the lumbosacral trunk, most commonly at the level of L4, and links the lumbar plexus to the sacral plexus. (c.f. Chap. 59 about Lumbosacral Conjoined Nerve Roots).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_22

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Fig. 22.1  Normal anatomical distribution of the cauda equina nerve roots within the thecal sac at the L1–L2 disk level (a). Postero-medial compression (arrows) of the thecal sac at a high spinal lumbar level may damage low radicular nerve roots such as L4–L5–S1 nerve roots (b)

22.2 Clinical Presentations

22.3 Paraclinical Features

Signs and symptoms do not differ from those related to traditional lumbar discogenic or spinal lumbar stenosis. However, most patients with LDH have unilateral sciatic pain, while those with spinal lumbar stenosis often present with bilateral sciatica. The straight leg raising test result is often positive with associated lumbosacral spinal root stretching. Any related signs of a tumoral, vascular, infectious, or systemic condition should be considered in order to exclude other mimicking or associated pathologies. Classic electrodiagnostic studies confirm the involvement of L5, S1, or both lumbosacral roots. These techniques should be indicated above all, when the patient’s clinical presentation and imaging did not correlate, particularly in the absence of any pathology at the lower lumbar level (i.e., at L4/L5 and L5/S1). To prevent wrong or delayed diagnosis, in addition, to correctly identifying the cause of the symptoms, some procedures will be helpful such as lumbar epidural blocks.

For a long time, patients were diagnosed using myelo-­ radiculography or myelo-computed tomography (CT). Nowadays, magnetic resonance imaging (MRI) is the primary imaging modality that may indicate the exact topography of the lesion, its nature, exact margins, and inner structures, as well as its relationships with adjacent structures (Figs. 22.2, 22.3, 22.4, 22.5, 22.6, and 22.7). The most common cause of sciatic pain related to high spinal lumbar lesions is L1–L2 and L2–L3 lumbar disk herniations, followed by L1–L2 and L2–L3 spinal stenosis. Interestingly, six patients reported in the literature had L3– L4 stenosis with associated spondylolisthesis. Furthermore, patients should be assessed by appropriate imaging tools and biological explorations to exclude potential hip, sacroiliac joint, and knee disorders, as well as potential underlying systemic diseases. Consultations with experts such as neurologists, orthopedists, physical therapists, and rheumatologists can aid in differential diagnoses. However, various etiologies may be associated with peripheral neuropathy but they rarely present as an isolated sciatic pain (c.f. Chap. 94 about Sciatic Peripheral Neuropathies).

22.3 Paraclinical Features

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Fig. 22.2  Case 1. Paracentral L2–L3 disk herniation (arrows) in a 54-year-old patient suffering only from right-sided sciatic pain with mild low back pain. Lumbosacral spinal sagittal (a) and axial (b) T2-weighted MR imaging

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Fig. 22.3  Case 2. This 23-year-old man came to our medical clinic for bilateral sciatica without a neurological deficit. Lumbar spinal MRI showed a T12–L1 posterior ring apophysis separation, a concomitant

adjacent disk herniation, and a monosegmental central spinal stenosis (arrows). Sagittal T1-weighted (a) and T2-weighted MRI (b) and axial T2-weighted MRI (c, d)

22.3 Paraclinical Features

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Fig. 22.4  Case 3. An L2–L3 central disk herniation (arrows) resulting in bilateral sciatic pain. Lumbar sagittal T1-weighted (a) and T2-weighted MRI (b) and axial T2-weighted MRI (c, d)

340 Fig. 22.5  Case 3. CT scan appearance of the L2–L3 herniated disk with concomitant degenerative lesions (arrows) as seen on sagittal reconstruction (a) and axial (b, c) views

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22.3 Paraclinical Features

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Fig. 22.6  Case 4. Extensive degenerative spinal canal narrowing from T11 to L5 manifesting as bilateral sciatica with neurogenic claudication. Note the T11–L1 vertebral osteophytosis with partial ossification

c

of the posterior longitudinal ligament (arrowheads), the L2–L3 and L4– L5 disk herniations (arrows) as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and reconstruction CT scan (c)

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22  Sciatica Due to High Lumbar Disk Herniations and Spinal Stenosis

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Fig. 22.7  Case 5. Recurrence of lumbar degenerative spinal stenosis at L2–L3 with a concomitant herniated disk (arrows) in a 75-year-old man operated on in another institution 4 years before. His main complaints

were left cruralgia with bilateral sciatica. Lumbosacral sagittal T1-weighted (a) and T2-weighted MRI (b), and STIR sequence (c) and axial T2-weighted MR imaging (d, e)

22.4 Treatment Options and Prognosis

All reported cases were operated on depending on their etiologies:

Conservative management is typically the primary therapeutic intervention in patients with intraspinal LDH as long as they have no red flag symptoms including neurological weakness, sphincter disturbances, or uncontrolled pain. Conservative measures consist of bed rest, pharmacological therapy, physical therapy interventions, lumbar bracing (infrequently), and limitation of physical activities. Posture-­ modifying exercises can improve symptoms by improving muscle strength, coordination, and flexibility. When symptoms persist beyond 4–6 weeks, transforaminal or interlaminar epidural steroid injections may be considered for a short term. Surgical management may be appropriate for such patients in a method equivalent to the presentations of clinical syndromes with imaging concordant traditional spinal lumbar degenerative disorders. In some cases with high lumbar disk lesions, motor-­ evoked potential monitoring was previously used during surgery and has been considered useful for the ultimate confirmation of the responsible spinal lesion and for predicting the outcome.

• Herniectomy/discectomy via interlaminar approach for lumbar disk herniation. • Laminectomy/laminotomy and arthrectomy, with or without fusion for patients with spinal stenosis (some of them have an associated spondylolisthesis). It is important to have a preoperative discussion with the patient and family about the possibility of needing a potential second surgery. To the best of our knowledge, no additional surgery has been needed in any of the reported patients. Surgical decompression results in the resolution of radicular symptoms in patients with this unusual condition. No case of recurrence has been described.

Further Reading Chen Y, Wei G, Li Z, Yu N, Gong F, Ji G.  Schmorl node induced multiple radiculopathy: a rare case report. Medicine (Baltimore). 2020;99:e22792. https://doi.org/10.1097/MD.0000000000022792. Eguchi Y, Ohtori S, Toyone T, Ozawa T, Yamauchi K, Yamashita M, et al. Surgical experience in cases of L5 and S1 symptoms caused

Further Reading by upper lumbar spinal stenosis of L2–L3 and L3–L4. J Spine. 2012;1:105. https://doi.org/10.4172/2165-­7939.1000105. Epstein BS, Epstein JA, Lavine L.  The effect of anatomic variations in the lumbar vertebrae and spinal canal on cauda equina and nerve root syndromes. Am J Roentgenol Radium Ther Nucl Med. 1964;91:1055–63. Hidalgo-Ovejero AM, García-Mata S, Martínez-Grande M, MaraviPetri E, Izco-Cabezón T.  L5 root compression caused by degenerative spinal stenosis of the L1-L2 and L2-L3 spaces. Spine (Phila Pa 1976). 1998;23:1891–4. https://doi.org/10.1097/00007632-­ 199809010-­00019. Hidalgo-Ovejero AM, García-Mata S, Sánchez-Villares JJ, Lasanta P, Izco-Cabezón T, Martínez-Grande M. L5 root compression resulting from an L2-L3 disc herniation. Am J Orthop (Belle Mead NJ). 2003;32:392–4. Kikuchi S, Hasue M, Nishiyama K, Ito T.  Anatomic features of the furcal nerve and its clinical significance. Spine (Phila Pa 1976). 1986;11:1002–7. https://doi.org/10.1097/00007632-­ 198612000-­00006. Korovessis P, Baikousis A, Stamatakis M, Katonis P. Monoradiculopathy of the fifth lumbar nerve root due to lumbar disc herniation

343 between lumbar one and lumbar two vertebrae. J Spinal Disord. 1998;11:350–3. Larner AJ.  False localising signs. J Neurol Neurosurg Psychiatry. 2003;74:415–8. https://doi.org/10.1136/jnnp.74.4.415. McClelland S 3rd, Kim SS.  Successful operative management of an upper lumbar spinal canal stenosis resulting in multilevel lower nerve root radiculopathy. J Neurosci Rural Pract. 2015;6:108–11. https://doi.org/10.4103/0976-­3147.143216. Shirado O, Matsukawa S, Kaneda K.  Herniation of the disc between the first and second lumbar vertebrae with a monoradiculopathy of the fifth lumbar nerve root. J Bone Joint Surg Am. 1996;78:1422–6. https://doi.org/10.2106/00004623-­199609000-­00022. Stein AA, Vrionis F, Espinosa PS, Moskowitz S. Report of an isolated L5 radiculopathy caused by an L2-3 disc herniation and review of the literature. Cureus. 2018;10:e2552. https://doi.org/10.7759/ cureus.2552. Yasuda M, Nakura T, Kamiya T, Takayasu M. Motor evoked potential study suggesting L5 radiculopathy caused by l1-2 disc herniation: case report. Neurol Med Chir (Tokyo). 2011;51:253–5. https://doi. org/10.2176/nmc.51.253.

Anterior Retroperitoneal Lumbar Disk Herniations

23.1 Generalities and Relevance Unlike extraforaminal lumbar disk herniation (LDH) (c.f. Chap. 17), anterior retroperitoneal LDH (ARLDH) represents a disk fragment migrating too anteriorly in the retroperitoneal space, sometimes far away from the original intervertebral disk space (Figs. 23.1 and 23.2). Accordingly, some authors improperly use the term “extreme lateral” or “far lateral” disk herniation for designating ARLDH.  First described in the 1980s with the introduction of computed tomography (CT) scan, most cases with ARLDH are asymptomatic. The anterior disk fragment may reach the retroperitoneum in two ways as follows:

23

Symptomatic ARLDHs are rare since only about 20 cases have been documented in the literature, mainly in the lower lumbar vertebral column. The majority of patients with ARLDH present various and unspecific clinical signs and symptoms that are suggestive of visceral pain. Neurological presentations are extremely rare since less than a dozen cases have been reported in the literature to date mainly as lumbosacral radicular pain with or without deficits, whereas low back pain is often moderate or absent. Although asymptomatic, the association of ARLDH with other lumbosacral degenerative diseases is not rare (e.g.,

• Laterally from the foraminal or extraforaminal part of the disk. • Directly from the anterior or anterolateral portion of the affected disk.

Fig. 23.1  Axial views of lumbar disk space showing an anterior lumbar disk herniation (red color)

Fig. 23.2  Axial T2-weighted MRI lumbar disk space showing different topographic zones of lumbar disk herniation: central zone (in blue), subarticular zone (in red), foraminal zone (in yellow), extraforaminal zone (in orange), and anterior zone (in green). The anterior zone is too anterior to the extraforaminal zone in the retroperitoneal space

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_23

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foraminal/extraforaminal LDH, ligamentous calcification/ ossification, spondylolisthesis, spinal stenosis, or degenerative scoliosis). As with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as compression theory, ischemic theory, and chemical irritative theories. However, compressive neurological structures do not concern only lumbar or sacral radicular nerves but also their corresponding nerve ganglions, part of the proximal lumbosacral plexus, and even lumbar sympathetic structure. Because of the rarity of ARLDHs, most neurosurgeons and spinal surgeons do not have enough experience with this condition. Many documented cases were diagnosed only during surgery. Consequently, management of most patients with anterior extension of disk fragment, with or without foraminal herniation, may result in poor outcomes and persistent sciatic pain, despite proper decompressive surgical procedures.

23.2 Clinical Presentations For some authors, many cases with an isolated anterior extension of disk herniation will remain asymptomatic for a long time until further degenerative changes occur. Therefore, ARLDH will be found only incidentally on spinal imaging, particularly in the elderly. Age and sex distribution of patients with symptomatic ARLDH are the same as those found with typical lumbar intraspinal counterparts except that the age is somewhat older. Most patients are male subjects aged between 50 and 70 years old. Clinical presentation of ARLDH varies from traditional intraspinal forms (namely central and subarticular LDH). Most patients present various and unspecific clinical signs and symptoms that are unrelated to lumbosacral root compression or irritation. In 2013, Tang et al. reported a remarkable Chinese series of 12 patients who suffered from long-term abdominal pain due to anterior herniation of the lumbar disk. This epigastric or hypogastric pain was unrelated to diet, position, or weather. Interestingly, three cases among them have also concomitant lower limb cold pain without typical radiculopathy. In one case report, the disk fragment was responsible for an extrinsic unilateral ureteral obstruction with progressive hydronephrosis. Neurological presentations are extremely rare since only a dozen documented cases have been reported in the literature before. Most patients complain of lumbosacral radicular pain which tends to be chronic for several months or years history, whereas low back pain is often minor or absent. Neurological deficits are not rare and include sensory and/or

23  Anterior Retroperitoneal Lumbar Disk Herniations

motor deficits with or without reflex abnormalities. One patient developed a completely painless foot drop. Remarkably, the straight leg raising test (AKA Lasègue sign) was negative due to the absence of classic intraspinal root conflict. Electrophysiological studies including conduction explorations and electromyography will be useful in the assessment of a possible sciatic neuropathy or even lumbosacral plexopathy. Overall, the diagnosis of ARLDH is often not made preoperatively according to clinical signs and symptoms and even with imaging features.

23.3 Imaging Features Preoperative diagnosis of a symptomatic ventral fragment of LDH is very difficult on spinal imaging. Myelography (saccoradiculography) results have been negative in similar cases because the nerve sheath ends proximal to the outer zone of the foramen. Perhaps discography could have been helpful in diagnosing anterior and extraforaminal disk herniation. The diagnosis becomes more complicated, especially when sequestered herniation occurs at some distance from the foramen or when the disk fragment does have no continuity with the intervertebral space. In some cases, the lesion was overlooked at first spinal imaging because most radiologists focus mainly on the intraspinal region (inside the confines of the spinal canal) and unless there are coexisting posterior or foraminal components, there is no evidence of nerve root compression. CT scan can suspect a presacral, paravertebral, or retroperitoneal soft-tissue lesion, but they usually fail to indicate its precise nature. Generally, the pathological tissue has a similar density as the disk material. The disk fragment is rarely calcified but can be associated with possible secondary degenerative osteoarticular changes such as concomitant osteophytosis, calcified/ossified posterior longitudinal ligament, facet joint arthrosis, and disk narrowing. Despite the introduction of CT scan and high-resolution magnetic resonance imaging (MRI), some anterior disk fragments can be firstly missed, unrecognized, or confused for retroperitoneal tumors or nerve sheath tumors. MRI is superior to a CT scan in visualizing all constituents of the LDH.  MRI revealed a retroperitoneal mass, medial to the psoas muscle and anterior to the spinal column, far lateral from the adjacent foramen (Figs. 23.3, 23.4, 23.5, 23.6, and 23.7). Paraspinal fat displacement or obliteration may be present. In addition, variable degrees of inflammatory changes in the adjacent fat and muscle can be associated. The disk fragment can be found cranially or caudally from the corresponding lumbosacral nerve. The sagittal pro-

23.3  Imaging Features

347

a

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Fig. 23.3  Anterior retroperitoneal right-sided L5–S1 disk herniation (arrows) as seen on axial T2-weighted MRI (a, b)

a

b

c

d

Fig. 23.4  Massive L5–S1 anterior disk herniation (arrows) as seen on sagittal T1-weighted (a, b) and T2-weighted (c, d) MRI in a patient with concomitant spinal stenosis

jection is especially useful in identifying ventral LDH. Some authors added 5–30° angled frontal view oblique caudally and anteriorly, following the course of the nerve roots. The radiologist should consider looking beyond the foramen and even anteriorly in the retroperitoneal zone. MR neurography is a useful technic in helping to clearly determine lesions responsible for possible retroperitoneal plexopathy. Ventral sequestered disk herniations usually appear heterogeneous, with a hypo-isointense signal on T1-weighted

MRI and a hypo-hyperintense signal on T2-weighted MRI, depending on the time of existence. Usually, gadolinium-­ enhanced MRI does not show central enhancement of the herniated disk fragment, but a slight diffuse or peripheral enhancing complex can be observed. In accordance with previously documented cases, the diagnosis of ARLDH is very difficult to make preoperatively, especially when the disk fragment is not in continuity with its original intervertebral disk or when he migrated too far from the intervertebral foramen.

348

23  Anterior Retroperitoneal Lumbar Disk Herniations

a

b

Fig. 23.5  Anterior retroperitoneal left-sided L5–S1 disk herniation (dotted frame) combined with foraminal/extraforaminal herniated disk (arrows) and marginal ridge. Note that the anterior mass is far lateral from the adjacent foramen. Axial T2-weighted MRI (a, b)

a

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Fig. 23.6  Central lumbar spinal degenerative stenosis with anterior retroperitoneal L4–L5 disk herniation (arrows). Sagittal T1-weighted (a) and T2-weighted MRI (b), and axial T2-weighted MRI (c)

23.4  Treatment Options and Prognosis

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b

Fig. 23.7  Anterior retroperitoneal left-sided L5–S1 disk herniation (dotted oval form) combined with foraminal/extraforaminal stenosis (arrows) and marginal ridge. Axial T2-weighted MRI (a, b)

The association of ARLDH with other lumbosacral degenerative diseases should be considered (Figs. 23.4, 23.5, 23.6, and 23.7). Imaging features are unspecific and can mimic other lesions in the retroperitoneal lumbosacral area as follows:

cal approach. An inaccurate preoperative diagnosis could result in incomplete surgical exploration of the involved nervous structure and, consequently, could result in surgical failure. A further revised surgical approach is not rare. The appropriate surgical accesses are lateral (e.g., via a trans-psoas approach) or anterior (trans-abdominal). It is –– Schwannoma and neurofibroma. preferable to explore the nervous structure using microsurgi–– Metastasis or primary retroperitoneal tumors. cal technics and intraoperative neuromonitoring to avoid fur–– Retroperitoneal adenopathy. ther neurological damage. The surgeon should be aware of –– Large vertebral osteophytes. retroperitoneal vascular structures. Disk material can be –– Prominent paraspinal venous plexus. identified caudally or cranially to the corresponding nerve. –– Psoas abscess. Furthermore, this likely preserved the patient’s spine stabil–– Discitis. ity and, as a result, avoided the need for an additional spinal fusion. However, most surgeons are unfamiliar with these Sometimes, further variable imaging techniques and pro- approaches and the nerve cannot be tracked from medial to cedures (CT and MRI of pelvis, myelogram, positron-­ lateral. emission tomography (PET) scan, bone survey, gastroscopy, A traditional midline approach is not indicated with this vascular ultrasound, lumbar sympathetic nerve block or type of LDH. However, some authors have successfully used abdominal CT scan) are employed to reach a diagnosis and a microsurgical lateral extraforaminal transmuscular exclude other possible etiologies. approach. Consequently, cases with concomitant intraspinal or foraminal counterparts (having a double crush syndrome) 23.4 Treatment Options and Prognosis should be managed consequently. All operated cases with ARLDH had satisfactory to good Treatment of symptomatic ARLDH is often surgical through postoperative clinical results except those presenting preopanterior or posterolateral decompression and removal of the erative severe neurological deficit. No case of postoperative migrated and compressive disk material. Patients who pres- recurrence has been reported. ent lower limb motor weakness need an urgent surgical Because of the high rate of postoperative neuropathic pain procedure. after removing this type of LDH, intraoperative manipulaConsidering the detailed location of the ARLDH is cru- tion of the neural ganglion should be avoided, as much as cial for surgeons who must choose the best appropriate surgi- possible.

350

Further Reading Avila MJ, Chua RV.  Extraforaminal lumbar herniated disc mimicking foraminal tumor: case report, literature review, and the role for minimally invasive approach for resection. J Craniovertebr Junction Spine. 2022;13:101–5. https://doi.org/10.4103/jcvjs.jcvjs_105_21. Clarke HA, Fleming ID.  Disk disease and occult malignancies. South Med J. 1973;66:449–54. https://doi.org/10.1097/00007611-­ 197304000-­00014. Cusimano MD, Bukala BP, Bilbao J.  Extreme lateral disc herniation manifesting as nerve sheath tumor. Case report. J Neurosurg. 1995;82:654–6. https://doi.org/10.3171/jns.1995.82.4.0654. Garg K, Nagi ON, Suri S, Garg SK.  CT of anterior intervertebral disc herniation. Australas Radiol. 1988;32:458–9. https://doi. org/10.1111/j.1440-­1673.1988.tb02777.x. Haines CM, Samtani RG, Bernatz JT, Abugideiri M, O’Brien JR. Far-­ lateral disc herniation treated by lateral lumbar interbody fusion without complete fragment excision: a case report and review of the literature. Cureus. 2018;10:e3404. https://doi.org/10.7759/ cureus.3404. Johansen JG.  Demonstration of anterior intervertebral disc herniation by CT. Neuroradiology. 1987;29:214. https://doi.org/10.1007/ BF00327556. Kachramanoglou C, Farmer SF, Choi D.  Sequestered disc fragment mimicking a psoas abscess. Spine J. 2012;12:e1–4. https://doi. org/10.1016/j.spinee.2012.08.022. Kotil K, Akcetin M, Bilge T.  A minimally invasive transmuscular approach to far-lateral L5-S1 level disc herniations: a prospective study. J Spinal Disord Tech. 2007;20:132–8. https://doi. org/10.1097/01.bsd.0000211268.43744.2a. Levene HB, Nimmagadda A, Levi AD.  An unusual case of footdrop: anterior disc herniation mimicking a nerve sheath tumor. Neurosurgery. 2010;66:E419–20. https://doi.org/10.1227/01. NEU.0000363406.81956.A9. Oh YM, Shin YS, Jeong YB, Eun JP. Anterior retroperitoneal herniation of the lumbar disk causing hydronephrosis: case report with a review of literatures. Neurosurg Q. 2015;25:481–3. https://doi. org/10.1097/WNQ.0000000000000091. Osborn AG, Hood RS, Sherry RG, Smoker WR, Harnsberger HR. CT/ MR spectrum of far lateral and anterior lumbosacral disk herniations. AJNR Am J Neuroradiol. 1988;9:775–8.

23  Anterior Retroperitoneal Lumbar Disk Herniations Ozpeynirci Y, Braun M, Lubotzki I, Schmitz B, Antoniadis G. Extra-­ foraminal intraneural L5-S1 disc herniation mimicking a retroperitoneal peripheral nerve sheath tumour: case report and review of the literature. Cureus. 2019;11:e4956. https://doi.org/10.7759/ cureus.4956. Parmar G, Soin P, Sharma P, French C, Han B, Kochar PS.  Sequestered disc herniation mimicking psoas abscess: a rare case report. Radiol Case Rep. 2021;17:223–6. https://doi.org/10.1016/j. radcr.2021.10.024. Perves A, Morvan G. L5-S1 herniated disk migrated to the anterior part of the right sacral wing with compression of the right lumbosacral roots. Rev Chir Orthop Reparatrice Appar Mot. 1996;82:557–60. Porchet F, Fankhauser H, de Tribolet N.  Extreme lateral lumbar disc herniation: clinical presentation in 178 patients. Acta Neurochir (Wien). 1994;127:203–9. https://doi.org/10.1007/BF01808767. Saadeddin M, Razik MA, el Bakry AK.  Retroperitoneal liposarcoma simulating a prolapsed intervertebral disc. A case report. Int Orthop. 1989;13:125–8. https://doi.org/10.1007/BF00266373. Sadek AR, Dare C, McGillion S, Nader-Sepahi A, Skiadas V. Lumbar intravertebral disc herniation secondary to idiopathic calcific discitis. Br J Neurosurg. 2019;33:586–90. https://doi.org/10.1080/02688 697.2017.1394445. Sharma MS, Morris JM, Pichelmann MA, Spinner RJ. L5-S1 extraforaminal intraneural disc herniation mimicking a malignant peripheral nerve sheath tumor. Spine J. 2012;12:e7–e12. https://doi. org/10.1016/j.spinee.2012.10.033. Tang YZ, Shannon ML, Lai GH, Li XY, Li N, Ni JX.  Anterior herniation of lumbar disc induces persistent visceral pain: discogenic visceral pain: discogenic visceral pain. Chin Med J (Engl). 2013;126:4691–5. Tschugg A, Tschugg S, Hartmann S, Rhomberg P, Thomé C. Far caudally migrated extraforaminal lumbosacral disc herniation treated by a microsurgical lateral extraforaminal transmuscular approach: case report. J Neurosurg Spine. 2016;24:385–8. https://doi.org/10.3 171/2015.7.SPINE15342. Witzmann A, Hammer B, Fischer J.  Free sequestered disc herniation at the S2 level misdiagnosed as neuroma. Neuroradiology. 1991;33:92–3. https://doi.org/10.1007/BF00593349. Wong-Chung JK, Naseeb SA, Kaneker SG, Aradi AJ. Anterior disc protrusion as a cause for abdominal symptoms in childhood discitis. A case report. Spine (Phila Pa 1976). 1999;24:918–20. https://doi. org/10.1097/00007632-­199905010-­00016.

Pediatric Lumbar Disk Herniations

24.1 Generalities and Relevance Pediatric (children and adolescents) lumbar disk herniations (LDHs) are relatively rare representing less than 5% of all LDHs. For many authors, pediatric forms of LDH are distinct from those occurring in adults due to some different clinical–pathological features. In contrast to the adult population, where the main etiology of LDH is degenerative, many factors have been recognized as the possible causes of pediatric LDH, especially trauma and intensive sport activity (Table 24.1). The correlation between obesity and pediatric LDH remains unclear. There is also a possible role of facet tropism in the pathology of LDH in adolescents. The majority of LDHs involve low lumbar intervertebral levels, particularly L5–S1 and L4–L5 disks with other levels and multilevel disease documented, but unusual. Table 24.1  Main factors involved in the pediatric age group with LDH Traumatic experience Intensive sport activity Genetic factors Congenital spine anomalies

In 30–60% of patients Weightlifters and tennis players are particularly at risk Particularly first-degree family members with the same condition (in up to 60% of patients) Transitional vertebra (lumbarization and sacralization), spina bifida, hyperlordosis, scoliosis, Scheuermann kyphosis, or spondylolisthesis In 5–30% of patients. Mostly in adolescent males (c.f. Chap. 27)

Posterior ring apophysis separation Lumbosacral facet Asymmetries (facet tropism) joint

24

Herniated disk material in pediatric age group tends to be soft, viscous, rubbery, hydrated, and strongly attached to the cartilaginous end plate unlike degenerative material usually encountered in adult LDH (Figs. 24.1 and 24.2). Hard or calcified disks are mostly associated with a posterior ring apophysis separation (PRAS) in adolescents (Figs.  24.3, 24.4, 24.5, and 24.6). As seen with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as compression theory, ischemic theory, and chemical inflammatory theory. In 1945, Herman Wahren, a Swedish surgeon, was the first to report a pediatric LDH in a 12-year-old girl following a gymnastic injury at school. If the incidence of LDH is 40% in adults, this incidence is less than 3% in children and adolescents. However, the prevalence of pediatric LDH seems to be much higher in the Japanese population (up to 22%) compared to that reported in Caucasian populations. It was reported that the pediatric population represents less than 7% of all patients hospitalized for LDH. There is male dominance with twice as many boys as girls. It is very rare for isolated LDH to occur in children aged younger than 10 years. Due to the low incidence of LDH in children and adolescents, these patients are generally misdiagnosed initially and have a prolonged length of time from the onset of symptoms to the final diagnosis. With a pediatric LDH and before any surgery, the treating physician must take into account that a growing spine is vulnerable to surgery and postoperative spinal deformities are not rare in the pediatric population.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_24

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24  Pediatric Lumbar Disk Herniations

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b

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Fig. 24.1  Case 1. L4–L5 central disk herniation (arrows) in a 16-year-old patient as seen on axial CT scan (a), sagittal (b), and axial (c) T2-weighted MRI

Fig. 24.2  Case 1. Photograph showing the herniated disk material in this adolescent patient. The disk material was soft, viscous, rubbery, and hydrated. The appearance of disk material collected (a) and spread (b)

a

b

24.1 Generalities and Relevance

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Fig. 24.3  Case 2. This 15-year-old patient presented with nontraumatic bilateral sciatica for 3 months. There was an L4–L5 central spinal stenosis with adjacent central disk herniation (arrows) as seen on sagit-

tal T1-weighted (a) and T2-weighted MRI (b) and axial T2-weighted MR imaging (c, d)

354 Fig. 24.4  Case 2. Preoperative sagittal reconstruction (a) and axial (b) CT scan showing the so-called calcified L4–L5 disk herniation (arrows). In fact, it was an L4–L5 posterior ring apophysis separation (arrows) from the L4 posteroinferior endplate (c)

24  Pediatric Lumbar Disk Herniations

a

b

c

a

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Fig. 24.5  Case 2. Operative view of the L4–L5 posterior ring apophysis separation (bilateral approach via L4 laminectomy) (a). Intraoperative photograph following surgical decompression and discectomy (nerve root and thecal sac are released) (b)

24.2 Clinical Presentations Fig. 24.6  Case 2. Postoperative lumbosacral CT scan showing the removal of the L4–L5 ring apophysis. Sagittal reconstruction (a) and axial (b, c) CT scan

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24.2 Clinical Presentations As with other forms of LDH, the initial evaluation should include a sufficient and detailed history and a neurological, spinal, and somatic examination. The majority of the patients are male adolescents. Clinical presentations of LDH in the pediatric age group are normally comparable to those encountered in the adult population except that most pediatric patients have the following: • A positive straight leg raising test (up to 90%). • Some cases might have truncated sciatic pain mimicking a hamstring syndrome (AKA proximal hamstring tendinopathy) (Fig. 24.7). • Predominant mechanical signs including low back pain, scoliosis, and paravertebral muscle spasm. • Few neurological symptoms such as numbness and motor weakness. • Exceptionally a cauda equina syndrome (only one previous presentation in a 13-year-old child).

Classically, many patients may present with painful scoliosis, where the LDH is typically on the same side of the convexity of lumbar scoliosis (Fig.  24.8). Children with LDH tend to have a greater limitation of movement than adults. For many authors, the severity of spinal and neurological symptoms did not have a strong correlation with the size of the herniated disk. Regarding the rare group of patients younger than 10 years old, attention should be given to the traditional lumbosacral radicular symptoms and signs that are more likely to be ignored as younger children tend to lack cooperation during examinations. Some diagnoses should be suspected as the cause of low back pain or sciatica in any young patient such as neoplasms (i.e., lumbar osteoid osteoma and sarcoma), infections (i.e., Garre’s chronic sclerosing osteomyelitis, discitis, and pyomyositis), and spinal congenital deformities.

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24  Pediatric Lumbar Disk Herniations

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Fig. 24.7  Case 3. This 17-year-old patient has suffered from atypical left coxalgia for more than 4 years. It was during a pelvic CT scan procedure that an L5–S1 posterior ring apophysis separation with concomitant central disk herniation was diagnosed (arrows). Clinically, the

a

b

e

patient presented rather a hamstring syndrome rather than radicular sciatica. Anteroposterior pelvic plain radiography (a) and axial CT scan (b). It was only later that a lumbosacral spinal CT scan was done on both parenchymal (c, d) and bone (e) windows

c

Fig. 24.8  Case 4. Preoperative patient clinical presentation (a–c) showing a left lateral shift (sciatic scoliotic list) with a flat back and slight trunk flexion (arrows) away from the right (contralateral) side of sciatica in an adolescent

24.3 Imaging Features

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24.3 Imaging Features

Postural abnormalities are best assessed on plain radiography. Computed tomography (CT) scans of the spine perMagnetic resonance imaging (MRI) is still the gold standard formed in these patients are very helpful for diagnosing for diagnosing LDH or lumbosacral nerve root anomalies. vertebral fractures, bone anomalies, or posterior avulsed rim Based on their exact anatomical localization, some LDHs are plate (namely PRAS) impinging on the lumbar canal central, while the majority are centro-lateral into the spinal (Figs. 24.3 and 24.5). Unlike the adult population, two consecutive disk levels canal. In pediatric patients, disk herniations remain subligamen- are rarely involved. As with other traditional LDHs, there is no real correlatous in most cases (Figs. 24.1, 24.3, 24.9, and 24.10), whereas extruded disks are rare. The materials are usually well-­ tion between the size of the disk herniation on spinal imaghydrated and elastic in appearance. Degenerative changes ing and the degree of clinical symptomatology in the pediatric are rarely seen, often in obese adolescents. Posterior ring population. This variance is explained by the existence of apophysis separation could not be appreciated on MRI due to other factors besides pure mechanical compression such as inflammatory and vascular phenomena. the small size of the bone fragment.

a

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Fig. 24.9  Case 4. Preoperative lumbosacral CT scan on sagittal reconstructions (a, b) and axial (c, d) views showing straightness of the lumbar spine with central L4–L5 disk herniation (arrows)

358 Fig. 24.10  Case 4. Preoperative lumbosacral MRI in the same patient on sagittal (a) and axial (b) T2-weighted sequences. Note the L4–L5 central disk herniation (arrows)

24  Pediatric Lumbar Disk Herniations

a

24.4 Treatment Options and Prognosis The key treatment of pediatric LDHs is to relieve symptoms, improve quality of life, and prevent further spinal complications. In the absence of neurological deficits, conservative management is typically the primary therapeutic intervention in pediatric patients with LDH. This consists of bed rest, analgesic and anti-inflammatory medications, physical therapy, bracing (rarely), and limitation of physical activities. There are some successful results using direct epidural steroid injections. Nevertheless, it seems that conservative measures are not as effective for children and adolescents with LDH as they are for adult patients. Short- to long-term success rates of conservative treatment for children and adolescents with LDH without neurological compromise varied between 25 and 50%.

b

Intradiscal chemonucleolysis was previously proposed by some authors before any surgery. Chemonucleolysis is known to be associated with less trauma and postoperative adhesion, earlier remobilization, shorter hospitalization, and reduced cost. However, chemonucleolysis is not appropriate for large disk herniations and up to 25% of patients will require additional surgery. Like in adults, modalities of surgical treatment for pediatric LDH consist of percutaneous microendoscopic discectomy and open discectomy (including microsurgical discectomy, discectomy with laminotomy or laminectomy, and spinal fusion). All these surgical techniques have been shown to be safe and effective in the pediatric age group. However, clinicians should always consider spinal growth and the timing of spinal maturity when managing the pediatric spine. The soft disks found in pediatric patients are difficult to remove due to their rubbery/elastic consistency and can be

24.5 Outcomes and Prognosis

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excised in piecemeal only (Fig. 24.2). Therefore, the risks of recurrence due to residual disk are relatively great. Spinal fusion is not recommended for pediatric LDH except in some special conditions as follows: • LDH with spondylolisthesis or obvious instability. • Multiple-level laminectomy. • The incompetence of the facet joints due to other causes.

24.5 Outcomes and Prognosis Postoperative complications are consistent with those in adults (i.e., hematoma, delayed wound healing, infection) except for the relatively high rate of iatrogenic spinal defor-

a

b

mities related to multiple-level laminectomy, excessive bone or ligament resection, and damage to the facet joints. Recurrent LDH at the same operating disk level represents 5–10% of pediatric patients. Interestingly, failed back syndrome, which is often encountered in adults, is relatively rare in the pediatric population. The results of disk surgery in the pediatric age group are reported to be successful (good to excellent) in more than 90% of patients, principally for the improvement of sciatic and low back pain (Figs. 24.8 and 24.11). However, as with other traditional forms of LDH, patients with neurological deficits are more resistant to improvement. Overall, the literature does not support the notion that surgical outcomes are worse in pediatrics than in the adult population. On the contrary, surgical results are rather equivalent or better. c

Fig. 24.11  Case 4. Postoperative patient presentation the next day after surgery. Significant improvement of the patient’s postural deformities (a–c)

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Further Reading Akhaddar A.  Letter to the Editor regarding “Transforaminal endoscopic discectomy for hard or calcified lumbar disc herniation: a new surgical technique and clinical outcomes”. World Neurosurg. 2020;144:316–7. https://doi.org/10.1016/j.wneu.2020.07.202. Akhaddar A, Arabi H.  Isolated painless scoliosis in lumbar disc herniation. Surg Neurol Int. 2020;11:159. https://doi.org/10.25259/ SNI_287_2020. Beck J, Brisby H, Baranto A, Westin O.  Low lordosis is a common finding in young lumbar disc herniation patients. J Exp Orthop. 2020;7:38. https://doi.org/10.1186/s40634-­020-­00253-­7. Cahill J, Frost G, Solanki GA. Paediatric lumbar disc herniation in the very young: a case-based update. Childs Nerv Syst. 2011;27:687– 91. https://doi.org/10.1007/s00381-­010-­1369-­6. Cahill KS, Dunn I, Gunnarsson T, Proctor MR. Lumbar microdiscectomy in pediatric patients: a large single-institution series. J Neurosurg Spine. 2010;12:165–70. https://doi.org/10.3171/2009.9.SP INE09756. Dang L, Chen Z, Liu X, Guo Z, Qi Q, Li W, et al. Lumbar disk herniation in children and adolescents: the significance of configurations of the lumbar spine. Neurosurgery. 2015;77:954–9. https://doi. org/10.1227/NEU.0000000000000983. Dang L, Liu Z. A review of current treatment for lumbar disc herniation in children and adolescents. Eur Spine J. 2010;19(2):205–14. https://doi.org/10.1007/s00586-­009-­1202-­7. Dewing CB, Provencher MT, Riffenburgh RH, Kerr S, Manos RE. The outcomes of lumbar microdiscectomy in a young, active population: correlation by herniation type and level. Spine (Phila Pa 1976). 2008;33:33–8. https://doi.org/10.1097/BRS.0b013e31815e3a42. Durham SR, Sun PP, Sutton LN.  Surgically treated lumbar disc disease in the pediatric population: an outcome study. J Neurosurg. 2000;92:1–6. https://doi.org/10.3171/spi.2000.92.1.0001. Garrido E. Lumbar disc herniation in the pediatric patient. Neurosurg Clin N Am. 1993;4:149–52. Haidar R, Ghanem I, Saad S, Uthman I.  Lumbar disc herniation in young children. Acta Paediatr. 2010;99:19–23. https://doi. org/10.1111/j.1651-­2227.2009.01460.x. Ishihara H, Matsui H, Hirano N, Tsuji H.  Lumbar intervertebral disc herniation in children less than 16  years of age. Long-term follow-up study of surgically managed cases. Spine (Phila Pa 1976). 1997;22:2044–9. https://doi.org/10.1097/00007632-­ 199709010-­00022. Karademir M, Eser O, Karavelioglu E. Adolescent lumbar disc herniation: impact, diagnosis, and treatment. J Back Musculoskelet Rehabil. 2017;30:347–52. https://doi.org/10.3233/BMR-­160572. Kim YS, Park IJ, Rhyu KW, Lee SU, Jeong C.  Surgical excision of the lumbar disc herniation in elementary school age. Asian Spine J. 2009;3:10–5. https://doi.org/10.4184/asj.2009.3.1.10. Kumar R, Kumar V, Das NK, Behari S, Mahapatra AK.  Adolescent lumbar disc disease: findings and outcome. Childs Nerv Syst. 2007;23:1295–9. https://doi.org/10.1007/s00381-­007-­0370-­1. Kurihara A, Kataoka O. Lumbar disc herniation in children and adolescents. A review of 70 operated cases and their minimum 5-year follow-up studies. Spine (Phila Pa 1976). 1980;5:443–51. Lavelle WF, Bianco A, Mason R, Betz RR, Albanese SA. Pediatric disk herniation. J Am Acad Orthop Surg. 2011;19:649–56. https://doi. org/10.5435/00124635-­201111000-­00001. Lin RH, Chen HC, Pan HC, Chen HT, Chang CC, Tzeng CY, et  al. Efficacy of percutaneous endoscopic lumbar discectomy for pediatric lumbar disc herniation and degeneration on magnetic resonance imaging: case series and literature review. J Int Med Res. 2021;49:300060520986685. https://doi. org/10.1177/0300060520986685. Luukkonen M, Partanen K, Vapalahti M.  Lumbar disc herniations in children: a long-term clinical and magnetic resonance imag-

24  Pediatric Lumbar Disk Herniations ing follow-up study. Br J Neurosurg. 1997;11:280–5. https://doi. org/10.1080/02688699746041. Martínez-Lage JF, Fernández Cornejo V, López F, Poza M.  Lumbar disc herniation in early childhood: case report and literature review. Childs Nerv Syst. 2003;19:258–60. https://doi.org/10.1007/s00381-­ 003-­0720-­6. McAvoy M, McCrea HJ, Chavakula V, Choi H, Bi WL, Mekary RA, et al. Long-term outcomes of lumbar microdiscectomy in the pediatric population: a large single-institution case series. J Neurosurg Pediatr. 2019:1–9. https://doi.org/10.3171/2019.6.PEDS18716. Montejo JD, Camara-Quintana JQ, Duran D, Rockefeller JM, Conine SB, Blaise AM, et  al. Tubular approach to minimally invasive microdiscectomy for pediatric lumbar disc herniation. J Neurosurg Pediatr. 2018;21:449–55. https://doi.org/10.3171/2017.11. PEDS17293. Ozgen S, Konya D, Toktas OZ, Dagcinar A, Ozek MM. Lumbar disc herniation in adolescence. Pediatr Neurosurg. 2007;43:77–81. https://doi.org/10.1159/000098377. Raghu ALB, Wiggins A, Kandasamy J.  Surgical management of lumbar disc herniation in children and adolescents. Clin Neurol Neurosurg. 2019;185:105486. https://doi.org/10.1016/j.clineuro.2019.105486. Sarma P, Thirupathi RT, Srinivas D, Somanna S. Adolescent prolapsed lumbar intervertebral disc: management strategies and outcome. J Pediatr Neurosci. 2016;11:20–4. https://doi.org/10.4103/1817­1745.181259. Shillito J Jr. Pediatric lumbar disc surgery: 20 patients under 15 years of age. Surg Neurol. 1996;46:14–8. https://doi.org/10.1016/0090-­ 3019(96)00035-­3. Shimony N, Louie C, Barrow D, Osburn B, Noureldine MHA, Tuite GF, Carey CM, Jallo GI, Rodriguez L.  Adolescent disc disease: risk factors and treatment success-related factors. World Neurosurg. 2021;148:e314–20. https://doi.org/10.1016/j.wneu.2020.12.126. Singhal A, Mitra A, Cochrane D, Steinbok P. Ring apophysis fracture in pediatric lumbar disc herniation: a common entity. Pediatr Neurosurg. 2013;49:16–20. https://doi.org/10.1159/000355127. Strömqvist F, Strömqvist B, Jönsson B, Gerdhem P, Karlsson MK. Lumbar disc herniation surgery in children: outcome and gender differences. Eur Spine J. 2016;25:657–63. https://doi.org/10.1007/ s00586-­015-­4149-­x. Theodore N, Ahmed AK, Fulton T, Mousses S, Yoo C, Goodwin CR, Danielson J, Sciubba DM, Giers MB, Kalani MYS.  Genetic predisposition to symptomatic lumbar disk herniation in pediatric and young adult patients. Spine (Phila Pa 1976). 2019;44:E640–9. https://doi.org/10.1097/BRS.0000000000002949. Tin SS, Wiwanitkit V. Sciatica in the young. Asian Spine J. 2014;8:703. https://doi.org/10.4184/asj.2014.8.5.703. Wahren H.  Herniated nucleus pulposus in a child of twelve years. Acta Orthop Scand. 1945;16:40–2. https://doi. org/10.3109/17453674508988913. Wang H, Cheng J, Xiao H, Li C, Zhou Y.  Adolescent lumbar disc herniation: experience from a large minimally invasive treatment centre for lumbar degenerative disease in Chongqing, China. Clin Neurol Neurosurg. 2013;115:1415–9. https://doi.org/10.1016/j.clineuro.2013.01.019. Wang H, Zhang Z, Zhou Y. Irregular alteration of facet orientation in lumbar segments: possible role in pathology of lumbar disc herniation in adolescents. World Neurosurg. 2016;86:321–7. https://doi. org/10.1016/j.wneu.2015.09.029. Wang X, Zeng J, Nie H, Chen G, Li Z, Jiang H, et  al. Percutaneous endoscopic interlaminar discectomy for pediatric lumbar disc herniation. Childs Nerv Syst. 2014;30:897–902. https://doi.org/10.1007/ s00381-­013-­2320-­4. Wang Y, Xu Y, Tian G, Dai G. Pediatric lumbar disc herniation: a report of two cases and review of the literature. Eur J Med Res. 2022;27:82. https://doi.org/10.1186/s40001-­022-­00696-­x.

Pregnant Women with Lumbar Disk Herniations

25.1 Generalities and Relevance During various times of pregnancy, there is an increasing risk of intervertebral lumbar disk herniation (LDH). The reported incidence of symptomatic LDH during pregnancy is about 1 in 10,000 pregnant women. Two important factors that may rise this incidence in the parturient population are high body mass index and increased age. As seen with other traditional symptomatic forms of LDHs, discogenic sciatica in pregnant women can be unilateral or bilateral, with or without low back pain. Parturients with severe neurological deficits are rare. In 1995, Myron Miles LaBan, an American physiatrist, described with his team the first case of discectomy for L5– S1 disk herniation in a pregnant woman during her 20th week of gestation. This 36-year-old woman underwent a laminectomy and discectomy for the progressive development of cauda equina syndrome (CES) with a good postoperative result. Later, at 39  weeks, a healthy child was delivered by cesarean section under general anesthesia because of coexisting fetal bradycardia. Many pathophysiologic mechanisms may contribute to LDH during pregnancy including the following: (a) Normal pregnancy-related changes due to the expansion of the uterus and the development of the fetus. (b) Postural changes and nutation of the pelvic girdle manifesting as an increase in lumbar lordosis and an anterior tilt of the pelvis. (c) Excessive axial load on the intervertebral disks, altering the biomechanics of the three-joint complex and accelerating disk degeneration, causing protrusion and LDH.

25

(d) Production of high concentrations of a hormone called “relaxin” which relaxes joints, muscles, and ligaments and helps the pelvis to expand. (e) Preexisting underlying spinal lumbosacral problems before the pregnancy. (f) Lifestyle, psychological and socioeconomic profiles. More often, a number of pregnant women will suffer from mild sciatic pain unrelated to LDH, particularly in the second and third trimesters of pregnancy, as the fetus progressively grows more (c.f. Chap. 90 about Non Discogenic Sciatica in Pregnancy). This phenomenon can be explained by various mechanisms as follows: • Compression of vascular elements leading to neural hypoxia or ischemia. • Excessive vomiting. • Fetal position within the uterine cavity and the abdomen (Fig. 25.1). The mechanism of injury likely involves compression of the fetal head against the underlying pelvis and lumbosacral trunk. • Sacral stress fracture (not associated with low bone mineral density). • Extreme positions for prolonged periods of time. Management of pregnant women with LDHs depends not only on how an intervention affects the mother’s health but also on its risk to the developing fetus/child. Therefore, optimal management should be discussed within a comprehensive multidisciplinary team whenever possible.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_25

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362 Fig. 25.1 Scannopelvimetry on sagittal (a) and axial (b) views showing the fetal position and especially the head location (circle dotted) within the pelvic cavity

25  Pregnant Women with Lumbar Disk Herniations

a

25.2 Clinical Presentations As for the nonpregnant population, the initial evaluation should include a sufficient and detailed history and a neurological, spinal, and somatic examination. Clinical presentations of LDH during pregnancy are normally comparable to those encountered in other traditional populations. The sciatic radicular pain can be unilateral or less often bilateral with or without lumbosacral back pain. Pain exacerbates with sitting or standing for long periods. Although severe neurological deficit (less than 10% of cases) and CES (about 2% of cases) are rare in pregnant women with LDH, physicians should assess and appropriately recognize the gravity of neurological symptoms. As with other traditional LDHs, there is no real correlation between the size of the LDH on spinal imaging and the degree of clinical symptomatology in the pregnant population. This variance is explained by the existence of other factors besides apparent mechanical compression such as inflammatory, vascular, and hormonal phenomena. Some other diagnoses should be suspected as the cause of low back pain or sciatica during pregnancy such as osteoporotic vertebral fractures and symptomatic vertebral angiomas.

25.3 Imaging Features Despite plain radiography and computed tomography scans, magnetic resonance imaging (MRI) is free of the adverse effects of ionizing radiation and can be safely used to inves-

b

tigate LDH in pregnancy. In addition, MRI is superior in the visualization of neurological and non-osseous structures. The imaging procedure is usually performed for assessment of the lumbar spine in axial and sagittal T1 and T2 sequences. However, in some atypical presentations, neuroimaging can be used for screening lumbosacral plexus or even sciatic nerve lesions causing potential sciatica. Classically, complementary electromyography is not requested for exploring traditional lumbosacral radicular pain in pregnant women.

25.4 Treatment Options The key treatment of symptomatic LDH in pregnant women is to relieve symptoms, improve quality of life, prevent further neurologic complications, and preserve the health and safety of the fetus. There is limited evidence to guide the therapeutic management of parturients with symptomatic LDH.  For many authors, decision-making for these patients needs a multidisciplinary team consisting of obstetricians, neonatologists, neurosurgeons/spinal surgeons, and anesthesiologists. Each decision must consequently be balanced with the risk and benefits for both the mother and her fetus/child. Overall, it is recommended that pregnant women with LDH are treated conservatively unless nonsurgical management has failed or there are red flag symptoms such as CES, fecal/urinary dysfunction, progressive neurological weakness of the lower extremities, and intractable radicular pain. It is important to consider that maternal stress and persistent

Further Reading

noxious stimuli can increase the risk of abortion or preterm birth. When needed, a variety of physiotherapies or self-care therapies may be helpful. This might comprise massage, stretching, swimming, hot/cold therapy, maternity support belts, and performing good posture and gentle exercises. Most of the analgesic medications habitually used to treat neuropathic pain are contraindicated in pregnancy. Some safety drugs can be used such as paracetamol (acetaminophen), some antioxidants, and neurotrophic agents such as alpha-lipoic acid (known as thioctic acid) and its reduced form, dihydrolipoic acid. However, nonsteroidal anti-­ inflammatory drugs are contraindicated during the first and third trimesters, due to the risk of spontaneous abortion, congenital malformations, and constriction of ductus arteriosus in utero, respectively. Glucocorticoids have the potential to cause some dose-dependent teratogenicities. If symptoms persist beyond one month in spite of bed rest and oral analgesia, epidural or transforaminal steroid injections can be considered. Like other traditional patient group with LDH, more than 85% of pregnant women will have improved symptoms within 6  weeks of starting conservative methods of treatment. However, if surgery is absolutely indicated, it is therefore recommended to postpone procedures beyond 24 weeks gestation in order to minimize the risk of spontaneous abortion and neonatal mortality rate. Then, the effects of patient ­positioning, anesthesia, fetal heart rate monitoring, plans for urgent delivery, monitoring of maternal blood pressure, aspiration prophylaxis, and tocolysis for the prevention of preterm labor must be measured. Like in the nonpregnant population, modalities of surgical treatment for pregnant women with LDH consist of traditional open discectomy techniques (including microsurgical discectomy, laminectomy, and even spinal fusion) and percutaneous microendoscopic discectomy. All these surgical techniques have been shown to be safe and effective in parturients. Best intraoperative patient positioning depends on the gestational age. The prone position is not recommended beyond 12 weeks of gestation due to abdominal compression. A left lateral position is preferable for patients in the later stages of the second trimester and the third-trimester to avoid aortocaval compression syndrome. Both general and regional anesthesia should be used with caution. However, regional anesthesia is preferred because it is more safety. Regarding the optimal route of delivery, some authors recommend a cesarean section if possible at the time of surgery for the LDH. For some other physicians, vaginal delivery does not report an elevated rate of persistent neurological symptoms. However, for Brown and his colleagues, labor

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before treatment for LDH can cause increased neurological injury due to the rise of epidural venous pressure.

25.5 Outcomes and Prognosis Compared to pregnant patients who are treated surgically, pregnant women managed conservatively had a higher complete recovery rate and reported a lower rate of persistent symptoms. However, as with other traditional forms of LDHs, patients with neurological deficits are more resistant to improvement. Patients managed conservatively reported a 100% successful birth rate with a healthy mother and infant compared with 93% of patients treated surgically. However, according to many authors, surgical management of LDH in pregnancy is now safe if a multidisciplinary approach is involved. Surgical complications are not significantly increased in pregnant women compared to nonpregnant women with LDH.

Further Reading Abou-Shameh MA, Dosani D, Gopal S, McLaren AG. Lumbar discectomy in pregnancy. Int J Gynaecol Obstet. 2006;92:167–9. https:// doi.org/10.1016/j.ijgo.2005.09.028. Ahern DP, Gibbons D, Johnson GP, Murphy TM, Schroeder GD, Vaccaro AR, et  al. Management of herniated lumbar disk disease and Cauda Equina Syndrome in pregnancy. Clin Spine Surg. 2019;32:412–6. https://doi.org/10.1097/BSD.0000000000000886. Al-Khodairy AW, Bovay P, Gobelet C. Sciatica in the female patient: anatomical considerations, aetiology and review of the literature. Eur Spine J. 2007;16:721–31. https://doi.org/10.1007/ s00586-­006-­0074-­3. Ardaillon H, Laviv Y, Arle JE, Kasper EM.  Lumbar disk herniation during pregnancy: a review on general management and timing of surgery. Acta Neurochir (Wien). 2018;160:1361–70. https://doi. org/10.1007/s00701-­017-­3098-­z. Babici D, Johansen PM, Newman SL, O’Connor TE, Miller TD. Microdiscectomy under local anesthesia and spinal block in a pregnant female. Cureus. 2021;13:e20241. https://doi.org/10.7759/ cureus.20241. Brown MD, Levi AD.  Surgery for lumbar disc herniation during pregnancy. Spine (Phila Pa 1976). 2001;26:440–3. https://doi. org/10.1097/00007632-­200102150-­00022. Di Martino A, Russo F, Denaro L, Denaro V. How to treat lumbar disc herniation in pregnancy? A systematic review on current standards. Eur Spine J. 2017;26:496–504. https://doi.org/10.1007/ s00586-­017-­5040-­8. Han IH.  Pregnancy and spinal problems. Curr Opin Obstet Gynecol. 2010;22:477–81. https://doi.org/10.1097/GCO.0b013e3283404ea1. Hayakawa K, Mizutani J, Suzuki N, Haas C, Kondo A, Otsuka S, et  al. Surgical management of the pregnant patient with lumbar disc herniation in the latter stage of the second trimester. Spine (Phila Pa 1976). 2017;42:E186–9. https://doi.org/10.1097/ BRS.0000000000001741. Iyilikçi L, Erbayraktar S, Tural AN, Celik M, Sannav S.  Anesthetic management of lumbar discectomy in a pregnant patient. J Anesth. 2004;18:45–7. https://doi.org/10.1007/s00540-­003-­0199-­z.

364 Kapetanakis S, Giovannopoulou E, Blontzos N, Kazakos G, Givissis P.  Surgical management for lumbar disc herniation in pregnancy. J Gynecol Obstet Hum Reprod. 2017;46:753–9. https://doi. org/10.1016/j.jogoh.2017.09.009. Kovari VZ, Horvath L.  Surgical management of cauda syndrome in third trimester of pregnancy focusing on spinal anesthesia and right lateral positioning during surgery as possible practices. Eur Spine J. 2018;27:483–8. https://doi.org/10.1007/s00586-­018-­5519-­y. LaBan MM, Rapp NS, von Oeyen P, Meerschaert JR. The lumbar herniated disk of pregnancy: a report of six cases identified by magnetic resonance imaging. Arch Phys Med Rehabil. 1995;76:476–9. https://doi.org/10.1016/s0003-­9993(95)80582-­6. Nyrhi L, Kuitunen I, Ponkilainen V, Mäntymäki H, Huttunen TT, Mattila VM. Incidence of lumbar discectomy during pregnancy and within 12 months post-partum in Finland between 1999 and 2017: a retrospective register-based cohort study. Spine J. 2023;23:287–94. https://doi.org/10.1016/j.spinee.2022.10.015. Paslaru FG, Giovani A, Iancu G, Panaitescu A, Peltecu G, Gorgan RM.  Methods of delivery in pregnant women with lumbar disc

25  Pregnant Women with Lumbar Disk Herniations herniation: a narrative review of general management and case report. J Med Life. 2020;13:517–22. https://doi.org/10.25122/ jml-­2020-­0166. S DCR, Shetty AP, Kanna RM, Rajasekaran S. Cauda equina syndrome in an obese pregnant patient secondary to double level lumbar disc herniation—A case report and review of literature. Spinal Cord Ser Cases. 2019;5:33. https://doi.org/10.1038/s41394-­019-­0179-­7. Smith MW, Marcus PS, Wurtz LD.  Orthopedic issues in pregnancy. Obstet Gynecol Surv. 2008;63:103–11. https://doi.org/10.1097/ OGX.0b013e318160161c. Whiles E, Shafafy R, Valsamis EM, Horton C, Morassi GL, Stokes O, et  al. The management of symptomatic lumbar disc herniation in pregnancy: a systematic review. Global Spine J. 2020;10:908–18. https://doi.org/10.1177/2192568219886264. Zheng Q, Hu X, Zhang Y, Wang Y. Lumbar disc herniation in a pregnant woman treated with full-endoscopic interlaminar discectomy without X-ray exposure: a case report. J Orthop Sci. 2023;28:911–4. https://doi.org/10.1016/j.jos.2020.10.021.

Spontaneous Regression of Lumbar Disk Herniations

26.1 Generalities and Relevance Therapeutic possibilities for symptomatic lumbar disk herniation (LDH) include both conservative and surgical treatment. Most patients benefit from conservative treatment; however, surgery is recommended in some conditions especially when cauda equine syndrome (CES), motor weakness, or pain refractory to conservative treatment exists. The radicular pain is not only due to herniated disk compression on the nerve but also due to inflammation, edema, and radicular blood congestion phenomena. The choice between conservative and surgical treatment remains a source of controversy in the literature. The definition of spontaneous regression of an LDH corresponds to a reduction in the size of the herniated disk material without resorting to a surgical procedure. The percentage of disk regression differs between studies by more than 20%, 50%, or 70%. The complete disappearance of LDH (100%) is an unusual finding. Regression of herniated disks has been described at different spinal segments and levels (mainly the three last lumbar disks) and with various clinical presentations, above all radicular pain (Figs. 26.1 and 26.2). The first “suspicion” of spontaneous regression of LDH was published by Key in 1945 using repeated epidurography. Afterward, many cases have been reported along with the development and extensive use of spinal imaging techniques. Indeed, spontaneous resorption of an LDH was first observed by computed tomography (CT) scan in 1984 by Guinto et al. and by magnetic resonance imaging (MRI) in 1990 by Saal et al. This condition revealed that LDH could be reduced by itself or via nonoperative methods. Since that, there is increasing concern regarding spontaneous regression or disappearance of herniated intervertebral disks without surgical management.

26

The exact mechanism of spontaneous LDH regression remains unknown. However, the following hypotheses have been previously suggested: (a) Retraction of the herniated disk back into the intervertebral space. (b) Regression secondary to gradual dehydration and shrinkage. (c) Enzymatic degradation and phagocytosis of “foreign body” cartilaginous tissue in the epidural space due to inflammatory reaction and neovascularization of disk herniation (more convincing hypothesis). In this context, cytokines released from macrophages [e.g., tumor necrosis factor-alpha (TNF-α)], matrix metalloproteinase (MMP), and vascular endothelial growth factor (VEGF) are considered to play a role in the mechanism of hernia regression. A combination of two or more mechanisms is also possible in the regression and disappearance of herniated disk tissue. Many factors related to the resorption phenomenon have been recognized. However, the most predictive factors include the following: • Large-sized disk herniation. • Sequestrated intervertebral disk herniation especially those with extensive rim enhancement in gadolinium-­ enhanced T1-weighted MRI. • High signal intensity of the LDH on T2-weighted MRI. • Lateral LDH (inconstantly incriminated). For some authors, laterally sequestrated migrating LDH are among most cases that are likely to resorb.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_26

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366 Fig. 26.1 Spontaneous regression of a C5–C6 disk herniation (arrows) as seen on sagittal (a) and axial (b) T2-weighted MRI and 3 years after the initial MRI (c, d)

26  Spontaneous Regression of Lumbar Disk Herniations

a

b

c

d

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26.2 Clinical Presentations Fig. 26.2 Spontaneous regression of an L5–S1 disk herniation (arrows) as seen on axial (a) and sagittal (b) T2-weighted MRI and 2 years after the initial MRI (c, d)

a

b

c

d

26.2 Clinical Presentations According to the literature, patients who presented spontaneous regression of LDH might have the following clinical features as follows: • Lower back pain (40–65% of cases). • Lumbosacral radiculopathy (50–85%). • Both lower back pain and lumbosacral radiculopathy (about 60%). • Positive straight leg tests (40–55%). • Hyporeflexia (35%). • Motor weakness (30–40%). • Sensory disturbances (45%).

Many patients voluntarily refused surgical decompression for LDH despite being indicated for extruded or sequestered and even some of them had a motor weakness. To the best of our knowledge, no case was presented with a CES. A higher incidence of lumbar disk regression is seen in patients in their fifth decade with a male predominance (between 55 and 70%). Overall, recovery of the lumbosacral radicular pain occurred earlier before the reduction of the size of the herniated disk as appreciated on MRI. The average time of recovery from radicular pain is between 3 and 6  weeks, but it can sometimes take many months. Generally, patients whose clinical symptoms improved during the first 6  weeks may have more rapid

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26  Spontaneous Regression of Lumbar Disk Herniations

regression of their LDH and a decrease of their nerve root inflammation on follow-up MRI.

26.3 Paraclinical Features The first confirmed patients with spontaneous regression of LDH were diagnosed using a CT scan in 1984 and MRI in 1990. Both MRI and CT have proved to be good imaging technics for following up on patients with LDH who undergo conservative treatment. L4–L5 and L5–S1 are the most frequently affected spinal levels, followed by L3–L4, and less frequently L2–L3.

a

c

However, the last two intervertebral disks are associated with sciatic pain syndrome and, above all, extrusion or sequestration in the classification of disk herniation. The largest LDHs on MRI are most likely to show the greatest regression in dimension over time (Figs. 26.2, 26.3, 26.4, and 26.5). Additionally, herniated disk with rim enhancement on post-gadolinium T1-weighted MRI disappears or markedly decreases in more than three-quarters of cases. Rim-surrounded enhancement is related to the accumulation of gadolinium substance within the vascularized granulation tissue (increased inflammatory response) contiguous to the avascular epidural sequestrated disk mass.

b

d

Fig. 26.3  Spontaneous regression of an extruded and migrated L4–L5 disk herniation (arrows) as seen on axial (a, b) T2-weighted MRI and 30 months after the initial MRI (c, d). (Courtesy of Pr. Hatim Belfquih)

26.3 Paraclinical Features

a

369

b

c

d

Fig. 26.4  Spontaneous regression of an extruded and migrated L4–L5 disk herniation (arrows) as seen on sagittal T1-weighted (a) and T2-weighted (b) MRI and 30 months later on the control MRI (c, d). (Courtesy of Pr. Hatim Belfquih)

Overall, predictive factors for spontaneous regression of LDH in MRI are as follows: –– –– –– ––

Extruded and sequestrated types of herniation. Migrated LDH. Transligamentous LDH. Herniation with contrast enhancement known as “bull’s eye sign.” –– High signal intensity of the LDH on T2-weighted MRI. The mean time from the first diagnostic MRI of a herniated disk to radiographic resolution was between 5 and

10 months. This average time varied between 4 and 9 months for sequestration and about 14 months for extrusion. Time taken for spontaneous regression of LDH by more than half of its size varies between 3 and 12 months. Disk regression is more likely with greater thicknesses of the ring enhancement on post-gadolinium T1-weighted MRI. As previously seen, there is no correlation between clinical improvement and imaging morphological modifications in many patients. According to a recent meta-analysis carried out by Ming Zhong et al. in 2017, the overall incidence of resorption of LDHs was around 66.66%.

370

26  Spontaneous Regression of Lumbar Disk Herniations

a

b

c

d

e

f

Fig. 26.5  Initial lumbar axial CT scan (a–c) and control MRI showing complete spontaneous disappearance of a sequestrated L5–S1 herniated disk (arrows) (d–f) for a period of 2 years

26.4 Treatment Options and Prognosis The management approaches for symptomatic LDH include conservative therapies such as bed rest, oral anti-­inflammatory and analgesic drugs, spinal anesthesia blocks, and/or physiotherapy. Globally, surgery is indicated in CES or in the presence of symptoms such as motor weakness or pain refractory to conservative treatment. Although the benefits of early decompressive surgery were stated in most studies, some patients and treated clinicians chose the conservative treatment as the best option when radiculopathy is acceptable and CES is absent. However, there is still a controversy about choosing the best therapeutic options for promoting the resorption of the LDH. Spontaneous regression time is not clearly determined. It has been reported that the regression commonly occurs between 6 and 12 months. The majority of authors recommend conservative treatment for up to 2–3  months in the

absence of CES or neurological deficit and, if conservative management does not succeed, decompressive surgery should be considered. On the other hand, some authors and patients opt for conservative treatment alone in the absence of definitive surgical indications. These patients can be successfully treated with nonoperative procedures resulting in “good-to-excellent” outcomes for approximately 90% of them. However, some patients still need surgical intervention because of the neurological deficit and prolonged uncontrolled pain. One year after disease onset, about one-quarter of patients require surgery. Within the first 3  months of conservative treatment, about 15% of patients would undergo surgical intervention. Patients whose clinical symptoms improved during the first 6 weeks may have more rapid regression of their LDH and a decrease of their nerve root inflammation on follow-up MRI. Additionally, a ring enhancement around the herniated disk material on post-gadolinium T1 weighted (bull’s eye sign) is a significant indicator of resorption.

Further Reading

In an interesting series of 76 patients, only 16% of the patients had complete recovery, nearly 20% of all subjects developed permanent motor deficits, and 14.5% of cases underwent surgery. All operated patients have reported a total recovery. So, conservative treatment did not produce satisfactory benefits in all cases. Subsequently, all nonoperated patients should be followed up closely to avoid potentially more severe and complicated neurological outcomes. Usually, the clinical symptoms improve regardless of the resolution of LDH. According to Chui et al., the rate of spontaneous regression was found to be as follows: –– –– –– ––

96% for disk sequestration. 70% for disk extrusion. 41% for disk protrusion. 13% for disk bulging.

Further Reading Ahn SH, Ahn MW, Byun WM. Effect of the transligamentous extension of lumbar disc herniations on their regression and the clinical outcome of sciatica. Spine (Phila Pa 1976). 2000;25:475–80. https:// doi.org/10.1097/00007632-­200002150-­00014. Altun I, Yüksel KZ.  Lumbar herniated disc: spontaneous regression. Korean J Pain. 2017;30:44–50. https://doi.org/10.3344/ kjp.2017.30.1.44. Benson RT, Tavares SP, Robertson SC, Sharp R, Marshall RW. Conservatively treated massive prolapsed discs: a 7-year follow-­up. Ann R Coll Surg Engl. 2010;92:147–53. https://doi.org/10.1308/0035884 10X12518836438840. Birbilis TA, Matis GK, Theodoropoulou EN.  Spontaneous regression of a lumbar disc herniation: case report. Med Sci Monit. 2007;13:CS121–3. Bozzao A, Gallucci M, Masciocchi C, Aprile I, Barile A, Passariello R. Lumbar disk herniation: MR imaging assessment of natural history in patients treated without surgery. Radiology. 1992;185:135– 41. https://doi.org/10.1148/radiology.185.1.1523297. Bush K, Cowan N, Katz DE, Gishen P.  The natural history of sciatica associated with disc pathology. A prospective study with clinical and independent radiologic follow-up. Spine (Phila Pa 1976). 1992;17:1205–12. https://doi.org/10.1097/00007632-­ 199210000-­00013. Chiu CC, Chuang TY, Chang KH, Wu CH, Lin PW, Hsu WY.  The probability of spontaneous regression of lumbar herniated disc: a systematic review. Clin Rehabil. 2015;29:184–95. https://doi. org/10.1177/0269215514540919. Gezici AR, Ergün R. Spontaneous regression of a huge subligamentous extruded disc herniation: short report of an illustrative case. Acta Neurochir (Wien). 2009;151:1299–300. https://doi.org/10.1007/ s00701-­009-­0370-­x. Guinto FC Jr, Hashim H, Stumer M.  CT demonstration of disk regression after conservative therapy. AJNR Am J Neuroradiol. 1984;5:632–3. Hong SJ, Kim DY, Kim H, Kim S, Shin KM, Kang SS. Resorption of massive lumbar disc herniation on MRI treated with epidural steroid injection: a retrospective study of 28 cases. Pain Physician. 2016;19:381–8.

371 Hornung AL, Barajas JN, Rudisill SS, Aboushaala K, Butler A, Park G, et al. Prediction of lumbar disc herniation resorption in symptomatic patients: a prospective, multi-imaging and clinical phenotype study. Spine J. 2023;23:247–60. https://doi.org/10.1016/j. spinee.2022.10.003. Hu C, Lin B, Li Z, Chen X, Gao K. Spontaneous regression of a large sequestered lumbar disc herniation: a case report and literature review. J Int Med Res. 2021;49:3000605211058987. https://doi. org/10.1177/03000605211058987. Ito T, Yamada M, Ikuta F, Fukuda T, Hoshi SI, Kawaji Y, et al. Histologic evidence of absorption of sequestration-type herniated disc. Spine (Phila Pa 1976). 1996;21:230–4. https://doi.org/10.1097/00007632-­ 199601150-­00014. Iwabuchi M, Murakami K, Ara F, Otani K, Kikuchi S.  The predictive factors for the resorption of a lumbar disc herniation on plain MRI. Fukushima J Med Sci. 2010;56:91–7. https://doi.org/10.5387/ fms.56.91. Key JA.  The conservative and operative treatment of lesions of the intervertebral discs in the low back. Surgery. 1945;17:291–303. Kim SG, Yang JC, Kim TW, Park KH.  Spontaneous regression of extruded lumbar disc herniation: three cases report. Korean J Spine. 2013;10:78–81. https://doi.org/10.14245/kjs.2013.10.2.78. Macki M, Hernandez-Hermann M, Bydon M, Gokaslan A, McGovern K, Bydon A.  Spontaneous regression of sequestrated lumbar disc herniations: literature review. Clin Neurol Neurosurg. 2014;120:136–41. https://doi.org/10.1016/j.clineuro.2014.02.013. Oktay K, Ozsoy KM, Dere UA, Cetinalp NE, Arslan M, Erman T, et al. Spontaneous regression of lumbar disc herniations: a retrospective analysis of 5 patients. Niger J Clin Pract. 2019;22:1785–9. https:// doi.org/10.4103/njcp.njcp_437_18. Orief T, Orz Y, Attia W, Almusrea K.  Spontaneous resorption of sequestrated intervertebral disc herniation. World Neurosurg. 2012;77:146–52. https://doi.org/10.1016/j.wneu.2011.04.021. Saal JA, Saal JS, Herzog RJ.  The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine (Phila Pa 1976). 1990;15:683–6. https://doi.org/10.1097/00007632-­ 199007000-­00013. Sabuncuoğlu H, Ozdoğan S, Timurkaynak E. Spontaneous regression of extruded lumbar disc herniation: report of two illustrative case and review of the literature. Turk Neurosurg. 2008;18:392–6. Sakai T, Tsuji T, Asazuma T, Yato Y, Matsubara O, Nemoto K. Spontaneous resorption in recurrent intradural lumbar disc herniation. Case report. J Neurosurg Spine. 2007;6:574–8. https://doi.org/10.3171/ spi.2007.6.6.11. Slavin KV, Raja A, Thornton J, Wagner FC Jr. Spontaneous regression of a large lumbar disc herniation: report of an illustrative case. Surg Neurol. 2001;56:333–6. https://doi.org/10.1016/s0090-­ 3019(01)00607-­3. Splendiani A, Puglielli E, De Amicis R, Barile A, Masciocchi C, Gallucci M.  Spontaneous resolution of lumbar disk herniation: predictive signs for prognostic evaluation. Neuroradiology. 2004;46:916–22. https://doi.org/10.1007/s00234-­004-­1232-­0. Sucuoğlu H, Barut AY.  Clinical and radiological follow-up results of patients with sequestered lumbar disc herniation: a prospective cohort study. Med Princ Pract. 2021;30:244–52. https://doi. org/10.1159/000515308. Takada E, Takahashi M, Shimada K.  Natural history of lumbar disc hernia with radicular leg pain: spontaneous MRI changes of the herniated mass and correlation with clinical outcome. J Orthop Surg. 2001;9:1–7. Turk O, Antar V, Yaldiz C. Spontaneous regression of herniated nucleus pulposus: the clinical findings of 76 patients. Medicine (Baltimore). 2019;98:e14667. https://doi.org/10.1097/MD.0000000000014667. Wang Y, Dai G, Jiang L, Liao S. The incidence of regression after the non-surgical treatment of symptomatic lumbar disc herniation: a

372 systematic review and meta-analysis. BMC Musculoskelet Disord. 2020;21:530. https://doi.org/10.1186/s12891-­020-­03548-­z. Wang Y, Liao SC, Dai GG, Jiang L. Resorption of upwardly displaced lumbar disk herniation after nonsurgical treatment: a case report. World J Clin Cases. 2020;8:4609–14. https://doi.org/10.12998/ wjcc.v8.i19.4609. Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine (Phila Pa 1976). 1983;8:131–40.

26  Spontaneous Regression of Lumbar Disk Herniations Yang X, Zhang Q, Hao X, Guo X, Wang L. Spontaneous regression of herniated lumbar discs: report of one illustrative case and review of the literature. Clin Neurol Neurosurg. 2016;143:86–9. https://doi. org/10.1016/j.clineuro.2016.02.020. Zhong M, Liu JT, Jiang H, Mo W, Yu PF, Li XC, et al. Incidence of spontaneous resorption of lumbar disc herniation: a meta-analysis. Pain Physician. 2017;20:E45–52.

Posterior Ring Apophysis Separation

27.1 Generalities and Relevance Posterior ring apophysis separation (PRAS) is an unusual pathological entity characterized by the separation of a bony fragment at the posterior superior or inferior endplates of the vertebral body in the weak junction between ring apophysis and the adjacent vertebral body (the site of attachment of the Sharpey fibers of the intervertebral disk) (Fig.  27.1). For many authors, they represent a true bony fracture occurring in the immature skeleton, usually in the lower lumbar spine. Various terms are referred to this condition including “limbus vertebral fracture” and “apophyseal ring fracture,” “posterior retro-extramarginal disk hernia,” “slipped vertebral epiphysis,” or even “posterior Schmorl node.” The majority of PRAS occurs in children before the apophyseal ring fuses to the vertebral body. In adults, a PRAS should not be confused with an acute fracture, an osteophytosis, or a calcified/ossified posterior longitudinal ligament.

27

Although the first case of PRAS has been described in 1946 by the Swiss pathologist Hanns Von Meyenburg (1887– 1971), this entity is generally unrecognized and misdiagnosed as a calcified herniated disk. However, there has recently been a growing interest in this phenomenon with the development of spinal imaging techniques. The association of PRAS with lumbar disk herniation (LDH) represents a distinct subgroup of disk herniation due to some different clinic-pathological features. PRAS represents up to 8% of all ages of patients with LDH.  However, there is a disparity between the pediatric (6–28%) and adult populations (less than 5%). Overall, this condition is typically found in adolescents and young adults (early twenties), three times more likely in men probably due to greater strenuous physical activity. Traditionally, trauma was considered the main etiological factor in the development of adolescent PRAS, especially in active athletes. However, trauma has not been reported in many patients. Therefore, other factors could be involved. In

Fig. 27.1  Illustration of a sagittal section of the lumbar intervertebral space showing the constituent parts of the disk. Note the sites of the posterior ring apophysis separation (PRAS) (stars)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_27

373

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27  Posterior Ring Apophysis Separation

adults, chronic strenuous physical activities affecting the lumbosacral spine may be the primary event leading to the onset of symptoms. Generally, there is a controversy in the pathogenesis of PRAS, whether an overworked disk produces avulsion injury or the latter results in annular disruption and disk herniation. The majority of PRAS involve the low lumbar spine, particularly at the posterior cephalad endplate of the vertebra of L5 and S1 with other vertebral levels, and multilevel diseases are rare. Fig. 27.2  Illustrations on axial views showing the main types of posterior ring apophysis separation (arrows) compared to normal (a). The bony fragment is completely (b) or partially (c) separated from the posterior edge of the vertebral body. The ring apophysis separation extends across the entire posterior vertebral body (d)

a

b

c

d

Table 27.1  Takata classification completed by Epstein Type I Type II Type III Type IV

Many classifications have been developed to better understand the location and type of PRAS for therapeutic purposes (Fig. 27.2; Tables 27.1 and 27.2). The association of PRAS and LDH has been increasingly accepted as a significant contributor to low back pain and lumbosacral radicular symptoms. Also, some cases may induce lumbar spinal stenosis and sometimes present with cauda equina syndrome. As we have already noticed, histological examination of the bony fragment shows fibrocartilaginous tissue containing

Avulsion fractures of the posterior cortical rim Central cortical and cancellous fragments Lateralized chip fracture bodies Extending across entire vertebral bodies

Table 27.2  Our personal classification Type I

Type II Stage A Stage B

The bony fragment adjacent to the disk was partially separated from the posterior edge of the vertebral body (the osseous fragment still hinged to the body of the vertebra) The bony fragment was completely separated from the posterior edge of the vertebral body. The bony fragment can be central, lateral, foraminal, and even extraforaminal Disk material was displaced to the posterior margin of the bony fragment Disk material was displaced beyond the posterior margin of the bony fragment

27.3 Imaging Features

375

may present with painful reactive scoliosis, where the PRAS/ LDH is typically on the same side of the convexity of lumbar scoliosis. Pediatric populations with PRAS/LDH tend to have a greater limitation of movement than adults. Neurological signs include motor weakness in the lower extremities and/or sensory defect and loss of deep tendon reflexes according to the radicular nerves involved. The straight leg raising is usually found and was often less than 60°, especially in the pediatric age group. Cauda equina syndrome is rare. However, it seems that the symptoms of patients with PRAS are more painful and severe than those with LDH alone due to the hard apophysis fragment.

27.3 Imaging Features Fig. 27.3  Microscopic image of a posterior ring apophysis fragment (PRAS) showing a compact bone material with areas of bone necrosis (arrows). Note the normal bone appearance in the periphery (stars) (hematoxylin–eosin stain, original magnification ×40). (Courtesy of Pr. Mohamed Amine Azami)

The most important diagnostic features are the border defect of the posterior vertebral body and the osseous fragment near the edge of the endplate. According to the size, location, and relationship of the bony fragment in comparison with the posterior edge of the vertebral body, the PRAS can be as follows: • • • • •

Fig. 27.4  Histopathological appearance of a PRAS. Fibrocartilaginous tissue and areas of necrotic bone (arrow) without osteoblastic formations (hematoxylin–eosin stain, original magnification ×100)

small portions of sequestered bone without osteoblastic formations (Figs. 27.3 and 27.4).

27.2 Clinical Presentations Clinical presentations of patients with PRAS, combined or not with LDH, are generally similar to those encountered in patients with LDH alone, including intractable low back pain and uni- or bilateral lumbosacral radiculopathy. Some patients may present intermittent claudication when lumbar spinal stenosis exists. Physical examination findings include paravertebral muscle spasm and tenderness. Classically, many young patients

Small or large. Central, lateral, foraminal, or even extraforaminal. Attached or separated. Superior or inferior endplate. One or multiple levels.

Thus, variable combinations are possible. These findings are often occult on plain radiography, often being missed because of the very small size of the fragment or lack of familiarity with this entity. However, postural abnormalities are will assessed on X-ray examination. Computed tomography (CT) scans with sagittal reconstructions are the procedure of choice for diagnosing and should always be considered if a clinically suspected PRAS is not demonstrated on magnetic resonance imaging (MRI). The “Bitten apple appearance” on the axial bone window CT scan is highly suggestive of PRAS (Fig. 27.5). CT scans provide the best delineation of the bony defect in the vertebral body, the bone fragment impinging on the lumbar canal, and the associated posterior disk herniation (Figs. 27.6, 27.7, 27.8, 27.9, 27.10, 27.11, and 27.12). Some cases may be associated with Scheuermann’s disease. MRI is a less accurate method to visualize PRAS because it is difficult to distinguish the bone fragment from the low signal intensity of the disk or the posterior longitudinal ligament. Less than 25% of PRAS lesions are identified on MRI (Figs. 27.13, 27.14, 27.15, 27.16, and 27.17). On axial and sagittal MR imaging, the bony fragment appears as a hyposignal area protruding into the spinal canal. On sagittal MRI, the displaced fragment may form a Y- or 7-shaped con-

376

a

27  Posterior Ring Apophysis Separation

b

c

Fig. 27.5  Photograph of a bitten apple (a). Note that most posterior ring apophysis separations are associated with a “bitten apple sign” on CT scan as seen on axial views on both parenchymal (b) and bone (c) windows

b

a

d

e

c

f

Fig. 27.6  According to the size and location of the bony fragment in comparison with the posterior edge of the vertebral body, the PRAS (arrows) can be small (a–c) or large (d–f), as well as central (a, d), lateral (b, e), or foraminal (c, f). Axial CT scan on parenchymal windows (a–f)

27.3 Imaging Features

377

a

b

c

d

e

f

Fig. 27.7  Large forms of lumbosacral posterior ring apophysis separation (arrows) may induce true lumbar spinal stenosis. Axial CT scan on parenchymal windows (a–f)

a

b

Fig. 27.8  According to the location of the bony fragment in comparison with the posterior edge of the vertebral body, the PRAS (arrows) can be attached (a) or separated (b–d), from the superior (b, d) or infe-

c

d

rior endplate (c, d), solitary (a–c), or multiple (d). Sagittal reconstruction CT scan on bone windows (a–d)

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27  Posterior Ring Apophysis Separation

a

b

c

d

e

Fig. 27.9  Posterior ring apophysis separation of the L5 superior endplate (arrowheads) with concomitant L4–L5 disk herniation (arrows) in a 27-year-old man. Lumbar sagittal reconstruction (a) and axial CT scan (b–d)

figuration, elevating an intact posterior longitudinal ligament. MRI also shows a prolapsed intervertebral disk and any associated nerve root compression, useful for guiding surgical decisions and intervention. LDH remains subligamentous in most cases, whereas extruded disks are rare. On spinal imaging, PRAS may be radiologically confused with other diseases such as the following: • Posterior longitudinal ligament calcification or ossification (Fig. 27.18). • Ankylosing Spondylitis (Figs. 27.19 and 27.20). • Discal calcification (Fig. 27.21). • Posterior degenerative ridge osteophytes (Fig. 27.22). • Spondylodiscitis (Fig. 27.23).

• Vertebral body fractures (Fig. 27.24). • Posterior Schmorl’s node (This node is named after the German pathologist Christian Georg Schmorl (1861– 1932) who first described them in 1927). • Some osteoblastic or cartilaginous tumors such as osteochondroma. Lumbar intervertebral disk calcification (AKA discal calcification) is a non-specific radiological finding encountered in various conditions (Table 27.3). This may occur in isolation or in conjunction with other sites of spinal or extraspinal calcification. This phenomenon can involve either the central part (nucleus pulposus) or the peripheral part (annulus fibrosus) of the disk or both.

27.3 Imaging Features

379

a

b

c

d

Fig. 27.10  Posterior ring apophysis separation of the L5 superior endplate (arrows) in a 41-year-old man. Lumbar sagittal reconstruction (a, b) and axial CT scan (c, d)

380

27  Posterior Ring Apophysis Separation

a

b

c

d

Fig. 27.11  Right-sided subarticular posterior ring apophysis separation of the L4 inferior endplate (arrows) in a 53-year-old woman. Lumbar axial CT scan on parenchymal (a, b) and bone (c, d) windows

27.3 Imaging Features

381

a

b

c

Fig. 27.12  Right-sided foraminal posterior ring apophysis separation of the L5 superior endplate (arrows) in a 44-year-old man. Lumbar axial CT scan on parenchymal (a, b) and bone (c) windows Fig. 27.13 Case A. Concomitant L3–L4 and L4–L5 PRAS (arrows) in this 38-year-old patient as seen on sagittal (a) and axial (b, c) T2-weighted MR imaging

a

b

c

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27  Posterior Ring Apophysis Separation

a

b

c

Fig. 27.14  Case A. Double lumbar PRAS (arrows) in the same patient as seen on sagittal reconstruction (a) and axial (b, c) CT scan

27.3 Imaging Features

a

383

b

c

d

Fig. 27.15  Case B. Lumbar sagittal T1-weighted (a) and T2-weighted (b) MRI and axial T2-weighted MRI (c, d) showing a monosegmental L3–L4 spinal stenosis with a concomitant adjacent central disk hernia-

tion and a posterior ring apophysis separation of the L4 inferior endplate (arrows) in a 16-year-old patient

384

27  Posterior Ring Apophysis Separation

a

b

c

Fig. 27.16  Case B. Lumbar sagittal reconstruction (a) and axial CT scan (b, c) showing the posterior ring apophysis separation of the L4 inferior endplate (arrows) misdiagnosed as a “calcified” L4–L5 disk herniation

27.3 Imaging Features

a

385

b

d

c e

Fig. 27.17  Sagittal (a) and axial (b, c) T2-weighted MRI as well as sagittal reconstruction (d) and axial (e) CT scan in a 48-year-old man with left-sided sciatica. Initially, the MRI had shown an L3–L4 disk

herniation (a, b) (arrows); however, there was a posterior ring apophysis separation on CT scan (c, d) (arrows)

386

27  Posterior Ring Apophysis Separation

a

b

c

d

e

Fig. 27.18  Sagittal T2-weighted MRI (a) and reconstruction CT scan (b) and axial T2-weighted MR imaging (c) and CT scan images (d, e) showing ossification of the posterior longitudinal ligament on L4–L5

and L5–S1 in a 53-year-old woman (arrows). The ossification was seen to compress the thecal sac anteriorly, medially, and laterally

27.3 Imaging Features

a

387

b

c

d

Fig. 27.19  Ankylosing spondylitis with diffuse anterior (curly brackets) and posterior (arrows) spinal ligamentous calcifications/ossifications in a 56-year-old man as seen on sagittal (a, b) and axial (c, d) CT

scan. Note the sclerosis and proliferation on the iliac side of the sacroiliac joints (stars) (d)

388

27  Posterior Ring Apophysis Separation

a

c

b

d

Fig. 27.20  Intervertebral disk calcifications in a 54-year-old man with ankylosing spondylosis (arrows). Sagittal lumbosacral CT scan on parenchymal (a) and bone windows (b) and on axial views (c, d)

a

c

d

b

Fig. 27.21  L4–L5 intervertebral disk calcification in an adult man (idiopathic calcified nucleus pulposus) (arrows). Axial lumbosacral CT scan on parenchymal (a) and bone windows (b) and on coronal (c) and sagittal reconstructions images (d)

27.3 Imaging Features

a

c

389

b

d

Fig. 27.22  L4–L5 posterior degenerative ridge osteophytes (arrows) causing central spinal stenosis in a 45-year-old man as seen on sagittal reconstruction (a) and axial (b–d) CT scan

390

a

27  Posterior Ring Apophysis Separation

b

d

c

Fig. 27.23  Acute L4–L5 spondylodiscitis (arrows) with concomitant anterior epidural abscess (star) as seen on lumbosacral sagittal (a) and axial (b) T2-weighted MRI and on axial (c) and sagittal reconstruction (d) CT scan

27.4 Treatment Options and Prognosis Fig. 27.24 Pathological osteoporotic vertebral fracture of L4 with spinal canal compromise (arrows) in a 62-year-old woman as seen on lumbosacral sagittal reconstruction CT scan on bone windows (a, b)

a

Table 27.3  Main etiologies of intervertebral lumbar disk calcification – Degenerative –  Ring apophysis separation – Postoperative – Post-traumatic –  Ochronosis (nucleus pulposus calcification with osteopenia) –  Axial spondyloarthritis –  Chondrocalcinosis or pseudogout – Hemochromatosis –  Hypervitaminosis D –  Juvenile idiopathic arthritis – Amyloidosis – Poliomyelitis – Acromegaly – Hyperparathyroidism

27.4 Treatment Options and Prognosis In the absence of neurological deficits, conservative management is typically the primary therapeutic intervention in patients with PRAS. This consists of bed rest, analgesic and anti-inflammatory medications, physical therapy, lumbar

391

b

bracing (rarely), and limitation of physical activities. If conservative therapy is unsuccessful or persistent low back pain unfavorably compromises the patient’s daily activities, regardless of existing neurological deficits, the need for surgical decompression is highlighted. Few authors debate the value of nonoperative treatment for this disease. Nevertheless, we have already documented that the bony fragment will eventually resorb with time (Figs. 27.25 and 27.26). Some other authors suggested that “the fracture” could heal with residual bony lumbar spinal stenosis. Due to its rarity and diversity of classification modality, there is a lack of an agreed treatment strategy, and many ­different attitudes exist, including the choice of decompressive modalities, whether removal of apophyseal fragments or/and LDH, and the necessity of further spinal fusion. Overall, clinicians should always consider spinal growth and the timing of spinal maturity when managing the pediatric spine. An enlarged laminectomy field and foraminotomy are helpful to define the anatomy and delimit the lesion. It is preferable to explore the nerve root and the dura using

392

27  Posterior Ring Apophysis Separation

a

b

c

d

Fig. 27.25  Case C. Spontaneous regression of an L5–S1 posterior ring apophysis separation (arrows) as seen on axial (a, b) CT scan and 2 years after the initial CT scan (c, d) in a 50-year-old woman

a

b

c

Fig. 27.26  Case C. Spontaneous regression of the L5–S1 PRAS (arrows) as seen on sagittal reconstruction CT scan (a, b) and 2 years later in the same patient (c, d)

27.4 Treatment Options and Prognosis

393

microsurgical technics to avoid further neurological damage. Endoscopic and minimally invasive approaches are undesirable, especially in patients with large apophyseal fragments. We propose that a type I PRAS (with immobile fragments) must be left alone (only decompression can be achieved), whereas a type II PRAS (with mobile fragments) must be excised. The main cause of acute typical sciatica in type I PRAS seems to be the herniated disk rather than the bony fragment, particularly in stage B. Sometimes transaxillary dissection is required to relieve nerve impingement. Some authors may start by identification and resection of disk material and entry into the interspace to facilitate access to the osseous apophyseal fragment. For some Japanese surgeons, complete and safe resection of bony fragments is facilitated by impacting and separating the PRAS from the posterior vertebral body margin by using a shoe-shaped impactor that allows protection of both nerve root sleeves and thecal sac.

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PRAS located laterally can be excised together with the disk via a unilateral approach, but for a lesion located centrally and significantly occupying the central lumbar canal space, decompression can be performed using bilateral piecemeal excision or even laminectomy (Figs. 27.15, 27.16, 27.27, 27.28, 27.29, 27.30, and 27.31). Microdrill can be used to remove bone fragments. To avoid iatrogenic spinal instability, posterolateral arthrodesis may be used in some cases when an extensive bilateral laminectomy is achieved (Figs. 27.32 and 27.33). Concerning intraoperative and postoperative complications (especially new postoperative neurological deficits and dural tears), the rate is consistent with those in patients with LDH alone. Almost all patients surgically treated for PRAS showed good-to-excellent results in up to 80%. However, patients with large apophyseal fragments and those with severe preoperative neurological deficits had a greater chance of poor results. The existence of PRAS was not associated with recurrent LDH.

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Fig. 27.27  Case B. Intraoperative view of the central posterior apophysis ring fragment (arrow) following bilateral L4 laminectomy (a). Operative view after PRAS fragment removal (b). PRAS fragment appearance (c)

394 Fig. 27.28 Case B. Postoperative CT scan after L4–L5 PRAS removal. Lumbar sagittal reconstruction (a) and axial CT scan (b, c)

27  Posterior Ring Apophysis Separation

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27.4 Treatment Options and Prognosis

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Fig. 27.29  Case D. Right-sided lateral posterior ring apophysis separation of the S1 superior endplate (arrows). Lumbosacral sagittal reconstruction (a, b) and axial (c, d) CT scan on parenchymal (b, d) and bone (a, c) windows

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Fig. 27.30  Case D. Intraoperative view of the lateral posterior apophysis ring fragment (star) following an enlarged L5–S1 interlaminar approach on the right side. Operative view before (a) and after PRAS fragment removal (b)

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Fig. 27.31  Enlarged L4–L5 interspinous approach for a large central posterior apophysis ring fragment (arrows) (a–d). Preoperative axial CT scan (a). Note the L4–L5 yellow ligaments (arrowheads) (b), the

thecal sac appearance after bilateral flavectomy (curly bracket) (c), and the disk space (star) after PRAS removal (b)

27.4 Treatment Options and Prognosis

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Fig. 27.32  Case E. This 23-year-old man came to our medical clinic for back pain and bilateral sciatica without any neurological deficit. Lumbar spinal MRI showed a T12–L1 posterior ring apophysis separa-

tion, a concomitant adjacent disk herniation, and a monosegmental central spinal stenosis (arrows). Sagittal T1-weighted (a) and T2-weighted MRI (b) and axial T2-weighted MRI (c, d)

398 Fig. 27.33 Case E. Postoperative anteroposterior (a) and lateral (b) thoraco-lumbar plain radiography following extensive bilateral posterior decompression and screw-rod fixation system

27  Posterior Ring Apophysis Separation

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Further Reading Akhaddar A.  Letter to the Editor regarding “Transforaminal endoscopic discectomy for hard or calcified lumbar disc herniation: a new surgical technique and clinical outcomes”. World Neurosurg. 2020;144:316–7. https://doi.org/10.1016/j.wneu.2020.07.202. Akhaddar A, Belfquih H, Oukabli M, Boucetta M. Posterior ring apophysis separation combined with lumbar disc herniation in adults: a 10-year experience in the surgical management of 87 cases. J Neurosurg Spine. 2011;14:475–83. https://doi.org/10.3171/2010.11. SPINE10392. Akhaddar A, Belabyad S.  Spontaneous regression of posterior ring apophysis separation in lumbar spine. World Neurosurg. 2018;119:304–5. https://doi.org/10.1016/j.wneu.2018.08.062. Akhaddar A, Boucetta M. Combined lumbar retroisthmic cleft and posterior ring apophysis separation in an adult. Spine J. 2012;12:716–7. https://doi.org/10.1016/j.spinee.2012.06.012. Alagheband SJ, Clapp AD, Narducci DM, Cudahy R, Pujalte G. Limbus vertebra. Cureus. 2021;13:e13954. https://doi.org/10.7759/ cureus.13954. Albeck MJ, Madsen FF, Wagner A, Gjerris F. Fracture of the lumbar vertebral ring apophysis imitating disc herniation. Acta Neurochir (Wien). 1991;113:52–6. https://doi.org/10.1007/BF01402115. Alvarenga JA, Ueta FT, Del Curto D, Ueta RH, Martins DE, Wajchenberg M, Puertas EB. Apophyseal ring fracture associated with two levels extruded disc herniation: case report and review of the literature. Einstein (Sao Paulo). 2014;12:230–1. https://doi.org/10.1590/ s1679-­45082014rc2736. Asazuma T, Nobuta M, Sato M, Yamagishi M, Fujikawa K.  Lumbar disc herniation associated with separation of the posterior ring

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a­ pophysis: analysis of five surgical cases and review of the literature. Acta Neurochir (Wien). 2003;145:461–6. https://doi.org/10.1007/ s00701-­003-­0044-­z. Baba H, Uchida K, Furusawa N, Maezawa Y, Azuchi M, Kamitani K, et al. Posterior limbus vertebral lesions causing lumbosacral radiculopathy and the cauda equina syndrome. Spinal Cord. 1996;34:427– 32. https://doi.org/10.1038/sc.1996.76. Bae JS, Rhee WT, Kim WJ, Ha SI, Lim JH, Jang IT. Clinical and radiologic analysis of posterior apophyseal ring separation associated with lumbar disc herniation. J Korean Neurosurg Soc. 2013;53:145– 9. https://doi.org/10.3340/jkns.2013.53.3.145. Chang CH, Lee ZL, Chen WJ, Tan CF, Chen LH. Clinical significance of ring apophysis fracture in adolescent lumbar disc herniation. Spine (Phila Pa 1976). 2008;33:1750–4. https://doi.org/10.1097/ BRS.0b013e31817d1d12. Costa L, de Reuver S, Kan L, Seevinck P, Kruyt MC, Schlosser TPC, et al. Ossification and fusion of the vertebral ring apophysis as an important part of spinal maturation. J Clin Med. 2021;10:3217. https://doi.org/10.3390/jcm10153217. Epstein NE. Lumbar surgery for 56 limbus fractures emphasizing noncalcified type III lesions. Spine (Phila Pa 1976). 1992;17:1489–96. https://doi.org/10.1097/00007632-­199212000-­00008. Epstein NE, Epstein JA. Limbus lumbar vertebral fractures in 27 adolescents and adults. Spine (Phila Pa 1976). 1991;16:962–6. https:// doi.org/10.1097/00007632-­199108000-­00017. He JT, Chen JW, Wei P. Surgical treatment for posterior rim separation of the lumbar and sacral vertebrae. Orthop Surg. 2013;5:177–82. https://doi.org/10.1111/os.12053. Huang PY, Yeh LR, Tzeng WS, Tsai MY, Shih TT, Pan HB, Chen CK. Imaging features of posterior limbus vertebrae. Clin Imaging. 2012;36:797–802. https://doi.org/10.1016/j.clinimag.2012.01.031.

Further Reading Inoue T, Inokuchi A, Izumi T, Imamura R, Hamada T, Nakamura K, Ebihara T, Inoue H, Kuroki Y, Arizono T. Co-existence of lumbar disc herniation and posterior ring apophyseal fracture: it is not rare and computed tomography is useful. Cureus. 2023;15:e35475. https://doi.org/10.7759/cureus.35475. Kadam G, Narsinghpura K, Deshmukh S, Desai S. Traumatic lumbar vertebral ring apophysis fracture with disk herniation in an adolescent. Radiol Case Rep. 2017;12:427–30. https://doi.org/10.1016/j. radcr.2016.11.026. Leroux JL, Fuentes JM, Baixas P, Benezech J, Chertok P, Blotman F.  Lumbar posterior marginal node (LPMN) in adults. Report of fifteen cases. Spine (Phila Pa 1976). 1992;17:1505–8. https://doi. org/10.1097/00007632-­199212000-­00011. Lowrey JJ.  Dislocated lumbar vertebral epiphysis in adolescent children. Report of three cases. J Neurosurg. 1973;38:232–4. https:// doi.org/10.3171/jns.1973.38.2.0232. Martínez-Lage JF, Poza M, Arcas P.  Avulsed lumbar vertebral rim plate in an adolescent: trauma or malformation? Childs Nerv Syst. 1998;14:131–4. https://doi.org/10.1007/s003810050195. Matsumoto M, Watanabe K, Tuji T, Ishii K, Takaishi H, Nakamura M, et al. Microendoscopic discectomy for lumbar disc herniation with bony fragment due to apophyseal separation. Minim Invasive Neurosurg. 2007;50:335–9. https://doi.org/10.1055/s-­2007-­993202. Mendez JS, Huete IL, Tagle PM.  Limbus lumbar and sacral vertebral fractures. Neurol Res. 2002;24:139–44. https://doi. org/10.1179/016164102101199675. Okada M, Yoshida M, Minamide A, Nomura K, Maio K, Yamada H.  Microendoscope-assisted decompression surgery with resection of bony fragment for treating a separation of lumbar posterior ring apophysis in young athletes. Global Spine J. 2021;11:889–95. https://doi.org/10.1177/2192568220929290.

399 Scarfò GB, Muzii VF, Mariottini A, Bolognini A, Cartolari R. Posterior retroextramarginal disc hernia (PREMDH): definition, diagnosis, and treatment. Surg Neurol. 1996;46:205–11. https://doi. org/10.1016/0090-­3019(96)00154-­1. Seo YN, Heo YJ, Lee SM. The characteristics and incidence of posterior apophyseal ring fracture in patients in their early twenties with herniated lumbar disc. Neurospine. 2018;15:138–43. https://doi. org/10.14245/ns.1836002.001. Skobowytsh-Okolot B. “Posterior apophysis” in L.IV—the cause of neuroradicular disturbance. Acta Orthop Scand. 1962;32:341–51. https://doi.org/10.3109/17453676208989592. Von Meyenburg H.  About separation of the posterior vertebral body edge as the cause of sciatica. Radiol Clin. 1946;15:215–24. Wu X, Ma W, Du H, Gurung K. A review of current treatment of lumbar posterior ring apophysis fracture with lumbar disc herniation. Eur Spine J. 2013;22:475–88. https://doi.org/10.1007/s00586-­012-­ 2580-­9. Wu XY, Ma W. Posterior lumbar ring apophysis fracture. Orthop Surg. 2011;3:72–7. https://doi.org/10.1111/j.1757-­7861.2010.00122.x. Yuan S, Wu Q, Zang L, Fan N, Du P, Wang A, Wang T, Si F, Li J, Kong X.  Posterior apophyseal ring fracture in adult lumbar disc herniation: an 8-year experience in minimally invasive surgical management of 48 cases. Neurospine. 2022;19:586–93. https://doi. org/10.14245/ns.2244346.173. Zheng ZZ, Tu Z, Li Y, Dai Y, Wu PF, Jiang B, et al. Full-endoscopic lumbar discectomy for lumbar disc herniation with posterior ring apophysis fracture: a retrospective study. World Neurosurg. 2018:S1878-8750(18)32877–8. https://doi.org/10.1016/j. wneu.2018.12.054.

Recurrent Lumbar Disk Herniations

28.1 Generalities and Relevance The definition of recurrent lumbar disk herniation (R-LDH) means the presence of herniated disk material at the same intervertebral level, homolateral (on the same side) or contralateral (on the opposite side), in a patient who has undergone discectomy and experienced a pain-free interval of at least 6 months since the surgical procedure. However, many other definitions exist. For some authors, “real” R-LDH is the occurrence of herniated disk material at the same side and level as the previously operated disk herniation. For others, the pain-free interval should not be restricted to a minimum of 6 months but one year or even 18 months. It is well known that re-herniation is the primary cause of surgical failure and morbidity in patients treated with a lumbar discectomy (c.f. Chap. 76 about Postoperative Spinal Etiologies of Sciatica). In 1938, J Grafton Love (1903–1987) and Maurice Walsh published their results in 100 patients operated on for an LDH, and for the first time, they reported a case of re-­ herniation and the concept of herniated disk recurrence. Nowadays, the rate of recurrent LDH varies from 5 to 25%. This great range may reflect surgical technique used, variability in follow-up, and diverse definitions of recurrence as specified before. The higher rate is reported in series with longer follow-ups. More than one recurrence is rare not exceeding 2% of all operated cases. Some factors may increase the risk of postoperative recurrence of LDH including the following: • • • • • •

Age (especially between 40 and 50 years old). Smoking. Obesity: body mass index >25 kg/m2. Diabetes mellitus. Type of disk herniation: especially disk protrusion. Biomechanical factors (more range of motion especially when sagittal motion >10° and lower preoperative disk height index).

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• Factors related to the primary discectomy (larger annular defects and limited discectomy during primary surgery. • Presence of lumbosacral transitional vertebrae. Before any therapeutic management, medical practitioners should distinct between disk recurrence, postoperative epidural fibrosis, neural scarring, residual disk herniation, and bone hypertrophy, or osteophytosis. Reoperation for R-LDH can present a formidable challenge due to spinal root scarring and epidural fibrosis. Furthermore, revised surgery leads to additional physical and psychological suffering for patients and considerable expenses for society.

28.2 Clinical Presentations As with other presentations of LDH, the initial evaluation should include a sufficient and detailed history and a neurologic, spinal, and somatic examination. Regarding the timing, approximately 50% of all R-LDH occur within the first year following the surgical procedure. However, recurrence may occur as long as 8 years after the primary discectomy. An early recurrence of LDH within 30 days of discharge after a primary discectomy is more related to persistent herniated disk material than a true LDH. Clinical presentations of R-LDH are normally comparable to those encountered in patients with the Novo (first-­ time) herniated disk. However, in some cases, there is persistent low back pain or radicular pain according to the radicular nerves involved. Some patients may present intermittent claudication when lumbar spinal stenosis coexists. Sometimes, the symptoms are more painful and severe than those presented prior to the first decompression surgery. For many authors, the severity of spinal and neurological symptoms did not have a strong correlation with the size of the re-herniated disk material.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_28

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Some diagnoses should be suspected as the cause of persistent or recurrent low back pain or sciatica in any patient who has undergone a previous discectomy such as epidural fibrosis, neural scarring, persistent herniated disk material, adhesive arachnoiditis, iatrogenic spinal instability, discitis and/or osteomyelitis, nerve root injury, and postoperative granuloma.

To identify postoperative pathological changes, radiologists and treating practitioners must be familiar with changes appropriate to early (6 months). A pseudo-mass lesion appearance at the area of previous surgery is a common non-pathological finding, especially in the early postoperative period (before 6  months). Nerve root enhancement with gadolinium is normal before 6 months. Adhesions within the dural sac at the surgical level generally disappear within several 28.3 Imaging Features weeks. Pathological modifications of the anterior epidural space Many modalities have been used to assess the lumbar spine can reflect mass effect due to scarring/fibrosis or the disk following surgical procedures. However, post-gadolinium-­ material. The distinction between these two entities is fundaenhanced magnetic resonance imaging (MRI) is still the gold mental in selecting the best appropriate treatment option. standard for diagnosing R-LDH. Other sequences have been Indeed, scarring and fibrosis often will not benefit from surproposed to increase the sensitivity and specificity of MRI gery but the re-herniated disk may. Both have similar signal such as fat saturation, T2-weighted turbo–spin echo, turbo intensities on no-gadolinium T1-weighted MRI in the late fluid-attenuated inversion recovery, short-tau inversion postoperative phase (after 6  months). However, scarring recovery, and differing contrast media. often displays intermediate signal intensity and may be If needed, computed tomography (CT) scan with axial hypointense after 2-year period postoperatively. Scarring images and sagittal reconstructions on bone windows are and fibrosis enhance heterogeneously due to their blood important to provide the best delineation of the bony and cal- supply. cified lesions and other degenerative changes (Figs. 28.1 and The re-herniated disk usually appears as a polypoid mass 28.2). CT scan has also a role in surgical planning. hypointense on both T1- and T2-weighted sequences. It is

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Fig. 28.1  Axial lumbar spinal CT scan (a, b) showing a central L4–L5 disk herniation (yellow arrows) in a 47-year-old patient operated on 18 months earlier for an L4–L5 disk herniation via a left-sided L4–L5 interlaminar approach (black arrows)

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Fig. 28.2  Recurrent central L4–L5 disk herniation with compressive gas pseudocysts (arrows) in a 56-year-old patient operated on one year earlier for an L4–L5 disk herniation with central spinal stenosis. Lumbosacral sagittal reconstruction (a, b) and axial (c, d) CT scan

commonly adjacent and in continuity with its original intervertebral disk unless sequestrated or migrated. There is often a hypointense rim of the posterior longitudinal ligament delineating the recurrent disk, enhancing following post-­ gadolinium injection. The intervertebral disk itself does not enhance because it has no vascular supply (Figs. 28.3, 28.4, 28.5, 28.6, 28.7, 28.8, 28.9, 28.10, 28.11, 28.12, 28.13, 28.14, 28.15, and 28.16). Retraction of the thecal sac in the direction of a soft-tissue lesion is suggestive of a scar, whereas displacement away from such a mass is suggestive of a herniated disk. Diagnosis is more difficult when there is compressive profuse epidural fibrosis.

It is well known that the correlation between the degree of persistent or recurrent postoperative clinical symptomatology and results of postoperative spinal imaging is poorly specific in nature and is difficult to interpret due to the existence of other factors besides pure mechanical compression such as inflammatory and/or vascular phenomena. In addition, discordance between neuroimaging and intraoperative findings is more common than expected, occurring in up to one-third of the cases confirmed intraoperatively. Overall, therapeutic management is principally guided by characteristics of the primary preoperative imaging, elements from the previous operative report, and the patient clinical presentation.

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Fig. 28.3  Recurrent right-sided L5–S1 disk herniation at the same level and the same side (arrows) 14 months following discectomy for discogenic sciatica in a 35-year-old man. Axial (a) and sagittal

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T1-weighted MRI before (b) and after (c) gadolinium injection and on T2-weighted MRI (d)

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Fig. 28.4  Case A. Recurrent central L4–L5 disk herniation at the same level and the same side (arrows) 12 months following discectomy for right-sided discogenic sciatica. Sagittal T1-weighted (a) T2-weighted

Fig. 28.5  Case A (The same case as in Fig. 28.4). Photograph showing the disk fragment that was removed (herniated disk material) and the discectomy material (right)

MRI (b) and on axial T2-weighted MRI (c–e). Note the two S1 nerve roots (yellow circles)

406 Fig. 28.6  Case B. This 51-year-old man was operated on for a central L5–S1 disk herniation (arrows) with a good outcome. Sagittal (a) and axial (b) T2-weighted MRI

Fig. 28.7  Case B. Recurrent right-sided sciatic pain 4 months later. Sagittal (a) and axial (b) T2-weighted postoperative MRI showing a recurrent L5–S1 disk herniation (arrows)

28  Recurrent Lumbar Disk Herniations

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28.3 Imaging Features Fig. 28.8  Recurrent central L5–S1 disk herniation at the same level (arrows) 3 years following discectomy for discogenic sciatica in a 48-year-old woman. Sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted MRI (c, d). Note the asymmetrical paraspinal muscle morphology (stars) indicating asymmetrical muscle innervation and/or activity

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Fig. 28.9  Sciatic pain recurrence on the left side in a 50-year-old woman previously operated on for L5 spinal stenosis (L5 bilateral laminectomy). Sagittal (a) and axial (b) T2-weighted MRI showing a recurrent central/paracentral L4–L5 disk herniation (arrows)

408 Fig. 28.10  Sciatic pain recurrence on the right side in a 61-year-old man previously operated on for L4–L5 spinal stenosis (L4–L5 bilateral laminectomy—curly brace). Sagittal (a) and axial (b, c) T2-weighted MRI showing a recurrent central/right paracentral L4–L5 disk herniation (arrows)

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Fig. 28.11  Recurrent L4–L5 disk herniation as seen on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted MRI (c, d). The disk fragment was migrated rostrally (arrows) to the L4–L5 intervertebral space behind the posterior vertebral wall of L4 Fig. 28.12  Recurrent right subarticular L5–S1 disk herniation at the same level and the same side (arrows) 14 months following discectomy for discogenic sciatica. Sagittal (a) and axial (b, c) T2-weighted MR imaging. Note the two S1 nerve roots (yellow circles)

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Fig. 28.13  This 37-year-old woman was operated on for an L4–L5 left-sided discogenic sciatica. Re-herniation occurred about 2 years later at the same level and at the same side (arrows) as shown on sagittal T1-weighted (a) and T2-weighted MRI (b) and on axial T2-weighted MRI (c, d)

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Fig. 28.14  This 43-year-old patient was operated on for an L4–L5 left-sided discogenic sciatica (the black arrows show the previous interlaminar approach). Re-herniation occurred one year later at the same

level and at the same side (arrows) as shown on sagittal (a, b) and axial (c, d) T2-weighted MR imaging

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Fig. 28.15  Recurrent giant L4–L5 disk herniation (yellow arrows) in a 56-year-old man operated via a left-sided L4–L5 interlaminar approach (black arrows) 2 years earlier. Lumbosacral sagittal (a, b) and axial (c, d) T2-weighted MR imaging

28.4 Treatment Options and Prognosis Fig. 28.16  Recurrent L5–S1 disk herniation (yellow arrows) in a 47-year-old man operated 10 years earlier via a left-sided L5–S1 interlaminar approach (black arrows). Lumbosacral sagittal (a) and axial (b, c) T2-weighted MR imaging

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28.4 Treatment Options and Prognosis The key treatment of R-LDH is as with a first-time LDH. The goal is to relieve symptoms, improve quality of life, and prevent further spinal complications. In the absence of progressive neurological deficits, cauda equina syndrome, or intractable pain, conservative management is typically the primary therapeutic intervention in patients with re-herniation of the lumbar disk. This consists of short-term bed rest, analgesic and anti-inflammatory medications, epidural injection, physical therapy, bracing (infrequently), and limitation of heavy physical activities. Nevertheless, it seems that conservative measures are not as effective for patients with R-LDH as they are for those with primary LDH. When conservative measures fail to show improvement, some patients with R-LDH are indicated for revision surgery. Various types of surgical procedures have been described for reoperation. These include revision discectomy (open dis-

cectomy or microscopic discectomy) with or without fusion. This is a technically demanding task due to the indistinguishable dissection plane between neural and fibrous/scar tissues. Consequently, the risk of complications may increase, which also may concern the clinical outcomes. The traditional surgical technique for recurrence uses more exposure and extensive tissue dissection. Great attention is needed to recognize the bony margins of the previous operative site. Identification and dissection of scar and fibrosis from the dura mater and the nerve root(s) are significantly supported by using a microscope. Sometimes the nerve root may be mistaken for the annulus fibrosis through which the nucleus pulposus is ­considered to be herniated out and can be imprudently incised. Anatomy should be carefully delineated further. It is usually easier to dissect laterally in the lumbar canal and work medially. If the doubt persists, it is preferable to perform a very lateral discectomy in order to gain more space and achieve a first indirect decompression. Once this relative decompression

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has been obtained, the nerve root will be better visualized and mobilized medially allowing the removal of the disk fragment. Then, the discectomy can be secondarily completed. For all these reasons, microendoscopic and other mininvasive techniques are not recommended by many authors. Classically, a scar or fibrosis does not benefit from reoperation and in fact may result in worse outcomes. Instrumented lumbar interbody fusion is not routinely required unless there is spinal instability or significant deformity. Potential complications consist of an increased incidence of dural tear and CSF fistula, laceration and nerve root injury, an increased incidence of failure to relieve symptoms, and the recurrence of symptoms and postoperative pain. Among all these problems, the dural tear is the most common complication in revision surgery for R-LDH. The dural tear was 2.5–5 times more frequent in revision surgery than in the first surgical procedure for LDH.  Also, subsequent iatrogenic meningitis is not rare and can be life-threatening. Surgical options for R-LDH are limited by various factors, may require longer operative time, and are associated with a higher rate of complications. However, reoperation seems to be associated with a similar chance of good clinical outcome comparable with that achieved following initial discectomies. For some authors, patients undergoing reoperation had good postoperative satisfaction in more than 80% of cases despite the frequency of low back pain and residual leg numbness. Rarely, anterior lumbar microdiscectomy with anterior interbody fusion can be discussed as an alternative for the treatment of some selected patients with multiple recurrent LDH.  Through a laparoscopic or open anterior surgical approach, recurrent herniated disk fragments can be removed and interbody fusion can be completed at the same site. However, this anterior approach has also been associated with the risk of some specific complications such as vascular injury and retrograde ejaculation.

Further Reading Ajiboye RM, Drysch A, Mosich GM, Sharma A, Pourtaheri S. Surgical treatment of recurrent lumbar disk herniation: a systematic review and meta-analysis. Orthopedics. 2018;41:e457–69. https://doi. org/10.3928/01477447-­20180621-­01. Akhaddar A, Oukabli M, Albouzidi A, Boucetta M.  Recurrent lumbosciatica because of cotton granuloma after surgery for lumbar disc herniation. Spine J. 2011;11:363–4. https://doi.org/10.1016/j. spinee.2011.03.002. Anichini G, Landi A, Caporlingua F, Beer-Furlan A, Brogna C, Delfini R, et al. Lumbar endoscopic microdiscectomy: where are we now? An updated literature review focused on clinical outcome, complications, and rate of recurrence. Biomed Res Int. 2015;2015:417801. https://doi.org/10.1155/2015/417801.

28  Recurrent Lumbar Disk Herniations Baba H, Chen Q, Kamitani K, Imura S, Tomita K.  Revision surgery for lumbar disc herniation. An analysis of 45 patients. Int Orthop. 1995;19:98–102. https://doi.org/10.1007/BF00179969. Brooks M, Dower A, Abdul Jalil MF, Kohan S. Radiological predictors of recurrent lumbar disc herniation: a systematic review and meta-­ analysis. J Neurosurg Spine. 2020;34:481. https://doi.org/10.3171/ 2020.6.SPINE20598. Dalal SS, Dupree DA, Samuel AM, Vaishnav AS, Gang CH, Qureshi SA, et al. Reoperations after primary and revision lumbar discectomy: study of a national-level cohort with eight years follow-up. Spine J. 2022;22:1983–9. https://doi.org/10.1016/j.spinee.2022.06.005. Deinsberger W, Wollesen I, Jödicke A, Lenzen J, Böker DK. Long-term socioeconomic outcome of lumbar disc microsurgery. Zentralbl Neurochir. 1997;58:171–6. Dower A, Chatterji R, Swart A, Winder MJ. Surgical management of recurrent lumbar disc herniation and the role of fusion. J Clin Neurosci. 2016;23:44–50. https://doi.org/10.1016/j.jocn.2015.04.024. Drazin D, Ugiliweneza B, Al-Khouja L, Yang D, Johnson P, Kim T, et  al. Treatment of recurrent disc herniation: a systematic review. Cureus. 2016;8:e622. https://doi.org/10.7759/cureus.622. Hlubek RJ, Mundis GM Jr. Treatment for recurrent lumbar disc herniation. Curr Rev Musculoskelet Med. 2017;10:517–20. https://doi. org/10.1007/s12178-­017-­9450-­3. Huang W, Han Z, Liu J, Yu L, Yu X.  Risk factors for recurrent lumbar disc herniation: a systematic review and meta-analysis. Medicine (Baltimore). 2016;95:e2378. https://doi.org/10.1097/ MD.0000000000002378. Isaacs RE, Podichetty V, Fessler RG. Microendoscopic discectomy for recurrent disc herniations. Neurosurg Focus. 2003;15:E11. https:// doi.org/10.3171/foc.2003.15.3.11. Keskimäki I, Seitsalo S, Osterman H, Rissanen P.  Reoperations after lumbar disc surgery: a population-based study of regional and interspecialty variations. Spine (Phila Pa 1976). 2000;25:1500–8. https://doi.org/10.1097/00007632-­200006150-­00008. Kim MS, Park KW, Hwang C, Lee YK, Koo KH, Chang BS, et  al. Recurrence rate of lumbar disc herniation after open discectomy in active young men. Spine (Phila Pa 1976). 2009;34:24–9. https://doi. org/10.1097/BRS.0b013e31818f9116. Landi A, Grasso G, Mancarella C, Dugoni DE, Gregori F, Iacopino G, et  al. Recurrent lumbar disc herniation: is there a correlation with the surgical technique? A multivariate analysis. J Craniovertebr Junction Spine. 2018;9:260–6. https://doi.org/10.4103/jcvjs. JCVJS_94_18. Lee JK, Amorosa L, Cho SK, Weidenbaum M, Kim Y. Recurrent lumbar disk herniation. J Am Acad Orthop Surg. 2010;18:327–37. https://doi.org/10.5435/00124635-­201006000-­00005. Luukkonen MT.  Medial facetectomy in recurrent lumbar nerve root compression. J Spinal Disord Tech. 2005;18:48–51. https://doi. org/10.1097/01.bsd.0000127702.75711.ae. McGirt MJ, Ambrossi GL, Datoo G, Sciubba DM, Witham TF, Wolinsky JP, et al. Recurrent disc herniation and long-term back pain after primary lumbar discectomy: review of outcomes reported for limited versus aggressive disc removal. Neurosurgery. 2009;64:338– 44. https://doi.org/10.1227/01.NEU.0000337574.58662.E2. Murphy TP, Panarello NM, Baird MD, Helgeson MD, Wagner SC. Should annular closure devices be utilized to reduce the risk of recurrent lumbar disk herniation? Clin Spine Surg. 2022;35:187–9. https://doi.org/10.1097/BSD.0000000000001104. Onyia CU, Menon SK. The debate on most ideal technique for managing recurrent lumbar disc herniation: a short review. Br J Neurosurg. 2017;31:701–8. https://doi.org/10.1080/02688697.2017.1368451. Osterman H, Sund R, Seitsalo S, Keskimäki I. Risk of multiple reoperations after lumbar discectomy: a population-based study. Spine (Phila Pa 1976). 2003;28:621–7. https://doi.org/10.1097/01. BRS.0000049908.15854.ED.

Further Reading Quah C, Syme G, Swamy GN, Nanjayan S, Fowler A, Calthorpe D. Obesity and recurrent intervertebral disc prolapse after lumbar microdiscectomy. Ann R Coll Surg Engl. 2014;96:140–3. https:// doi.org/10.1308/003588414X13814021676873. Rogerson A, Aidlen J, Jenis LG. Persistent radiculopathy after surgical treatment for lumbar disc herniation: causes and treatment options. Int Orthop. 2019;43:969–73. https://doi.org/10.1007/s00264-­018-­ 4246-­7. Sebaaly A, Lahoud MJ, Rizkallah M, Kreichati G, Kharrat K.  Etiology, evaluation, and treatment of failed Back surgery syndrome. Asian Spine J. 2018;12:574–85. https://doi.org/10.4184/ asj.2018.12.3.574. Shan ZM, Ren XS, Shi H, Zheng SJ, Zhang C, Zhuang SY, et  al. Machine learning prediction model and risk factor analysis of reoperation in recurrent lumbar disc herniation patients after percutaneous endoscopic lumbar discectomy. Global Spine J. 2023;10:21925682231173353. https://doi. org/10.1177/21925682231173353. Shepard N, Cho W. Recurrent lumbar disc herniation: a review. Global Spine J. 2019;9:202–9. https://doi.org/10.1177/2192568217745063. Shin BJ. Risk factors for recurrent lumbar disc herniations. Asian Spine J. 2014;8:211–5. https://doi.org/10.4184/asj.2014.8.2.211. Shin EH, Cho KJ, Kim YT, Park MH. Risk factors for recurrent lumbar disc herniation after discectomy. Int Orthop. 2019;43:963–7. https:// doi.org/10.1007/s00264-­018-­4201-­7. Siccoli A, Staartjes VE, Klukowska AM, Muizelaar JP, Schröder ML. Overweight and smoking promote recurrent lumbar disk her-

415 niation after discectomy. Eur Spine J. 2022;31:604–13. https://doi. org/10.1007/s00586-­022-­07116-­y. Swartz KR, Trost GR.  Recurrent lumbar disc herniation. Neurosurg Focus. 2003;15:E10. https://doi.org/10.3171/foc.2003.15.3.10. Turgut M, Akhaddar A, Turgut AT. Retention of nonabsorbable hemostatic materials (retained surgical sponge, Gossypiboma, Textiloma, Gauzoma, Muslinoma) after spinal surgery: a systematic review of cases reported during the last half-century. World Neurosurg. 2018;116:255–67. https://doi.org/10.1016/j.wneu.2018.05.119. Vinas-Rios JM, Sanchez-Aguilar M, Medina Govea FA, Von Beeg-­ Moreno V, Meyer F, DWG Registry-Group. Incidence of early postoperative complications requiring surgical revision for recurrent lumbar disc herniation after spinal surgery: a retrospective observational study of 9,310 patients from the German Spine Register. Patient Saf Surg. 2018;12:9. https://doi.org/10.1186/s13037-­018-­ 0157-­1. Wera GD, Marcus RE, Ghanayem AJ, Bohlman HH. Failure within one year following subtotal lumbar discectomy. J Bone Joint Surg Am. 2008;90:10–5. https://doi.org/10.2106/JBJS.F.01569. Yoshihara H, Chatterjee D, Paulino CB, Errico TJ.  Revision surgery for “real” recurrent lumbar disk herniation: a systematic review. Clin Spine Surg. 2016;29:111–8. https://doi.org/10.1097/ BSD.0000000000000365. Zhu F, Jia D, Zhang Y, Ning Y, Leng X, Feng C, et  al. Moderate to severe multifidus fatty atrophy is the risk factor for recurrence after microdiscectomy of lumbar disc herniation. Neurospine. 2023;20:637–50. https://doi.org/10.14245/ns.2346054.027.

29

Discal Cysts

29.1 Generalities and Relevance A discal cyst, also known as a “disk cyst,” is an unusual spinal entity defined as the communication of an intraspinal extradural cyst with the adjacent intervertebral disk. First described in the English literature by Kono et  al. in 1999, approximately 130 cases have been identified to date, exclusively in the lumbar spine. For some authors, discal cysts have some pathological similarities with postoperative discal pseudocysts. Most cases developed in the anterolateral lumbar epidural space, at a single level (mainly L4–L5) and unilateral. They may result in low back and lumbosacral radicular pain like more symptomatic typical lumbar disk herniation (LDH). The majority of discal cysts are described in males (about 90%) in their third or fourth decade of life (mean age of 33 years). Interestingly, patients of Asian ethnicity have an increased risk to develop a discal cyst. In histopathology study, the cysts contain clear serous or mucous fluid with a dense collagenous fibrous wall. Myxoid degeneration may also be seen, but there is no disk material inside the cyst. Unlike synovial cysts, there are no epithelial or synovial layers on the cystic wall. Nevertheless, the cyst fluid may contain sometimes gas or blood. All these characteristics are similar to those found in posterior longitudinal ligament cysts, but the latter does not communicate with the adjacent intervertebral disk. The etiology of discal cysts remains unclear, but three theories for the formation of these cysts have been suggested: (a) An excessive or persistent mechanical strain induces a focal degeneration of the lumbar posterior disk wall which produces a fluid collection. This collection will be surrounded by a pseudo-membrane formation and finally subsequent development of the disk cyst. (b) Following a primary lumbar intervertebral disk injury, extradural venous plexus bleeding leads to an anterior

extradural hematoma. The disk cyst finally occurs secondary to incomplete resorption of the hematoma. (c) The discal cysts may develop as a consequence of focal LDH and resorption following a reactive inflammatory response.

29.2 Clinical Presentations The clinical presentations depend on the volume of the cyst, its site, and its relationship to the surrounding bony, joints, and neural structures. However, signs and symptoms are difficult to differentiate from those of more typical lumbar disk herniation, manifesting as unilateral sciatica. The most common presenting feature is lumbosacral radicular pain (about 75%) involving a single nerve root followed by low back pain (about 55%), with neurological deficits (motor and/or sensitive) corresponding to the involved nerve root. Unlike degenerative LDH, the most frequent symptom is radicular pain and about 30–40% of patients had one or more neurological deficits.

29.3 Imaging Features On CT scan, the discal cyst appears as a benign low-density extradural cystic lesion attached to one of the lower lumbar intervertebral disks. Degenerative spinal joint disease may be encountered, but this is unusual in this young patient population. Some cyst walls are calcified and certain cysts may contain gas or hemorrhage. Bony CT scan may be useful for identifying possible secondary bone changes such as erosion of the posterior vertebral body (scalloping). If performed, contrast injected into the disk space (discography or CT discography) spreads into the cyst content. This invasive procedure could be useful in differentiating between discal cysts and other epidural spinal degenerative cysts but is rarely required for the diagnosis.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_29

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a

29  Discal Cysts

b

c

Fig. 29.1  A postoperative discal cyst (arrows) occurring after L4–L5 herniectomy and discectomy for disk herniation as seen on sagittal (a, b) and axial (c) T2-weighted MR imaging. (Courtesy of Pr. Abad Cherif El Asri)

MRI is the modality of choice for the diagnosis. Typically, the discal cyst appears as a well-defined thin-walled anterolateral epidural cystic lesion, in continuity with a lumbar intervertebral disk (Fig.  29.1). Occasionally, the cyst may extend into the lateral recess. The cyst contents are usually hypointense on the T1-weighted sequence and hyperintense on the T2-weighted sequence. Secondary bleeding may occur within the cyst, changing its signal characteristics, and it may present with a high signal on T1 and a heterogeneous low signal on T2-weighted images. The cyst was seen to compress the dura postero-medially and the nerve root laterally. Post-gadolinium MRI T1-weighted images may show rim enhancement; however, there is no communication with other adjacent anatomic structures. Imaging features may be atypical and can mimic other cystic lesions in the lumbosacral region as follows: –– –– –– –– –– –– –– ––

Posterior longitudinal ligament cyst. Tarlov or Arachnoid cysts. Synovial cyst. Ligamentum flavum cyst. Disk extrusion or sequestration. Nerve sheath cystic tumor. Epidural abscess or hematoma. Hydatid cyst.

29.4 Treatment Options and Prognosis Lumbar discal cysts can be managed conservatively or surgically. Conservative treatment modalities include bed rest, pain control medications, physiotherapy, and percutaneous steroid injection resulting in more or less control of the patient’s pain. In addition, these modalities may be useful as temporizing measures. Some rare discal cysts may resolve spontaneously. For patients with tolerable pain or without neurologic deficits, the literature suggests initially conservative treatment. However, it seems that discal cysts are less controllable with conservative therapy, and surgical treatment may often be considered as the initial management. The aim of surgery is to remove the cyst and decompress the neural roots. There are various surgical techniques for nerve decompression, such as imaging (fluoroscopic or CT scan)-guided cyst aspiration (with or without steroid injection), endoscopic (transforaminal or interlaminar approaches), and microscopic resection of the cyst (the most used procedure), with or without corresponding intervertebral discectomy (still controversial). The cyst may be adherent to the dura mater or to the nerve root, especially the voluminous cyst. Most cases will be operated on via interlaminar approach and unilateral flavec-

Further Reading

tomy followed by complete cyst excision. If needed, a more extensive approach will be used such as a hemilaminectomy. Care should be taken to minimize nerve root damage, and the possibility of CSF leaks. Postoperative complications are mild and rare. The majority of patients showed satisfactory clinical results after surgery. Recurrence of a lumbar discal cyst is very rare following complete resection surgery.

Further Reading Aljuboori Z, Altstadt T. Symptomatic lumbar discal cyst: a rare entity that can mimic other lumbar cystic lesions. Cureus. 2019;11:e5453. https://doi.org/10.7759/cureus.5453. Arslan E, Demirci İ, Şimşek G, Kılınçaslan MO, Güreşci S, Hacıfazlıoğlu Ç. Which treatment method should be preferred for lumbar discal cysts? A case report and a review of the literature. Neurol Neurochir Pol. 2014;48:71–5. https://doi.org/10.1016/j. pjnns.2013.04.003. Aydin S, Abuzayed B, Yildirim H, Bozkus H, Vural M. Discal cysts of the lumbar spine: report of five cases and review of the literature. Eur Spine J. 2010;19:1621–6. https://doi.org/10.1007/s00586-­010-­ 1395-­9. Bansil R, Hirano Y, Sakuma H, Watanabe K. Transition of a herniated lumbar disc to lumbar discal cyst: a case report. Surg Neurol Int. 2016;7:S701–4. https://doi.org/10.4103/2152-­7806.191081. Cao Z, Cong Y, Yin C, Wang Y, Wang Z, Liu X, et  al. A review and summary of patients with symptomatic postoperative discal pseudocysts of the lumbar spine. Orthop Surg. 2023;15:1256–63. https:// doi.org/10.1111/os.13689. Certo F, Visocchi M, Borderi A, Pennisi C, Albanese V, Barbagallo GM.  Lumbar intervertebral discal cyst: a rare cause of low back pain and radiculopathy. Case report and review of the current evidences on diagnosis and management. Evid Based Spine Care J. 2014;5:141–8. https://doi.org/10.1055/s-­0034-­1387806. Chen S, Suo S, Li C, Wang Y, Li J, Zhang F, Zhang W. Clinical application of percutaneous transforaminal endoscopic surgery in lumbar discal cyst. World Neurosurg. 2020;138:e665–73. https://doi. org/10.1016/j.wneu.2020.03.048. Chiba K, Toyama Y, Matsumoto M, Maruiwa H, Watanabe M, Nishizawa T. Intraspinal cyst communicating with the intervertebral disc in the lumbar spine: discal cyst. Spine (Phila Pa 1976). 2001;26:2112–8. https://doi.org/10.1097/00007632-­200110010-­00014. Cho SM, Rhee WT, Lee SY, Lee SB. Ganglion cyst of the posterior longitudinal ligament causing lumbar radiculopathy. J Korean Neurosurg Soc. 2010;47:298–301. https://doi.org/10.3340/jkns.2010.47.4.298. Fu CF, Tian ZS, Yao LY, Yao JH, Jin YZ, Liu Y, et  al. Postoperative discal pseudocyst and its similarities to discal cyst: a case report. World J Clin Cases. 2021;9:1439–45. https://doi.org/10.12998/ wjcc.v9.i6.1439. Jadhav N, Sivakumar L, Talibi SS, Momoh P, Rasul F, Hussain R, et  al. Lumbar discal cyst and post-operative discal pseudocyst: a case series. J Surg Case Rep. 2022;2022:rjac239. https://doi. org/10.1093/jscr/rjac239.

419 Jeong GK, Bendo JA.  Lumbar intervertebral disc cyst as a cause of radiculopathy. Spine J. 2003;3:242–6. https://doi.org/10.1016/ s1529-­9430(02)00445-­x. Hyung-Jun K, Dae-Yong K, Tae-Ho K, Ho-Sang P, Jae-Sung K, Jae-­Won J, et al. Lumbar discal cyst causing bilateral radiculopathy. Surg Neurol Int. 2011;2:21. https://doi.org/10.4103/2152­7806.77026. Koga H, Yone K, Yamamoto T, Komiya S.  Percutaneous CT-guided puncture and steroid injection for the treatment of lumbar discal cyst: a case report. Spine (Phila Pa 1976). 2003;28:E212–6. https:// doi.org/10.1097/01.BRS.0000067279.53431.6A. Kono K, Nakamura H, Inoue Y, Okamura T, Shakudo M, Yamada R.  Intraspinal extradural cysts communicating with adjacent herniated disks: imaging characteristics and possible pathogenesis. AJNR Am J Neuroradiol. 1999;20:1373–7. Kornberg M. Nerve root compression by a ganglion cyst of the lumbar annulus fibrosus. A case report. Spine (Phila Pa 1976). 1995;20:1633– 5. https://doi.org/10.1097/00007632-­199507150-­00013. Kwon YK, Choi KC, Lee CD, Lee SH. Intraoperative discography for detecting concealed lumbar discal cysts. J Korean Neurosurg Soc. 2013;53:255–7. https://doi.org/10.3340/jkns.2013.53.4.255. Marshman LA, Benjamin JC, David KM, King A, Chawda SJ. “Disc cysts” and “posterior longitudinal ligament ganglion cysts”: synonymous entities? Report of three cases and literature review. Neurosurgery. 2005;57:E818. https://doi.org/10.1093/ neurosurgery/57.4.e818. Marushima A, Uemura K, Sato N, Maruno T, Matsumura A.  Osteolytic lumbar discal cyst: case report. Neurol Med Chir (Tokyo). 2008;48:363–6. https://doi.org/10.2176/nmc.48.363. Nabeta M, Yoshimoto H, Sato S, Hyakumachi T, Yanagibashi Y, Masuda T.  Discal cysts of the lumbar spine. Report of five cases. J Neurosurg Spine. 2007;6:85–9. https://doi.org/10.3171/ spi.2007.6.1.17. Park JW, Lee BJ, Jeon SR, Rhim SC, Park JH, Roh SW. Surgical treatment of lumbar spinal discal cyst: is it enough to remove the cyst only without following discectomy? Neurol Med Chir (Tokyo). 2019;59:204–12. https://doi.org/10.2176/nmc.oa.2018-­0219. Perillo T, Vitiello A, Perrotta M, Serino A, Manto A.  Discal cyst: a rare cause of low back pain and sciatica. Radiol Case Rep. 2022;17:3678–80. https://doi.org/10.1016/j.radcr.2022.07.018. Prasad G, Kabir SM, Saifuddin A, Casey AT. Spontaneous resolution of discal cyst around L5 nerve root: case report and review of literature. Br J Neurosurg. 2011;25:761–3. https://doi.org/10.3109/0268 8697.2011.555020. Singleton A, Agarwal V, Casagranda B, Hughes MA, Rothfus WE. Lumbar discal cyst in an elite athlete. Radiol Case Rep. 2015;8:764. https://doi.org/10.2484/rcr.v8i1.764. Wang C, Zhang L, Chen Y, Xu D, Wu X, Ma X. A rare discal cyst with concurrent double-level isthmic lumbar spondylolisthesis: a case report and literature review. Br J Neurosurg. 2020:1–6. https://doi. org/10.1080/02688697.2020.1864294. Wu HT, Pang QJ, Tang T, Liu JT, Zhou CG, Wang Y. Symptomatic disc pseudocyst after percutaneous endoscopic discectomy of lumbar disc herniation: 5 cases report and literature progress. Zhongguo Gu Shang. 2022;35:669–74. https://doi.org/10.12200/j.issn.1003­0034.2022.07.014. Yu HJ, Park CJ, Yim KH. Successful treatment of a symptomatic discal cyst by percutaneous C-arm guided aspiration. Korean J Pain. 2016;29:129–35. https://doi.org/10.3344/kjp.2016.29.2.129.

Intradural Lumbar Disk Herniations

30.1 Generalities and Relevance Intradural disk herniation is the extension of a fragment of the intervertebral disk material into the dural sac (Fig. 30.1). Herniation into the nerve root sleeve is rarer and is called “intraradicular disk herniation” (c.f. Chap. 31). Intradural lumbar disk herniation (LDH) is a rare entity first described by Walter Edward Dandy (1886–1946) in 1942. Since then, less than 200 cases have been documented in the literature to date, mainly in the lower vertebral column (lumbar spine in more than 90% of cases). Less than 0.5% of all LDHs are intradural. In the lumbosacral area, most patients complain of usual sciatic pain. As with other forms of discogenic sciatica, neurological symptoms can be explained by various mechanisms such as compression theory, ischemic theory, and chemical irritative theories. Neither the clinical presentations nor the imaging features are characteristic. Almost all documented cases were diag-

30

nosed during surgery. Moreover, with increasing development and use of minimally invasive lumbar discectomy that has limited surgical exposure, the potential of failure to recognize this atypical variant of LDH can be high with subsequent complications and poor results. Based on their anatomical localization, there are two types of intradural LDH as follows: Type A: disk fragment being in the dural sac (Fig. 30.1) Type B: disk fragment into the preganglionic portion of dural root sleeve. Only “type A” intradural LDH will be detailed in the present chapter. For intraradicular LDH, please refer to Chap. 31 of the present book. Unlike intraradicular LDH, the lesions are often large. The annulus fibrosus, the posterior longitudinal ligament, and the dura are pierced by the disk fragment. There are further variations on exact localization of the intradural disk material as follows: (a) Pseudo-intradural disk herniation: when the disk fragment penetrates only the outer layer of the dura. (b) True intradural disk herniation: when the disk fragment perforated the whole dura (outer and inner layers).

Fig. 30.1  Illustration of an intradural lumbar disk herniation (in red)

Additionally, the disk may be in continuity or not with the parent intervertebral disk at that level. Also, some rare cases have a transdural (AKA transfixed) migration of herniated disk fragments through both the posterior and anterior thecal sacs. True intradural LDH is by far the most frequent form of intradural disk herniation. Pseudo-intradural cases are rare and characterized by the absence of cerebrospinal fluid (CSF) leakage when the dural root sleeve is excised intraoperatively to remove the disk fragment. However, some cases may remain extra arachnoid. Most cases developed in the anterolateral lumbar epidural space, at a unilateral single level, and mainly in L4–L5 ver-

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tebral level (55%) followed by L3–L4 (16%) and L5–S1 (10%) levels. Intradural herniation rarely migrated far from the parent intervertebral disk space. The exact mechanism of intradural penetration by an intervertebral herniated disk remains unclear, although many cases have evidence of previous spinal surgical interventions or contiguous epidural disk herniations. Consequently, the following four main theories have been suggested: • Localized adhesions between the posterior longitudinal ligament and the vertebral body periosteum with the ventral surface of the dural sac. • This dense connection may limit the mobility of the thecal sac and nerve roots and thus allow for intradural penetration by disk material. These adhesions may be congenital or caused by traumatic irritation, previous surgery, chronic local inflammation, disk protrusion, osteophyte, or even ossified posterior longitudinal ligament. • Acute prolapse (e.g., subtle trauma) may cause acute pressure on the anterior wall of the dura and may eventually erode it to reach the intradural space. • Congenital fineness and weakness of the dura matter. • Narrowing of the spinal canal with lack of extradural space. A combination of two or more of these different mechanisms is possible. For example, acute or subtle traumatic forces might tear the adherent and weakened dura by disk fragments that will penetrate its interior. Osteophytes, ossified posterior longitudinal ligament, or hard disk fragments with a sharp end can easily weaken the dura matter.

30.2 Clinical Presentations The initial evaluation should include a sufficient and detailed history and physical exam. About one-third of patients had a history of prior spinal surgery. Overall, most authors reported that lumbosacral radicular pain and neurological findings are worse than in patients with classic extradural LDH. The majority of the patients with intradural LDH are male subjects (more than 70% of cases) that tend to be older than those with classic herniated disks. Most patients with intra-

30  Intradural Lumbar Disk Herniations

dural LDH are aged between 50 and 60  years old versus 40–50 years old for those with classic herniation. Most patients present with lumbar back pain and radicular symptoms, which tend to be chronic for a several-year history (about 80% of cases experience symptoms greater than one year). Acute clinical presentations are rare but some patients complain of increasing pain intensity just before their admission. The clinical manifestations are variable and depend on the precise site of the disk fragment and its relationship to the surrounding neural structures. However, signs and symptoms are difficult to differentiate from those of more traditional extradural lumbar disk herniation, manifesting as unilateral or bilateral sciatica. Interestingly, about 30% of cases present a cauda equina syndrome (CES). Remarkably, some rare patients presented symptoms and signs of intracranial hypotension secondary to a CSF leak at the site of the intradural disk fragment. Overall, the diagnosis of intradural disk herniation is not made preoperatively according to clinical and even imaging features.

30.3 Imaging Features Preoperative diagnosis of fragment disk herniation into the thecal sac is very difficult. In myelography (saccoradiculography), the lesion presents as an irregular total or subtotal block, but it is challenging to differentiate intradural disk herniation from other intradural lesions of the lumbar region (see below). Computed tomography (CT) scan with intrathecal contrast (myelo-CT) can suspect an intradural lesion, but they usually fail to indicate its precise nature. Generally, the pathological tissue has a similar density as the disk material (Fig. 30.2a). In some cases, the disk fragment can be calcified. Some authors showed an association of intradural gas on the CT scan with intradural migration of disk fragments. A bony CT scan may be useful for identifying possible secondary degenerative osteoarticular changes such as concomitant osteophytosis, calcified/ossified posterior longitudinal ligament, facet joint arthrosis, and disk narrowing. Magnetic resonance imaging (MRI) is superior to myelography and CT scan in visualizing all constituents of the LDH including local adhesion, inflammatory tissue, and associated disk herniation/protrusion (Figs. 30.2, 30.3, 30.4, 30.5,

30.3  Imaging Features

a

423

b

c

Fig. 30.2  Case 1. This 46-year-old man had prior spine surgery 10 years ago for a left L4–L5 disk herniation with initial good clinical results. An intradural disk herniation (arrows) was highly suspected on lumbosacral axial CT scan (a) and MRI (b, c)

a

b

c

Fig. 30.3  Case 1. L4–L5 intradural disk herniation as seen on sagittal T1-weighted (a) and T2-weighted MRI (b, c)

30.6). Some MRI features may help to guide the diagnosis such as “Y sign,” “crumble disk sign,” and “hawk-beak sign” (Table  30.1). Also, unusual ring-enhancing lesion on T1-weighted post-gadolinium images and lack of communication with other adjacent anatomic structures are suggested for intradural LDH.

In accordance with previously documented cases, the diagnosis of intradural LDH is very difficult to make preoperatively especially when the disk fragment is not in continuity with its original intervertebral disk (sequestered) or when the disk fragment is migrated.

424 Fig. 30.4  Case 1. L4–L5 intradural disk herniation confirmed intraoperatively. Note the crumble disk sign (head arrow) on sagittal T2-weighted MRI (a) and the hawk-beak sign (arrow) on axial T2-weighted MRI (b)

30  Intradural Lumbar Disk Herniations

a

a

b

c

b

Fig. 30.5  Case 2. This 48-year-old woman had prior spine surgery 18 months ago for a right L5–S1 disk herniation with initial good clinical results. An intradural L5–S1 disk herniation was suspected preop-

eratively on axial CT scan (arrow) (a) and axial T2-weighted MRI (arrows) (b, c). This intradural disk herniation was confirmed intraoperatively

It seems that clinical symptoms did not correlate with the size of disk fragment. Imaging features are unspecific and can mimic other lesions within or around the thecal sac in the lumbosacral area as follows:

–– –– –– –– –– –– ––

–– Schwannoma and neurofibroma. –– Meningioma.

Ependymoma. Metastasis. Epidermoid and dermoid cysts. Lipoma. Arachnoid cyst. Large disk extrusion or sequestration. Postoperative scar or fibrosus.

425

Further Reading

a

b

c

Fig. 30.6  Case 2. L5–S1 intradural disk herniation confirmed intraoperatively. Note the crumble disk sign (arrows) on sagittal T2-weighted MRI (a–c) Table 30.1  Main MRI features of an intradural location of disk herniation “Y sign”

The disk material splits the anterior surface of the dura mater but with intact arachnoid mater on T2-weighted sagittal images. “Crumble Irregularly bordered mass with loss of continuity of disk sign” the posterior longitudinal ligament and anterior thecal sac on T2-weighted sagittal images (Figs. 30.3, 30.4, and 30.6) “Hawk-beak A sharp beak-like lesion compresses the dural sac on sign” T2-weighted axial images (Figs. 30.2, 30.4, and 30.5) Ring-­ Peripheral enhancement around an intradural disk enhancing fragment on both axial and sagittal T1-weighted lesion post-gadolinium images

30.4 Treatment Options and Prognosis The treatment of intradural LDH is surgical decompression and removal of the ruptured disk material. To the best of our knowledge, no case report exists on successful conservative treatment of intradural disk herniation. CES needs an urgent surgical procedure.

An enlarged laminectomy field and foraminotomy are helpful to define the anatomy and delimit the lesion. It is preferable to explore the nerve root and the dura using microsurgical techniques to avoid further neurological damage. Endoscopic and minimally invasive approaches are undesirable. The thecal sac and some nerve roots are usually dense, tense, firm, and adherent. The extradural removal is possible in partially intradural forms, but this is very difficult in completely intradural and migrated types. Except iatrogenic incidental durotomy, CSF visualization during the procedure attests presence of a true intradural or intraradicular disk herniation. The intradural mass can also be detected by intraoperative ultrasound. Previous surgery at the same disk level is associated with difficulty of anatomic dissection of the involved structures and subsequent complications due to fibrosis and scarring adhesions. Negative extradural exploration of a level with evident clinical symptoms/signs, empty intervertebral disk, and obvious imaging features should raise suspicion of the diagnosis. Of course, the exposed level should be checked intra-

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operatively. Then, a careful posterior durotomy and transdural exploration should be done to remove any intradural disk material. At the end of the procedure, the surgeon should check for any extradural disk fragment and repair both the anterior and posterior surface dura. For some difficult cases, free autologous fascia or muscle grafts can be used with fibrin glue reinforcement. All published cases were managed surgically with satisfactory to good clinical results in about two-thirds of cases. In the remaining third of patients, there was some persistent neurological deficit, especially in those with preoperative CES.  Postoperative complications are mild, mainly CSF pseudomeningocele due to the surgical durotomy. The neuropathic pains are transient and no case of postoperative recurrence has been documented. Negative prognostic factors linked to unsatisfactory results are as follows: long symptom duration, CES, previous surgery at the same spinal level, and incomplete removal of the disk herniation.

Further Reading Akhaddar A, Boulahroud O, Elasri A, Boucetta M. Radicular interdural lumbar disc herniation. Eur Spine J. 2010;19(Suppl 2):S149–52. https://doi.org/10.1007/s00586-­009-­1200-­9. Ashraf A, Babar ZU. Intradural disc herniation: a case report and literature review. Cureus. 2020;12:e7600. https://doi.org/10.7759/ cureus.7600. Chen X, Cheng Y, Wu H. Intradural lumbar disc herniation of L2-L3: a case report and literature review. Front Surg. 2023;9:1047974. https://doi.org/10.3389/fsurg.2022.1047974. D’Andrea G, Trillò G, Roperto R, Celli P, Orlando ER, Ferrante L. Intradural lumbar disc herniations: the role of MRI in preoperative diagnosis and review of the literature. Neurosurg Rev. 2004;27:75–80. https://doi.org/10.1007/s10143-­003-­0296-­3. Dandy WE.  Serious complications of ruptured intervertebral disks. J Am Med Assoc. 1942;119:474–7. https://doi.org/10.1001/ jama.1942.02830230008002. Diehn FE, Maus TP, Morris JM, Carr CM, Kotsenas AL, Luetmer PH, et al. Uncommon manifestations of intervertebral disk pathologic conditions. Radiographics. 2016;36:801–23. https://doi. org/10.1148/rg.2016150223. Ducati LG, Silva MV, Brandão MM, Romero FR, Zanini MA. Intradural lumbar disc herniation: report of five cases with literature review. Eur Spine J. 2013;22(Suppl 3):S404–8. https://doi.org/10.1007/ s00586-­012-­2516-­4. Epstein NE, Syrquin MS, Epstein JA, Decker RE. Intradural disc herniations in the cervical, thoracic, and lumbar spine: report of three cases and review of the literature. J Spinal Disord. 1990;3:396– 403. Fiechter M, Ott A, Beck J, Weyerbrock A, Fournier JY. Intradural non-­ calcified thoracic disc herniation causing spontaneous intracranial hypotension: a case report. BMC Surg. 2019;19:66. https://doi. org/10.1186/s12893-­019-­0527-­3.

30  Intradural Lumbar Disk Herniations Francio VT, Wie CS, Murphy MT, Neal MT, Lyons MK, Gibbs WN, et al. Multispecialty perspective on intradural disc herniation: diagnosis and management—a case report. Anesth Pain Med (Seoul). 2022;17:221–7. https://doi.org/10.17085/apm.21100. Ge CY, Hao DJ, Yan L, Shan LQ, Zhao QP, He BR, et al. Intradural lumbar disc herniation: a case report and literature review. Clin Interv Aging. 2019;14:2295–9. https://doi.org/10.2147/CIA.S228717. Ghaffari-Rafi A, Nosova K, Kim K, Goodarzi A. Intradural disc herniation in the setting of congenital lumbar spinal stenosis. Neurochirurgie. 2022;68:335–41. https://doi.org/10.1016/j.neuchi.2021.04.006. Hidalgo-Ovejero AM, García-Mata S, Gozzi-Vallejo S, Izco-Cabezón T, Martínez-Morentín J, Martínez-Grande M. Intradural disc herniation and epidural gas: something more than a casual association? Spine (Phila Pa 1976). 2004;29:E463–7. https://doi.org/10.1097/01. brs.0000142433.21912.0d. Huliyappa HA, Singh RK, Singh SK, Jaiswal M, Jaiswal S, Srivastava C, et  al. Transdural herniated lumbar disc disease with muscle patch for closure of durotomy—a Brief review of literature. Neurol Neurochir Pol. 2017;51:149–55. https://doi.org/10.1016/j. pjnns.2016.12.002. Jin YZ, Zhao B, Zhao XF, Lu XD, Fan ZF, Wang CJ, et  al. Lumbar intradural disc herniation caused by injury: a case report and literature review. Orthop Surg. 2023;15:1694–701. https://doi. org/10.1111/os.13723. Luo D, Ji C, Xu H, Feng H, Zhang H, Li K.  Intradural disc herniation at L4/5 level causing Cauda equina syndrome: a case report. Medicine (Baltimore). 2020;99:e19025. https://doi.org/10.1097/ MD.0000000000019025. Mercier P, Hayek G, Ben Ali H, Tounsi R, Fournier D, Menei P, et al. Intradural lumbar disk hernias. A propos of 6 cases and review of the literature. Neurochirurgie. 1997;43:142–7. Moon SJ, Han MS, Lee GJ, Lee SK, Moon BJ, Lee JK. Unexpected Intradural lumbar disk herniation found during transforaminal endoscopic surgery. World Neurosurg. 2020;134:540–3. https://doi. org/10.1016/j.wneu.2019.11.121. Pedaballe AR, Mallepally AR, Tandon V, Sharma A, Chhabra HS. An unusual case of transdural herniation of a lumbar intervertebral disc: diagnostic and surgical challenges. World Neurosurg. 2019;128:385–9. https://doi.org/10.1016/j.wneu.2019.05.103. Rapoport BI, Hartl R, Schwartz TH. Cranial neuropathy due to intradural disc herniation. Neurosurgery. 2014;74:E561–5. https://doi. org/10.1227/NEU.0000000000000315. Schisano G, Franco A, Nina P. Intraradicular and intradural lumbar disc herniation: experiences with nine cases. Surg Neurol. 1995;44:536– 43. https://doi.org/10.1016/0090-­3019(95)00248-­0. Segi N, Ando K, Nakashima H, Machino M, Imagama S.  Intradural lumbar disc herniation from the lateral inner surface of the dura without a penetration hole: a case report. Cureus. 2022;14:e22418. https://doi.org/10.7759/cureus.22418. Theodorou DJ, Theodorou SJ, Kakitsubata Y, Papanastasiou EI, Gelalis ID. Posterior and anterior epidural and intradural migration of the sequestered intervertebral disc: Three cases and review of the literature. J Spinal Cord Med. 2022;45:305–10. https://doi.org/10.1080/1 0790268.2020.1730110. Thohar Arifin M, Ikbar KN, Brilliantika SP, Bakhtiar Y, Bunyamin J, Muttaqin Z.  Challenges in intradural disc herniation diagnosis and surgery: a case report. Ann Med Surg (Lond). 2020;58:156–9. https://doi.org/10.1016/j.amsu.2020.08.022. Yu Y, Yang Z, Xiang Y, Wan Y, Jin H, Fan P, et al. Unexpected intradural disc herniation instead of space-occupying tumor at L3-L4 level: a case report and literature review. Am J Transl Res. 2021;13:10891–5.

Intraradicular Lumbar Disc Herniations

31.1 Generalities and Relevance Intraradicular disc herniation is a special type of intradural disc herniation (c.f. Chap. 30) where an intervertebral disc fragment penetrates into the dural root sleeve (Fig.  31.1). This rare entity was first described by Barbera et al. in 1984. Since then, less than 30 cases have been documented to date, exclusively in the lumbar spine. Most patients complain of classic sciatic pain. As with other forms of discogenic sciatica, neurologic symptoms can be explained by various mechanisms such as compression theory, ischemic theory, as well as chemical irritative theories. Neither the clinical presentation nor imaging studies allow an exact preoperative diagnosis of the topography of the intraradicular disc herniation. All the cases are diagnosed during surgery. The main risk in this exceptional lesion is to

31

miss an intraradicular discal fragment leading to a poor result. Furthermore, with the increasing development and use of minimally invasive lumbar discectomy that has limited surgical exposure, the potential of failure to recognize this unusual variant can be high with subsequent complications and bad outcomes. Based on their anatomical localization, there are two types of intradural lumbar disc herniation (LDH): Type A: Disc fragment being in the dural sac (c.f. Chap. 30) Type B: Disc fragment into the preganglionic portion of the dural root sleeve Type B is really the intraradicular LDH (Fig. 31.1). Interestingly, in only two previously reported cases, the intraneural disc fragment was found in the postganglionic portion of the dural root sleeve in the extraforaminal area mimicking a benign or malignant nerve sheath tumor. However, intraneural migration of the herniated disc material is extremely rare and has been reported only once before. It has been also hypothesized that the herniated disc can damage the epineurium and infiltrate the nerve. There are further variations on the exact localization of the disc fragment: (a) Pseudointraradicular disc herniation: when the disc fragment penetrates only the outer layer of the dura. (b) True intraradicular disc herniation: when the disc fragment perforated the whole dura (outer and inner layers).

Fig. 31.1  Illustration of an intraradicular lumbar disc herniation (in red)

Additionally, the disc may be in continuity or not with the intervertebral disc space. True intraradicular LDH is by far the most frequent form of intraradicular disc herniation. Pseudointraradicular cases are characterized by the absence of CSF leakage when the dural root sleeve is excised intraoperatively to remove the disc fragment.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_31

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In 2010, we reported the first documented cases of radicular interdural lumbar disc herniation. In this variation of “pseudointraradicular” disc herniation, a disc fragment has been found between the two layers of the root dural sleeve. Most cases of intraradicular LDH developed in the anterolateral lumbar epidural space, at a unilateral single level, and mainly in the L5-S1 vertebral level. This last level is mostly affected probably because the root S1 is among the longest intracanalicular root in the lumbosacral area. The exact mechanism of intraradicular penetration by an intervertebral herniated disc remains unclear; although many cases have evidence of previous spinal surgical interventions or contiguous epidural disc herniations. Subsequently, the following three main theories have been suggested: • Localized adhesions between the posterior longitudinal ligament and the vertebral body periosteum with the ventral wall of both the dural sac and the dural root sleeve. • This dense connection may limit the mobility of the nerve roots and thus allow for intraradicular penetration by disc material. These adhesions may be congenital or caused by traumatic irritation, previous surgery, chronic local inflammation, disc protrusion, or even osteophyte. • Acute prolapse may cause acute pressure on the anterior wall of the dural root sleeve and may eventually erode it to reach the intraradicular space. • Congenital weakness of the dural root sleeve. A combination of two or more of these different mechanisms is possible. For example, the action of bending, stretching, or vibratory forces might tear the adherent and weakened dura by disc fragments that will penetrate into its interior. Osteophytes and hard disc fragments with a sharp end can easily weaken the dura.

31.2 Clinical Presentations The clinical presentations depend on the precise site of the disc fragment and its relationship to the surrounding neural structures. However, signs and symptoms are difficult to differentiate from those of more traditional extradural lumbar disc herniation, manifesting as unilateral sciatica. The initial evaluation should include a sufficient and detailed history and physical exam. About 20% of patients had a history of prior spinal surgery or transforaminal epidural injection. The majority of the patients with intraradicular LDH are aged between 40 and 70 years old with a predominantly male

31  Intraradicular Lumbar Disc Herniations

population. Three-quarters of cases had radicular syndromes corresponding to the involved nerve root (mainly S1). About 50% of patients had long histories of pain that worst a few weeks before admission in one-third of the cases. Among all cases reported, only two patients presented with cauda equina syndrome (CES). It seems that pain and neurological findings are worse than in patients with classic extradural LDH. Overall, the diagnosis is not made preoperatively according to clinical features.

31.3 Imaging Features Preoperative diagnosis of fragment disc herniation into a nerve root sleeve is very difficult. In saccoradiculography (myelography), the lesion presents as an irregular total or subtotal block but it is challenging to differentiate intraradicular disc herniation from other intradural mass lesions of the lumbar region (see below). Computed tomography (CT) scan with intrathecal contrast (myelo-CT) can suspect an intraradicular dural lesion but they usually fail to indicate its precise nature. However, a bony CT scan may be useful for identifying possible secondary degenerative articular and bone changes such as concomitant osteophytosis, facet joint arthrosis, and disc narrowing. Magnetic resonance imaging (MRI) is superior to myelography and CT scan in visualizing all constituents of the LDH including local adhesion, inflammatory tissue, and associated disc herniation/protrusion. Some MRI features may help to guide the diagnosis such as uncommon large root, irregular rounded or fusiform form of an extruded disc fragment, unusual ring-enhancing lesion on T1-weighted postgadolinium images, and lack of communication with other adjacent anatomic structures. In accordance with previously published cases, the diagnosis of intraradicular LDH is very difficult to make preoperatively especially when the disc fragment is not in continuity with the lumbar intervertebral disc (Fig. 31.2). It seems that clinical symptoms did not correlate with the size of the disc fragment. Imaging features are unspecific and can mimic other lesions within or around the dural sheath of the nerve root in the lumbosacral region like: –– –– –– –– ––

Schwannoma and neurofibroma Metastasis Epidermoid and lipoma Arachnoid cyst Conjoined nerve roots

31.4  Treatment Options and Prognosis

a

429

b

c

d

Fig. 31.2  Intraradicular (S1) lumbar disc herniation (arrows) as seen on sagittal T1- (a) and T2-weighted MRI (b) as well as on axial (c, d) T2-weighted MRI

–– –– –– ––

Disc extrusion or sequestration Swollen nerve roots Postoperative scar or fibrosis Epidural granuloma

31.4 Treatment Options and Prognosis The treatment of intraradicular LDH is surgical decompression and removal of the ruptured disc material (Fig.  31.3). An enlarged laminectomy field and foraminotomy are helpful to define the anatomy. It is preferable to explore the nerve root using microsurgical techniques to avoid potential complications. Minimally invasive and endoscopic approaches are undesirable. To the best of our knowledge, no case report exists on successful conservative treatment. Intraoperatively, the nerve root is usually immobile, hard, and swollen. The extradural removal is possible in partially intraradicular cases (pseudointraradicular disc herniation),

but this is very difficult in completely intraradicular cases (true intraradicular disc herniation). Except iatrogenic incidental durotomy, CSF visualization during the procedure attests the presence of a true intradural or intraradicular disc herniation. Negative extradural exploration of a level with evident clinical symptoms/signs, empty intervertebral disc, and obvious imaging features should raise suspicion of the diagnosis. Of course, the exposed level should be checked intraoperatively. Then, a careful transradicular exploration should be done to remove any intraradicular disc fragment. At the end of the procedure, the dural defect must be closed. A perineural suture is often difficult and has its own complications. So, many authors recommend using only a free autologous fascia, fat or muscle graft, and/or adhesive around the nerve root. It appears that intraradicular LDH is less controllable with conservative therapy, and surgical treatment may often be considered as the initial management.

430 Fig. 31.3 Intraoperative views (a, b) showing the large free disc fragment (arrows) at the moment of its extirpation from inside the left sheath of the S1 nerve root (star). Note the surgical specimen removed from the S1 radicular sheath (c)

31  Intraradicular Lumbar Disc Herniations

a

b

c

All published cases were managed surgically with satisfactory to good clinical results taking into account preoperative duration and degree of neurologic symptoms. Postoperative complications are mild; only one patient presented an infection and another persistent neurological deficit. The neuropathic pains are transient and no case of postoperative recurrence has been described.

Kasliwal MK, Shimer AL. Transradicular lumbar disc herniation: An extreme variant of intraradicular disc herniation. Indian J Orthop. 2015;49:672–5. https://doi.org/10.4103/0019-­5413.168770. Mut M, Berker M, Palaoğlu S.  Intraradicular disc herniations in the lumbar spine and a new classification of intradural disc herniations. Spinal Cord. 2001;39:545–8. https://doi.org/10.1038/sj.sc.3101204. Nazzal MM, Croissant PD, Ali MA, Kaidi AA. Intraradicular disc herniation: a case report and review of the literature. J Spinal Disord. 1995;8:86–8. Ozdemir N, Yilmaz HS, Acar UD, Tektas S.  Intraradicular lumbar disc herniation: report of two cases and review of the literature. Br J Neurosurg. 2004;18:637–43. https://doi. Further Reading org/10.1080/02688690400022938. Ozer E, Yurtsever C, Yücesoy K, Güner M. Lumbar intraradicular disc Açikgöz B, Ozcan OE, Iplikçioğlu C, Sağlam S. Intraradicular disc herherniation: report of a rare and preoperatively unpredictable case niation. Neurosurgery. 1986;19:673–4. and review of the literature. Spine J. 2007;7:106–10. https://doi. Akdemir H, Oktem IS, Koç RK, Kavuncu I. Postoperative intraradicular org/10.1016/j.spinee.2006.04.011. lumbar disc herniation: a case report. Neurosurg Rev. 1997;20:71– Tsuji H, Maruta K, Maeda A. Postoperative intraradicular intervertebral 4. https://doi.org/10.1007/BF01390531. disc herniation. Spine (Phila Pa 1976). 1991, 16:998–1000. https:// Akhaddar A, Boulahroud O, Elasri A, Boucetta M. Radicular interdudoi.org/10.1097/00007632-­199108000-­00028. ral lumbar disc herniation. Eur Spine J. 2010;19(Suppl 2):S149–52. Sharma MS, Morris JM, Pichelmann MA, Spinner RJ. L5-S1 extrafohttps://doi.org/10.1007/s00586-­009-­1200-­9. raminal intraneural disc herniation mimicking a malignant periphBarberá J, Gonzalez-Darder J, García-Vazquez F.  Intraradicular hereral nerve sheath tumor. Spine J. 2012;12:e7–e12. https://doi. niated lumbar disc. Case report. J Neurosurg. 1984;60:858–60. org/10.1016/j.spinee.2012.10.033. https://doi.org/10.3171/jns.1984.60.4.0858. Schisano G, Franco A, Nina P. Intraradicular and intradural lumbar disc Ergüngör MF, Kars HZ.  Intraradicular herniation of a lumbar herniation: experiences with nine cases. Surg Neurol. 1995;44:536– disc: a case report. Neurosurgery. 1987;21:909–11. https://doi. 43. https://doi.org/10.1016/0090-­3019(95)00248-­0. org/10.1227/00006123-­198712000-­00021. Schisano G, Nina P. Intraradicular lumbar disc herniation: case report Finkel HZ.  Intraradicular, intervertebral disc herniation. A case and review of the literature. Neurosurgery. 1998;43:400. https://doi. report. Spine (Phila Pa 1976). 1997;22:1028–9. https://doi. org/10.1097/00006123-­199808000-­00153. org/10.1097/00007632-­199705010-­00017. Süzer T, Tahta K, Coşkun E. Intraradicular lumbar disc herniation: case Jackson RP, Kornblatt MD.  Lumbar intraradicular disk herniation: report and review of the literature. Neurosurgery. 1997;41:956–8. report of three cases. Orthopedics. 1997;20:980–5. https://doi. https://doi.org/10.1097/00006123-­199710000-­00037. org/10.3928/0147-­7447-­19971001-­17. Turgut M.  Intradural intraradicular disc herniation in the lumbar Karabekir HS, Karagoz Guzey F, Kagnici Atar E, Yildizhan A. Intra-­ spine: apropos of a new case. Spine J. 2011;11:92–3. https://doi. radicular lumbar disc herniation: report of two cases. Spinal Cord. org/10.1016/j.spinee.2010.10.020. 2006;44:318–21. https://doi.org/10.1038/sj.sc.3101860. Turgut M, Tekin C, Unsal A. Intraradicular extruded disc herniation as Karavelioglu E, Eser O. Intraradicular lumbar disc herniation in a rare a rare cause of failed back surgery - case report and review of the localization: case report. Clin Neurol Neurosurg. 2013;115:232–4. literature. Neurol Neurochir Pol. 2008;42:251–4. https://doi.org/10.1016/j.clineuro.2012.05.001.

Sciatic Double Crush Syndrome at the Same Root Site

32.1 Generalities and Relevance The classic definition of double crush syndrome (DCS) describes a clinical entity of two (or rarely more) sites of compression along a single peripheral nerve. Concomitant compressive causes coexist and synergistically increase neurological symptom intensity. Furthermore, the poor result obtained after treatment at one site may be the consequence of persistent damage at another site along the same peripheral nerve. Double crush syndrome was first described in 1973 by two Canadian neurologists Adrian Upton and Alan McComas who postulated that a proximal lesion in a nerve would make that same nerve more vulnerable to additional distal lesions. This unusual condition is often little known and can confuse clinicians. In the beginning, many of the studies investigating the possibility of DCS involve lesions in the upper extremity. The most usually considered association is between low-­ cervical radiculopathies and carpal tunnel syndrome. On the other hand, very few cases of DCS are documented in the lower extremity (c.f. Chap. 109 about Sciatic Double Crush Syndrome involving Different Sites). The original definition of DCS, although based on comprehensive pathophysiologic processes, may be limited in scope because many studies have found that “compressive” pathology is not the only contributor to nerve damage. Indeed, a “double crush” is also more likely in settings where the overall health of the nerve is compromised. The list of such underlying problems is long and comprises endocrine (especially diabetes mellitus), nutritional, metabolic, genetic, iatrogenic, anatomical, infectious, and systemic pathologies. For some authors, “multifocal neuropathy” is a more appropriate term describing the multiple etiologies of the DCS. For others, these underlying disorders can act as the first “crush” on the nerve rather than spinal nerve compression. Diverse factors may play a role in the development of this syndrome. The most plausible mechanisms are: (a) Disturbance of axonal transport.

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(b) Deregulation of ion channel. (c) Immune-response inflammation in the dorsal root ganglions. (d) Formation of neuroma-in-continuity. (e) Other factors may also be involved such as dynamic factors (e.g., altered movement of nerve and loss of elasticity), underlying abnormality of the connective tissue, direct neural pressure (neural edema and/or ischemic change), and psychological or psychosocial aspects. (f) Combined mechanisms as a summation of two or more abovementioned mechanisms. Besides traditional nerve involvement at two distinct sites (namely proximal and distal), some authors described a particular form of DCS characterized by a double compression at the same anatomic neurological site, especially at the level of the lumbar nerve root. The most known aspect is represented by the DCS of a lumbar nerve root (mainly L4, L5, or S1) due to lumbar disc herniation and adjacent lateral recess stenosis in patients with spinal degenerative disease. The other etiologies are rarer. Instead, lower lumbar disc herniation (LDH) is mainly associated with intradural schwannomas (neurinomas) at the same level. The remaining cases include lower LDH with concomitant extradural malignant neurofibroma, intradural neurofibroma, intradural filum paraganglioma, or spinal stenosis. Because there are no standardized or validated criteria to define or diagnose DCS, no true consensus exists regarding its prevalence or general epidemiology. However, lower limbs are much less affected than upper limbs.

32.2 Clinical Presentations Clinical history is important to consider in order to direct the diagnosis toward a second or more cause. Also, underlying conditions are useful to know. A full physical examination including gait analysis and appropriate laboratory studies to rule out metabolic, endocrine, or rheumatologic abnormali-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_32

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a

32  Sciatic Double Crush Syndrome at the Same Root Site

b

d

c

e

f

Fig. 32.1  Double disc herniation at L4-L5 (arrowheads) and T10-T11 (arrows) in a 54-year-old woman who had left-sided L4 radicular pain. The pain improved after surgical resection of the two compressive

lesions. Sagittal (a) and axial (b, c) spinal thoracolumbar T2-weighted MRI. Axial (d, e) and sagittal (f) reconstruction CT scan

ties should be performed. A work-up of low-back pain beginning with palpation, active and passive range of motion, and the straight leg raise test should be performed. Additional palpation, compression, or percussion over the sciatic nerve trunk may produce pain and paresthesia extending on the course of the nerve (AKA Valleix Phenomenon). Patients with suspected neurogenic tumors should be explored for a possible relationship with neurofibromatosis. Then, a deep neurocutaneous and otologic examination will be required. Most patients with sciatic double crush syndrome at the same root site present in a gradual subacute or chronic manner. The two involved causes may be revealed simultaneously or remotely (step by step) generally after the failure of a first medical and/or surgical treatment. Signs and symptoms do not differ from those related to traditional lumbar discogenic sciatica. However, most patients have low-back pain with unilateral lumbosacral radicular pain unless there is a large neoplasm which is caused by bilateral and several adjacent nerve root symptoms. Some patients may present with hypoesthesia in L5 and/or S1 nerve territory with or without muscular weakness supplied by the L5 and/or S1 nerve roots. Some other symptoms, such as claudication or urologic disorders, maybe the results of both pathologies. In all previously published cases, the two concomitant underlying etiologies were not suspected before neuroimaging assessment (Fig. 32.1).

In some cases, separating lumbosacral radiculopathy from sciatic peripheral mononeuropathy or lumbosacral plexopathy on clinical grounds can be difficult or even impossible. Therefore, in such cases electrodiagnostic studies are decisive. Neurophysiological explorations can assess the relative severity of neurological damage and predict the prognosis or follow-up course of recovery.

32.3 Paraclinic Features Diagnosis of concomitant symptomatic lumbar disc herniation and other compressive causes at the same spinal segment are not possible without performing adequate neuroradiological investigations. For a long time, patients were diagnosed using myeloradiculography or myelo-computed tomography. However, in many cases, the concomitant spinal tumor was missed during primary imaging and surgery. Therefore, supplementary neuroimaging studies and operations were required due to inadequate postoperative results. Nowadays, magnetic resonance imaging (MRI) is the primary imaging modality that may indicate the exact topography of the lesion, its nature, exact margins, and inner structures, as well as its relationships with adjacent structures (Fig. 32.1). Furthermore, MRI assists the treating physician in the creation of a therapeutic plan.

Further Reading

On MRI, the concomitant intraspinal neoplasm is often well-delineated and enhanced following gadolinium injection. The diagnosis is easier if the tumor is intradural. Unless the associated tumor is small, there is usually a close anatomic relationship between neoplasm and herniated disc. However, large neoplasms cause lesions of several adjacent nerve roots. Sometimes, the space-occupying lesion may be confused with migrated, sequestrated, or even intradural disc herniation. Additionally, calcified disc sequestration or some posterior ring apophysis separation may mimic an intradural spinal tumor and have MRI findings similar to that of schwannomas. These incorrect diagnoses can have bad consequences on patient management. For some authors, the coexistence of LDH and neoplasm at the same level may be secondary to the weakening of the intervertebral disc by the tumor which induces herniation; however, most reported tumors are intradural. When clinical symptoms cannot be fully explicated by an identified etiology, the coexistence of another spinal pathology should be suggested. It is easy to establish the diagnoses when LDH and a space-occupying lesion are present in the same spinal region because both etiologies are shown on an MRI exploration.

32.4 Treatment Options and Prognosis The majority of patients with lumbosacral radiculopathy respond to conservative treatment, but for those with persistent symptoms, progressive signs of nerve root compression, or neurological deficit, surgical treatment must be considered. Regarding DCS at the same root site, it is important to recognize both problems, as treating only one site can result in residual symptoms from the uncorrected second location of impingement. Generally, when surgery is needed, most authors used a single operation to address both conditions. All published cases were managed via posterior approach and laminectomy. In one case, percutaneous endoscopic stenosis was used for lumbar decompression. Surgical treatment options include herniectomy, discectomy, foraminotomy, and tumor resection depending on the nature of the compressive lesions. Surgical outcomes for the treatment of DCS are difficult to study due to the rarity of the condition in the lower limbs. However, most patients reported a satisfactory (fair or better) functional outcome. Some patients had residual neurological squeals that alternated between slight paresthesia to radicular paresis. As experienced in the upper limbs, it seems that patients with DCS are less responsive to surgical treatment than patients with single lesions.

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When clinical symptoms cannot be fully explained by an identified pathology, the coexistence of another spinal pathology should be considered.

Further Reading Albert FK, Oldenkott P, Bieker G, Danz B. Lumbar intervertebral disk herniation with a concomitant nerve root neurinoma at the same site. Case report and review of the literature. Neurochirurgia (Stuttg). 1988;31:222–5. https://doi.org/10.1055/s-­2008-­1053942. Baek SW, Kim C, Chang H.  Intradural schwannoma complicated by lumbar disc herniation at the same level: a case report and review of the literature. Oncol Lett. 2014;8:936–8. https://doi.org/10.3892/ ol.2014.2181. Bhatia R, Jaunmuktane Z, Zrinzo A, Zrinzo L. Caught between a disc and a tumour: lumbar radiculopathy secondary to disc herniation and filum paraganglioma. Acta Neurochir (Wien). 2013;155:315–7. https://doi.org/10.1007/s00701-­012-­1537-­4. Fujii K, Abe T, Koda M, Funayama T, Noguchi H, Miura K, et  al. Cauda equina schwannoma with concomitant intervertebral disc herniation: a case report and review of literature. J Clin Neurosci. 2019;62:229–31. https://doi.org/10.1016/j.jocn.2018.12.033. Iwasaki M, Akiyama M, Koyanagi I, Niiya Y, Ihara T, Houkin K. Double crush of L5 spinal nerve root due to L4/5 lateral recess stenosis and bony spur formation of lumbosacral transitional vertebra pseudoarticulation: a case report and review. NMC Case Rep J. 2017;4:121–5. https://doi.org/10.2176/nmccrj.cr.2016-­0308. Kim HS, Singh R, Adsul NM, Oh SW, Noh JH, Jang IT.  Management of root-level double crush: case report with technical notes on contralateral interlaminar foraminotomy with full endoscopic uniportal approach. World Neurosurg. 2019;122:505–7. https://doi. org/10.1016/j.wneu.2018.11.110. Lesoin F, Jomin M, Delisse B, Cécile JP. Neurinoma and lumbar disk herniation. A case. Rev Rhum Mal Osteoartic. 1987;54:508–9. Liu SY, Lin YM, Wei TS, Lin SJ, Liu CC, Chou CW. Exacerbation of symptoms of lumbar disc herniation complicated by a schwannoma: a case report. Kaohsiung J Med Sci. 2007;23:480–5. https://doi. org/10.1016/S1607-­551X(08)70057-­3. Love JG, Rivers MH.  Spinal cord tumors simulating protruded intervertebral disks. JAMA. 1962;179:878–81. https://doi.org/10.1001/ jama.1962.03050110046009. Nishimura Y, Hara M, Awaya T, Ando R, Eguchi K, Nagashima Y, et al. Possible double crush syndrome caused by iatrogenic acquired lumbosacral epidermoid tumor and concomitant sacral tarlov cyst. NMC Case Rep J. 2020;7:195–9. https://doi.org/10.2176/nmccrj. cr.2019-­0236. Pan J, Wang Y, Huang Y. Coexistence of intervertebral disc herniation with intradural schwannoma in a lumbar segment: a case report. World J Surg Oncol. 2016;14:113. https://doi.org/10.1186/s12957-­ 016-­0864-­y. Sanguinetti C, Esposito L, Laudati A. Association of disk hernia and vertebral neurinoma. Chir Organi Mov. 1985;70:369–74. Schramm J, Umbach W. Simultaneous occurrence of spinal tumor and lumbar disk herniation. Neurochirurgia (Stuttg). 1977;20:22–8. https://doi.org/10.1055/s-­0028-­1090351. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet. 1973;2:359–62. https://doi.org/10.1016/s0140-­ 6736(73)93196-­6. Wilbourn AJ, Gilliatt RW. Double-crush syndrome: a critical analysis. Neurology. 1997;49:21–9. https://doi.org/10.1212/wnl.49.1.21.

Sciatica Due to Contralateral Lumbar Disc Herniations

33.1 Generalities and Relevance Generally, the term “sciatica” is known to be specific to the pain, and/or paresthesia, which is a direct consequence of sciatic nerve root (L4 to S3), lumbosacral plexus, or sciatic nerve irritation. Most cases of sciatica result from mechanical compression and inflammatory disorders. Spinal sciatica may result from a variety of degenerative problems dominated by low lumbar disc herniation (LDH). Typically, clinical symptoms (e.g., sciatic pain) correspond to the results of neuroimaging studies. However, in rare cases, an LDH can cause the contralateral lumbosacral radicular symptom. This false localizing presentation may lead to missed or delayed diagnosis as well as a possible risk of unnecessary lumbosacral spinal surgery. According to Larner, a “false localizing sign” can be defined as a confusing clinical condition in which the anatomical situation of the lesion causing neurologic symptoms is distant or remote from the anatomical site predicted by neurologic examination. Although “distant or remote” could be a relative notion, sciatic pain due to contralateral LDH might be proposed among the forms of false localizing signs in neurology. The first report of such an instance was described by Abdur R Choudhury et  al. in 1978. The authors reported three cases of lumbar radiculopathy on the anterior thigh on the opposite side to their corresponding upper LDH diagnosed on myeloradiculography, one case on L2-L3 vertebral level, and two others on L3-L4 vertebral level. However, the first description of true sciatic pain (involving left L5 radiculopathy) secondary to right-sided L4-L5 disc herniation was published by Albert W Auld and Jan G Dewall in 1979. Since then, less than 70 cases have been documented in the literature. The incidence of such patients is not known but this rare entity often develops among mature adult men between their fourth and sixth decade without specific risk factors. While this phenomenon is actually well recognized by most neurosurgeons and spinal surgeons, its exact patho-

33

physiology is poorly understood. Sciatic pain contralateral to the side of the disc herniation on neuroimaging has been attributed to the following mechanisms (Fig. 33.1): (a) Spondylotic changes and lateral recess stenosis contralateral to the side of disc herniation, which could be the cause of fixing and trapping of the opposite side of the dural sac with the emerging nerve roots. (b) In the absence of the dural ligaments (that fix the lumbar nerve root to the posterior longitudinal ligament), the ipsilateral nerve root can simply be displaced posteriorly without being compressed significantly, while the contralateral nerve root is shifted laterally along the pedicle into the lateral recess. (c) Traction force generated on the contralateral nerve root might be stronger than the force applied on the ipsilateral nerve root. In this hypothesis, the traction phenomenon predominates over that of compression. (d) Nerve root anomalies such as contralateral conjoined nerve roots or furcal nerve. (e) Inflammatory theory or “friction radiculitis”: the nerve root of the symptomatic side, contralateral to the side of the disc herniation, had been compressed to the superior facet or along the pedicle by the herniated disc from the opposite side, with resultant inflammatory findings including fibrosis, adhesion, redness, and swelling. (f) Asymmetrically hypertrophied ligamentum flavum. The thickness of the ligamenta flava, especially on the opposite side of the disc herniation. (g) Venous engorgement and congestion could generate impingement to the contralateral neural contents. (h) Migrated epidural adipose tissue (fat) toward the contralateral side of the herniated disc. (i) Changing posture by bending to the opposite side of the LDH. By analogy, some authors believe that this entity may be similar to the “Kernohan notch-like phenomenon”: a paradoxical intracranial neurological manifestation. Intracranial

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_33

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33  Sciatica Due to Contralateral Lumbar Disc Herniations

Fig. 33.1 Different pathophysiological mechanisms explaining the sciatic pain contralateral to the side of the lumbar disc herniation

space-occupying lesions displace the brain laterally, causing compression of the other side of the brain against the rigid skull bone or the ridge edge of the cerebellar tentorium, giving a false clinical localizing sign.

33.2 Clinical Presentations Signs and symptoms do not differ from those related to traditional lumbar discogenic sciatica. However, most patients have unilateral sciatic pain or the lumbosacral radicular pain was predominant on one side only. Some patients may present with hypoesthesia in L5 and/ or S1 nerve territory with or without muscular weakness supplied by the L5 and/or S1 nerve roots. Any related signs of lumbar spinal stenosis or spondylolisthesis should be considered in order to exclude other mimicking or associated pathologies. To prevent wrong or delayed diagnosis, in addition, to correctly identifying the cause of the symptoms, some procedures will be helpful in the management of these patients such as lumbar foraminal blocks on the symptomatic side.

33.3 Paraclinic Features First reported patients were diagnosed using myeloradiculography and/or myelo-computed tomography (CT). Nowadays, magnetic resonance imaging (MRI) is the primary imaging modality for the assessment of spinal sciatica. The most common cause of sciatic pain contralateral to the side of the LDH found on neuroimaging is L4-L5 disc herniation followed by those on L5-S1 level (Fig.  33.2). Interestingly, some patients had a concomitant relative spinal canal stenosis. Furthermore, some patients with atypical presentations should be assessed by appropriate imaging tools and biological explorations to exclude potential hip, sacroiliac joint, and knee disorders, as well as underlying systemic diseases. Consultations with experts such as neurologists, orthopedists, physical therapists, and rheumatologists can aid in differential diagnoses. On the other hand, various etiologies may be associated with peripheral neuropathy but they rarely present as an isolated sciatic pain (c.f. Chap. 94 about Sciatic Peripheral Neuropathies).

33.4  Treatment Options and Prognosis

a

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Fig. 33.2  Right paramedian L4-L5 disc herniation (arrows) in a 40-year-old man manifesting as unilateral sciatic pain on the left side. Sagittal (a, b) and axial (c) T2-weighted MR imaging. Note the normal appearance of the L3-L4 intervertebral disc (d)

Classic neurophysiological studies confirm the involvement of L5, S1, or both lumbosacral roots. These techniques should be indicated above all, when the patient’s clinical presentation and imaging did not correlate, particularly in absence of any lesion at the ipsilateral symptomatic side.

33.4 Treatment Options and Prognosis Initially, conservative treatment should be trialed with appropriate management that focuses on the level and side of both spinal degenerative disease and lumbosacral radicular pain. Surgical management will be valid for such patients in a method comparable to the presentations of clinical syndromes with imaging concordant traditional LDH. However, according to the previously documented cases in the literature, three surgical approaches have been described: (a) Unilateral approach ipsilateral to the LDH (b) Unilateral approach contralateral to the LDH (c) Bilateral exploration

In the beginning, many authors choose to surgically approach and explore both sides of these conditions in spite of the risks of iatrogenic disorders such as failed back surgery syndrome and spinal instability. In 2006, Hasan Kamil Sucu and Fazil Gelal reported the first series of five patients with contralateral lumbar disc herniation who were operated on only from the herniation side (asymptomatic side). When selecting to perform a unilateral exploration (on the asymptomatic side with imaging-­ apparent lesion), it is important to have a preoperative discussion with patients and their families about the possibility of needing a potential second surgery (on the symptomatic side). However, to the best of our knowledge, no additional surgery has been needed in any of the patients reported. Following the three surgical approaches previously described, all cases had excellent outcomes both on the pain and on the possible neurological deficit. No postoperative complications and no cases of recurrence have been described. Interestingly, in only one publication, a patient was operated on via a percutaneous lumbar endoscopic exploration approached from the side of ipsilateral “symptomatic” pain.

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Then, clinical improvement was obtained after surgery. According to the authors of this paper, Jun-Song Yang et al., the migrated epidural fat plays a significant role in the pain mechanism of LDH with contralateral radiculopathy. However, because this is only one case, this supposition needs to be confirmed in supplementary comparative studies.

Further Reading Abdul Jalil MF, Lam MF, Wang YY.  Is that lumbar disc symptomatic? Herniated lumbar disc associated with contralateral radiculopathy. BMJ Case Rep. 2014;2014:bcr2013202726. https://doi. org/10.1136/bcr-­2013-­202726. Akdeniz T, Kaner T, Tutkan I, Ozer AF. Unilateral surgical approach for lumbar disc herniation with contralateral symptoms. J Neurosurg Spine. 2012;17:124–7. https://doi.org/10.3171/2012.4.SP INE11365. Akhaddar A, Dao I, Belfquih H, Boucetta M. Chronic localized headache with ipsilateral hemiparesis. Headache. 2010;50:664–5. https://doi.org/10.1111/j.1526-­4610.2010.01642.x. Asan Z.  Lumbar disc herniations causing contralateral radicular symptoms: can they be explained by hypotenusal theory? World Neurosurg. 2018;114:e1297–301. https://doi.org/10.1016/j. wneu.2018.03.201. Auld AW, DeWall JG.  Myelographic defect on the side opposite the leg pain. A case report with an explanation of mechanism of action. Spine (Phila Pa 1976). 1979;4:174–5. https://doi. org/10.1097/00007632-­197903000-­00015. Choudhury AR, Taylor JC, Worthington BS, Whitaker R.  Lumbar radiculopathy contralateral to upper lumbar disc herniation: report of 3 cases. Br J Surg. 1978;65:842–4. https://doi.org/10.1002/ bjs.1800651205. Dogan I, Bozkurt M, Kahilogullari G, Yakar F, Zaimoglu M, Bakirarar B, et al. Is a unilateral surgical approach effective in patients with bilateral leg pain with unilateral lumbar disc herniation? A prospective nonrandomized clinical and surgical study. World Neurosurg. 2018;117:e316–22. https://doi.org/10.1016/j.wneu.2018.06.022. Eguchi Y, Ohtori S, Toyone T, Ozawa T, Yamauchi K, Yamashita M, et al. Surgical experience in cases of L5 and S1 symptoms caused by upper lumbar spinal stenosis of L2–L3 and L3–L4. J Spine. 2012;1:105. https://doi.org/10.4172/2165-­7939.1000105. Hayashi N, Iba H, Ohnaru K, Nakanishi K, Hasegawa T.  Radiculopathy contralateral to the side of disc herniation-microendoscopic observation. Spine Surg Relat Res. 2018;2:304–8. https://doi. org/10.22603/ssrr.2017-­0062. Kalemci O, Kizmazoglu C, Ozer E, Arda MN.  Lumbar disc herniation associated with contralateral neurological deficit: can venous congestion be the cause? Asian Spine J. 2013;7:60–2. https://doi. org/10.4184/asj.2013.7.1.60.

33  Sciatica Due to Contralateral Lumbar Disc Herniations Karabekir HS, Yildizhan A, Atar EK, Yaycioglu S, Gocmen-Mas N, Yazici C.  Effect of ligamenta flava hypertrophy on lumbar disc herniation with contralateral symptoms and signs: a clinical and morphometric study. Arch Med Sci. 2010;6:617–22. https://doi. org/10.5114/aoms.2010.14477. Kesornsak W, Wasinpongwanich K, Kuansongtham V.  Posterior epidural sequestrated disc presenting with contralateral radiculopathy: a very rare case. Spinal Cord Ser Cases. 2021;7:98. https://doi. org/10.1038/s41394-­021-­00460-­z. Kim P, Ju CI, Kim HS, Kim SW. Lumbar disc herniation presented with contralateral symptoms. J Korean Neurosurg Soc. 2017;60:220–4. https://doi.org/10.3340/jkns.2016.1010.015. Koh ZSD, Lin S, Hey HWD. Lumbar disc herniation presenting with contralateral symptoms: a case report. J Spine Surg. 2017;3:92–4. https://doi.org/10.21037/jss.2017.03.06. Kornberg M.  Sciatica contralateral to lumbar disk herniation. Orthopedics. 1994;17:362–4. https://doi.org/10.3928/0147-­7447-­ 19940401-­12. Larner AJ.  False localising signs. J Neurol Neurosurg Psychiatry. 2003;74:415–8. https://doi.org/10.1136/jnnp.74.4.415. Lee DY, Lee SH. Recurrent lumbar disc herniation with contralateral symptoms treated by percutaneous endoscopic discectomy. Kor J Spine. 2007;4:41–3. Mirovsky Y, Halperin N.  Eccentric compression of the spinal canal causing dominantly contralateral-side symptoms. J Spinal Disord. 2000;13:174–7. https://doi.org/10.1097/00002517-­ 200004000-­00014. Mobbs RJ, Steel TR. Migration of lumbar disc herniation: an unusual case. J Clin Neurosci. 2007;14:581–4. https://doi.org/10.1016/j. jocn.2006.04.002. Ruschel LG, Agnoletto GJ, Aragão A, Duarte JS, de Oliveira MF, Teles AR.  Lumbar disc herniation with contralateral radiculopathy: a systematic review on pathophysiology and surgical strategies. Neurosurg Rev. 2021;44:1071–81. https://doi.org/10.1007/s10143-­020-­ 01294-­3. Safdarian M, Farzaneh F, Rahimi-Movaghar V. Contralateral radiculopathy: a Kernohan-Woltman notch-like phenomenon. Asian J Neurosurg. 2018;13:165–7. https://doi.org/10.4103/1793-­5482.180954. Sucu HK, Gelal F.  Lumbar disk herniation with contralateral symptoms. Eur Spine J. 2006;15:570–4. https://doi.org/10.1007/s00586-­ 005-­0971-­x. Utsunomiya R, Sakai T, Wada K, Sairyo K, Kosaka H, Katoh S, et al. Hemorrhagic facet cyst in the lumbar spine causing contralateral leg symptoms: a case report. Asian Spine J. 2011;5:196–200. https:// doi.org/10.4184/asj.2011.5.3.196. Yang JS, Zhang DJ, Hao DJ.  Lumbar disc herniation with contralateral radiculopathy: do we neglect the epidural fat? Pain Physician. 2015;18:E253–6. Yi YJ, Kang SS, Yoon YJ, Shin KM. Contralateral complete L5 palsy following ipsilateral L4 selective transforaminal epidural block. Korean J Anesthesiol. 2013;65:S56–8. https://doi.org/10.4097/ kjae.2013.65.6S.S56.

Part III Spinal Non-discogenic Sciatica

Lumbar Spinal Stenosis

34.1 Generalities and Relevance Lumbar spinal stenosis (LSS) refers to a narrowing in the lumbar spinal canal. The reduction in the canal size could be in the spaces of: • Central canal • Lateral recesses • Neural foramen This condition may induce lumbosacral radiculopathy with or without neurological deficits as well as neurogenic claudication. Anatomically, the dimensions of the lumbar spinal canal may be subject to some variations. However, in the majority of normal cases, the sagittal (anteroposterior) diameter of the lower lumbar vertebral canal is more than 12 mm centrally and more than 4  mm in the lateral recesses and foramina. While the transverse interpedicular diameter is more than 25 mm. In 1949, the Dutch neurosurgeon Henk Verbiest (1909– 1997) presented the concept of “lumbar spinal stenosis,” characterized by neural elements that may be compressed by a particular form of “narrowing of the lumbar vertebral canal” not associated with any other spinal disorder. All of Verbiest’s patients were men and presented with symptoms of caudal nerve root compression on standing or walking, but not at rest. On myelography, all of the cases had a block in the lumbar spine. Since then numerous authors have discussed the pathogenesis, cause, and treatment of LSS. The causes of neurologic symptoms of LSS may be multifactorial but dominated by: • Direct mechanical compression • Compromise of blood supply to the cauda equina nerve roots

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Other factors should be considered such as: • Increased intrathecal pressure secondary to the stenosis • Venous epidural stasis • Dynamic sciatic pain (secondary to spinal intersegmental instability, bowstring disease) • Nerve root inflammation The severity of the spinal stenosis is graded classically from A through D based on the morphology of the dural sac on magnetic resonance imaging (MRI) (Table  34.1) and (Fig. 34.1). There are two main etiologies of LSS: congenital or acquired (Table  34.2); however, the majority of cases are degenerative occurring in the lower lumbar spine mainly on the L4-L5 level. Most degenerative LSS are secondary to zygapophyseal facet joint hypertrophy, ligamentum flavum thickening, and worsened by disc protrusion or even true lumbar disc herniation (LDH) (Figs.  34.2, 34.3, 34.4). Other degenerative Table 34.1  Schizas grading system for lumbar spinal stenosis (based on the morphology of the dural sac on axial T2-weighted MRI) (Fig. 34.1) Degree of Grade stenosis Description A No or minor Cerebrospinal fluid (CSF) is plainly visible in the thecal sac but the distribution is varied B Moderate The rootlets occupy the entire thecal sac but they can still be detailed Some CSF is still existing, giving a granular form to the sac C Severe The rootlets are not recognized CSF is not visible, giving a homogeneous gray signal to the sac. However, epidural fat exists posteriorly D Extreme The rootlets are not recognized Both CSF and posterior epidural fat are not visible

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_34

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Fig. 34.1  Schizas grading system for lumbar spinal stenosis from A through D based on the morphology of the dural sac on axial magnetic resonance imaging

Table 34.2  Different etiologies of lumbar spinal stenosis Congenital and developmental

Acquired

– Idiopathic (genetic) – Achondroplasia – Morquio’s syndrome – Spinal dysraphism – Osteopetrosis – Degenerative +++ – Facet joint diseases – Combined congenital and degenerative stenosis – Spondylolysis or spondylolisthesis – Scoliosis – Ossification of the posterior longitudinal ligament – Calcification/ossification of the ligamentum flavum – Posterior ring apophysis separation (PRAS) – Surgical/Iatrogenic (e.g., laminectomy, fusion) – Traumatic – Fibrosis – Neoplasm – Metabolic (e.g., Paget's disease, spondyloarthritis, diffuse idiopathic skeletal hyperostosis [aka Forestier's disease], epidural lipomatosis, acromegaly, pseudogout, renal osteodystrophy, hypoparathyroidism)

lesions may occur such as posterior vertebral osteophyte formation, synovial facet cysts, spondylolisthesis, hypertrophy of the posterior longitudinal ligament, or even posterior ring apophysis separation (c.f. corresponding chapters) (Figs. 34.5, 34.6, 34.7, 34.8, 34.9, 34.10, 34.11, 34.12, 34.13, 34.14, 34.15, 34.16). Degenerative LSS is most frequent at L4-L5 vertebral level, then at L3-L4 and L2-L3, and lastly at L5-S1. LSS can be monosegmental (involving one vertebral level) or multisegmental (Fig.  34.17). Indeed, it is not uncommon that this narrowing extends from L2 to L5 (Figs. 34.2, 34.3, 34.4, 34.17). More rarely, LSS may be congenital resulting from shortened pedicles and thickened lamina with medially placed facets (e.g., achondroplasia) (Figs.  34.18, 34.19, 34.20). Many cases are identified to be idiopathic. Unlike degenerative LSS, most congenital forms present global stenosis of the entire lumbar spine. Central and lateral recess stenosis can impinge the traversing nerve to the level below also known as the descending nerve root [e.g., at L4-L5, stenosis compresses the L5 nerve root(s)]. However, foraminal stenosis results in compression of the exiting nerve root [e.g., at L4-L5, foraminal stenosis compresses the L4 nerve root(s)].

34.1 Generalities and Relevance

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Fig. 34.2  L2-L5 multisegmental degenerative spinal stenosis (both central, lateral, and foraminal) as seen on lumbosacral sagittal (a) and axial (b–e) T2-weighted MRI. Note the tortuous and twisted appearance of the cauda equina nerve roots (arrows) Fig. 34.3 L3-S1 multisegmental degenerative global spinal stenosis (arrows) as seen on lumbosacral sagittal (a) and axial (b, c) T2-weighted MRI. Note the severity of central and lateral stenosis on L3-L4 (b) and L4-L5 (c) (dotted triangles). (Courtesy of Dr. Achraf Moussa.)

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Fig. 34.4  L2-L5 multisegmental degenerative global spinal stenosis as seen on lumbosacral sagittal T1- (a) and T2-weighted (b) MRI as well as on axial T2-weighted MRI (c–e). Note the tortuous and twisted appearance of the cauda equina nerve roots (arrows)

Clinicians should be aware that degenerative LSS may occur in isolation or associated with other spinal (e.g., cervical canal stenosis aka tandem spinal stenosis) (Figs.  34.21 and 34.22) or extraspinal degenerative joints such as hip and/ or knee osteoarthritis (aka hip-spine syndrome, knee-spine syndrome or hip-knee-spine syndrome) (Figs.  34.23 and 34.24).

Acquired LSS is a significant cause of disability in the population aged between 60 and 70  years. LSS is also the most significant cause of spinal surgery in the elderly. Patients with congenital forms tend to be at a younger age (30–50 years old) than degenerative and other acquired LSS.

34.1 Generalities and Relevance Fig. 34.5 Lumbar degenerative global spinal stenosis with severe zygapophyseal facet joint hypertrophy (arrows) as seen on axial CT scan on both parenchymal (a, b) and bone (c, d) windows

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446 Fig. 34.6 Lumbar degenerative global spinal stenosis with “trefoil appearance” of the spinal canal (dotted circles) in one patient (a, b) and zygapophyseal facet joint vacuum (arrows) in another patient (c, d) as seen on axial CT scan (a–d)

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34.1 Generalities and Relevance

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Fig. 34.7  Lumbar axial T2-weighted MRI in a normal subject (a) and different patients with degenerative spinal stenosis (b–d) showing the severity of ligamentum flavum thickness

Fig. 34.8  Lumbosacral axial CT scan through L5-S1 intervertebral level (a, b) showing the asymmetry of facet joint hypertrophy with left-sided intracanal osteophytosis (arrows)

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Fig. 34.9  L4-L5 right-sided synovial cyst (arrows) with severe central spinal stenosis as seen on sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c, d)

34.1 Generalities and Relevance

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Fig. 34.10  Sagittal T1- (a) and T2-weighted MRI (b) as well as axial T2-weighted MRI (c–e) showing grade I L4-L5 degenerative spondylolisthesis. Note the central and bilateral foraminal stenosis on the axial view (d)

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Fig. 34.11  Grade II L4-L5 spondylolisthesis (arrows) as shown on lateral plain radiography (a), sagittal T1- (b), and T2-weighted MRI (c)

34.1 Generalities and Relevance

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Fig. 34.12  Grade II L4-L5 isthmic spondylolisthesis (arrowhead) as shown on sagittal reconstructions (a, b) and axial (c) CT scan. Note the bilateral L4 isthmolysis (arrows)

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Fig. 34.13  Ossification of the posterior longitudinal ligament (arrows) shown on lumbar MRI and CT scan (arrows). Sagittal T2-weighted MRI (a), sagittal reconstruction (b), and axial (c, d) CT scan. There is a concomitant disc herniation on L4-L5 (arrowhead) (a)

34.1 Generalities and Relevance

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Fig. 34.14  Case A. Lumbar sagittal T1- (a) and T2-weighted (b) MRI as well as axial T2-weighted MRI (c, d) showing a monosegmental L3-L4 spinal stenosis with a concomitant adjacent central disc hernia-

tion and a posterior ring apophysis separation of the L4 inferior endplate (arrows) in a 40-year-old man

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Fig. 34.15  Case A. Lumbar axial (a–d) and sagittal reconstruction CT scan (e) showing the posterior ring apophysis separation of the L4 inferior endplate (arrows) misdiagnosed as a “calcified” L4-L5 disc herniation

34.1 Generalities and Relevance

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Fig. 34.16  Lumbar axial CT scan in six different patients with posterior ring apophysis separation (arrows) (a–f) causing narrowing of the lumbar vertebral canal. The majority of these cases were misdiagnosed

as a “calcified” disc herniation, ring fracture, or ossification of the posterior longitudinal ligament

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Fig. 34.17  Lumbosacral sagittal T2-weighted MRI showing mono- (a), bi- (b), and multisegmental (c, d) lumbar spinal stenosis (arrows)

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Fig. 34.18  Idiopathic congenital L4-L5 spinal stenosis as shown on anteroposterior (a) and lateral plain radiography (b) as well as on sagittal T1- (c), and T2-weighted MRI (d). Note the shortened pedicles of L4 and L5 (double arrows) (b)

34.1 Generalities and Relevance

457

Fig. 34.19  Lumbar axial CT scan showing an idiopathic congenital global spinal stenosis with a “trefoil appearance” of the spinal canal (arrows), shortened pedicles, thickened lamina, and medially placed facets

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Fig. 34.20  Lumbosacral congenital spinal stenosis (arrows) in an achondroplastic adult patient as seen on sagittal reconstruction CT scan (a), T1- (b), and T2-weighted MRI (c)

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Fig. 34.21  Concomitant L2-L5 and C3-C6 degenerative spinal stenosis (tandem spinal stenosis) as seen on lumbar sagittal (a) and axial (b, c) T2-weighted MRI as well as on cervical sagittal T2-weighted MRI (d)

34.1 Generalities and Relevance

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Fig. 34.22  Cervical spinal degenerative canal stenosis (arrows) with coexisting lumbar stenosis dotted frames as seen on spinal sagittal (a, b) and cervical axial (c, d) T2-weighted MRI

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Fig. 34.23  Lumbar degenerative spinal stenosis with right-sided hip osteoarthritis (arrows) (hip-spine syndrome) in the same patient. Lumbar spinal anteroposterior (a) and lateral (b) plain radiography with

anteroposterior hip plain radiography (c) as well as hip coronal reconstruction (d) and axial (e) CT scan

34.2 Clinical Presentations

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Fig. 34.24  Lumbar degenerative spinal stenosis with bilateral knee osteoarthritis (knee-spine syndrome) in the same patient. Lumbar spinal anteroposterior (a) and lateral (b) plain radiography with knee anteroposterior (c, d) and lateral (e, f) plain radiography

34.2 Clinical Presentations Diagnostic strategy starts with a thorough history and physical evaluation. Classically, the majority of symptomatic LSS produces gradually progressive low-back and lower extremities pain (namely radiculopathy) which can be unilateral or bilateral with or without numbness, paresthesia, or weakness. This condition is exacerbated by standing, prolonged ambulation (neurogenic claudication), and spinal lumbar extension, and is relieved by forward flexion, sitting, and rest. Many patients reported that they move more easily by bicycle. Neurogenic claudication (aka pseudoclaudication) should be distinguished from vascular claudication (aka intermittent claudication). Unlike vascular claudication, neurogenic one includes pain in the buttocks and posterior thigh areas. Also, gait instability is frequent due to diminished proprioception of the lower limbs. If patients present with new onset of sphincter dysfunction, saddle anesthesia, bilateral lower extremity weakness, cauda equina syndrome should be highly suspected and confirmed clinically. Other symptoms may be related to other causes of acquired LSS (c.f. Table 34.2). Frequently, neurologic examinations are normal or at least without focal neurologic findings. The straight leg test

is positive in only 10% of patients and Valsalva maneuvers rarely exacerbate the radicular pain (unlike patients with classic LDH). The spinal examination should seek potential spinal deformities such as scoliosis or kyphosis as well as postural changes (Fig. 34.25). Distal pedal pulses should also be evaluated in order to eliminate vascular claudication. In addition, complete neurologic, rheumatologic, urologic, gynecologic, and general exams should be necessary. In some cases, electrodiagnostic studies are decisive for separating lumbosacral radiculopathy from sciatic peripheral mononeuropathy or lumbosacral plexopathy. However, electromyographic examinations are often normal in patients with LSS. Urodynamic studies should be required if a history of dysuria or incontinence is found. Many other concomitant symptoms related to LDH, spondylolisthesis, spondylolysis, lumbar facet joint syndrome, spinal ligamentous thickening, or potential rheumatologic disease (e.g., knee and/or hip osteoarthritis) should be considered in clinical presentations. LSS may also mask typical signs and symptoms of many other causes of spinogenic or extra-spinogenic sciatica. Hyperreflexia and Babinski’s sign may suggest upper motor neuron involvement especially concomitant cervical myelopathy (aka tandem spinal stenosis).

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Fig. 34.25  Clinical pictures showing postural changes (kyphoscoliosis) in a 45-year-old patient with degenerative lumbar spinal stenosis and concomitant lateral L4-L5 disc herniation on the left side. Note the

right lateral shift (red arrows) away from the left (contralateral) side of the sciatica as well as the appearance of the patient’s flat back. Anterior (a), lateral (b), and posterior (c) views

34.3 Paraclinic Features

abnormality and the initial diagnosis of spinal stenosis (Figs. 34.11, 34.18, 34.23, and 34.24). Oblique radiographs may help visualize the pars interarticularis (c.f. Chaps. 35 and 36 about Spondylolysis and spondylolisthesis, respectively). Dynamic flexion-extension plain radiographs may be used in the evaluation of variable degrees of spinal segmental instability. CT scan, with or without hydrosoluble myelography, is much more accurate for diagnosing LSS (Fig. 34.26). It will allow measuring the diameters of the spinal canal (best on bone windows), and all the bony changes (Figs. 34.5, 34.6, 34.8, 34.12, 34.13, 34.15, and 34.16). Classically, a “trefoil” canal (three leaflets) is found on axial images (Figs. 34.6 and 34.19). Nongadolinium magnetic resonance imaging (MRI) of the lumbosacral column remains the key diagnosis for LSS.  MRI is excellent at detecting neural structures impingement and loss of CSF signal on T2-weighted image sequences (Figs. 34.2, 34.3, 34.4, 34.7, 34.9, 34.10, 34.11,

Spinal imaging is used to: –– –– –– –– –– ––

Confirm a clinical diagnosis Characterize the cause of spinal stenosis (c.f. Table 34.2) Provide the degree of narrowing Show the compressive lesions Assess the dynamic spinal instability Help decisions regarding potential decompressive surgery and preoperative planning

However, it is well known that LSS is a common incidental imaging finding, especially in the “asymptomatic” elderly. In addition, there is also a lack of correlation between the severity of the imaging features and the severity of symptoms reported by the patients. Lumbosacral anteroposterior and lateral standard radiographs are usually sufficient for identifying the skeletal

34.3 Paraclinic Features Fig. 34.26 Lumbosacral anteroposterior (a) and oblique (b) myelographic views using water-­ hydrosoluble contrast revealing an L4-L5 spinal stenosis with a bilateral cutoff of the filling of the L5 nerve root sleeve (arrows)

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34.14, 34.17, and 34.19). More sequences that are specific may create a myelogram-like appearance (Fig.  34.27). However, MRI is somewhat limited in adequately detecting the osseous degenerative abnormalities, especially at the lateral recess stenosis as well as correct assessment of lumbar scoliotic spines. Preoperative CT scan combined with MRI can be used in complex and severe cases to further define the anatomy

b

of the region of interest, and assess associated disorders such as lumbar disc lesions, facet joint arthrosis, spinal canal and foraminal stenosis, spinal ligament thickening, osteophytosis, ring apophysis separation, and further abnormalities. For postoperative evaluations, postgadolinium MRI is a useful method in differentiating peridural scar from recurrent LDH or stenosis.

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Fig. 34.27  Lumbosacral sagittal spinal T2-weighted MRI (a) and myelographic sequence using specific fluid-sensitive acquisition techniques (b) showing a lumbar degenerative spinal stenosis including a severe left-sided L4-L5 foraminal stenosis. Note the asymmetrical

paraspinal muscle morphology (stars) indicating asymmetrical muscle innervation and/or activity in this 65-year-old patient as seen on axial T2-weighted MR imaging (c, d)

34.4 Treatment Options and Prognosis

• Failure to respond to conservative treatment (for 3–6 months) • Progressive neurologic deficits • Severe neurogenic claudication • Intractable pain restricting daily functions • Spinal segmental instability associated with pain

The ultimate goal of management for lumbar spinal stenosis is to: • • • • •

Relieve pain and reduce symptoms Improve functional status Perform nervous decompression Stabilize any spinal instability Control causative factors if possible

Initial treatment for this condition is mainly conservative and consists of physical therapy programs, posture corrections, lumbar bracing, pharmacologic therapy (analgesics, nonsteroidal anti-inflammatory drugs, and muscle relaxants), and epidural corticosteroid injections. Surgical treatment depends on many factors as shown above; however, surgery is generally reserved for confirmed cases of LSS with the following conditions:

The urgency of treatment is dictated largely by the presence of severe neurologic symptoms such as muscle weakness of the lower limb(s) and cauda equina syndrome. The most frequently performed surgical procedure is a wide posterior laminectomy of affected segments with or without foraminotomies (Figs.  34.28, 34.29, 34.30, 34.31, 34.32, 34.33, 34.34, 34.35, 34.36, 34.37, 34.38, 34.39). Limited resection techniques have also been advocated such as hemilaminectomies and microdecompressive laminotomies. The specific role and benefit of spinal fusion (with or without instrumentation, or interbody fusion) in addition to decompression are not unanimous among surgeons.

34.4 Treatment Options and Prognosis

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Fig. 34.28 Surgical illustration showing a complete laminectomy via posterior bilateral approach. The spinous process and both laminae are removed (red arrow)

Retractor placed between paraverte bral muscles on both sides

Working channel

Thecal sac L 4-5

Fig. 34.29 Intraoperative views (a–d) for interspinous approach for one-level central spinal stenosis decompression. Note the thecal sac decompression at the end of the surgical decompression (star) (c) and the ligamentoplasty between both L4 and L5 spinous processes (arrow) (d)

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Fig. 34.30  Case B. L2-L5 degenerative spinal stenosis as shown on sagittal T1- (a), and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c–f)

However, fusion is required for patients with associated segmental instability, degenerative scoliosis, or those with iatrogenic instability (e.g., facetectomy of more than half of the facet joints) (Figs. 34.34, 34.35, 34.36, 34.37, 34.38). Some surgeons widely use interspinous spacer procedures during which an implant is inserted between the spinous processes. Recently, with the development of endoscopic techniques, many surgeons perform percutaneous minimally invasive approaches with promising results. Patients who endure endoscopic surgery seem to report less postoperative low-­ back pain, less hospital stay, and less perioperative blood loss. If needed, some additional surgical procedures may be added in conjunction with concomitant lesions related to

synovial cysts, disc herniations (Fig. 34.39), ring apophysis separation, spondylolysis/listhesis, or other causative factors. Tandem concomitant cervical and lumbar spinal stenoses are often managed by first decompression of the cervical spine and later decompression of the LSS (Figs. 34.21 and 34.22). Some surgeons operate both during the same operation. Careful selection of candidates for simultaneous surgery may decrease the length of hospitalization, consolidate the postoperative rehabilitation program, and reduce hospital-­associated charges. Surgical complications are unusual but their incidence increases with advancing age, increased blood loss, the extension of surgery time, and the number of operated verte-

34.4 Treatment Options and Prognosis

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Fig. 34.31  Case B. Intraoperative views for posterior median laminectomy (a–c). L1-L5 Spinal processes appearance after release of lumbar paravertebral muscles (a). Intraoperative appearance after removing the spinous processes from L4 to L2 (b). Note the thecal sac decompression at the end of the surgical procedure (stars) (c)

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Fig. 34.33  Case C. Intraoperative views for posterior median laminectomy (a, b). L3-S1 spinal processes appearance after the release of lumbar paravertebral muscles (a). Intraoperative appearance of the thecal sac after its decompression at the end of the surgical procedure (stars) (b)

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Fig. 34.32  Case C. L3-L5 degenerative spinal stenosis as shown on sagittal T1- (a), and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c, d)

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Fig. 34.34  Case D. Grade I L4-L5 degenerative spondylolisthesis with L4-L5 disc herniation (arrowheads) as seen on sagittal (a, b) and axial (c) T2-weighted MRI. Note the bilateral facet joint degenerative changes (arrows) and the extensive L2-L5 spinal stenosis

Fig. 34.35  Case D. Intraoperative view after L2-L4 laminectomy and foraminotomy as well as posterior fusion with screws and rods

bral levels. These include infections, neurologic deficits, dural tears, epidural hematoma, failed fusion (pseudarthrosis), instability, and failed back surgery syndrome, and are among the most frequent complications (c.f. Chap. 13 about Surgical Complications). Other general complications are inherent to any surgery and include but are not limited to anemia, surgical positioning, urinary tract infection, pneumonia, or renal failure. Nonoperative treatment is useful in more than 30% of patients without neurologic deficits. Symptoms are not automatically related to the imaging severity of the narrowing. Overall, surgery is necessary in less than 20% of cases of LSS.

34.4 Treatment Options and Prognosis

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Fig. 34.36  Case D. Postoperative CT scan showing the L3-L5 posterior fixation system as seen on sagittal (a) and coronal (b) reconstructions CT scan as well as on axial CT scan (c–e)

Postoperatively, immediate symptomatic improvement can be predictable in about 75–85% of cases (Figs. 34.40 and 34.41). Unfortunately, symptom relief often declines with time. Long-term improvement in neurological symptoms, ambulation, and pain is less than two-thirds of operated patients. The successful operative rate is slightly lower for foraminal and lateral recess stenosis. Overall, due to the recurrence of the disease proximal or distal to the decom-

pressed levels, about 20% of patients may need repeat surgery (Figs. 34.42 and 34.43). However, the general prognosis is limited by the nature of the causative factors as well as potential underlying diseases. Psychological and social factors may affect rehabilitation, especially in the elderly population. Therefore, it is important to provide them with social support and personal assistance when needed.

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Fig. 34.37  Case E. Recurrence of lumbar degenerative spinal stenosis at L2-L3 with L2-L3-L4 spinal segmental instability in a 75-year-old patient operated in another institution 4 years before. Lumbosacral sag-

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ittal reconstruction CT scan (a), sagittal T1- (b), T2-weighted MRI (c), and on STIR sequence (d)

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Fig. 34.38  Case E. Intraoperative view showing L2-L3 posterior decompression (stars) and L2-L5 fusion using a polyaxial screw-rod system (a). Postoperative anteroposterior (b) and lateral (c) plain radiography showing the L2-L5 posterior fixation system

34.4 Treatment Options and Prognosis

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Fig. 34.39  Intraoperative view of a bilateral laminectomy for monosegmental lumbar degenerative spinal stenosis with a concomitant left-­ sided L4-L5 disc herniation. Note the thecal sac decompression and the herniated disc material on the left side (star)

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Fig. 34.40  Case F. Lumbosacral sagittal T1- (a) and T2-weighted MRI (b) showing L4-L5 degenerative spinal stenosis with adjacent disc herniation (arrows). Postoperative MRI control on sagittal T2-weighted sequence showing a good thecal sac decompression (c)

472 Fig. 34.41 Case F. Lumbosacral axial T2-weighted MRI (a, b) showing L4-L5 degenerative spinal stenosis (arrowheads) with adjacent disc herniation (arrows). Postoperative MRI control on axial T2-weighted sequence showing a good thecal sac and bilateral foraminal decompression (c, d)

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34.4 Treatment Options and Prognosis

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Fig. 34.42  Sciatic pain recurrence on the left side in an adult patient previously operated on for lumbar spinal stenosis at another institution. Lumbar anteroposterior plain radiography showing the L5-L3 bilateral

laminectomy (a). Axial CT scan (b) and T2-weighted MRI (c) as well as axial T2-weighted MRI (d) showing the recurrent L3-L4 central and paracentral disc herniation

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Fig. 34.43  Bilateral lumboradicular pain recurrence with concomitant neurogenic claudication in an adult patient operated on 3 years ago for an L4-L5 disc herniation with a monosegmental lumbar spinal stenosis. Lumbar anteroposterior plain radiography showing the L4 bilateral

laminectomy (a). Sagittal (b) and axial (c, d) T2-weighted MRI as well as axial CT scan on parenchymal window (e) showing the recurrent L2-L4 spinal stenosis (arrows)

Further Reading

Deasy J.  Acquired lumbar spinal stenosis. JAAPA. 2015;28:19–23. https://doi.org/10.1097/01.JAA.0000462052.47882.fd. Deer T, Sayed D, Michels J, Josephson Y, Li S, Calodney AK. A review of lumbar spinal stenosis with intermittent neurogenic claudication: disease and diagnosis. Pain Med. 2019;20:S32–44. https://doi. org/10.1093/pm/pnz161. Devin CJ, McCullough KA, Morris BJ, Yates AJ, Kang JD. Hip-spine syndrome. J Am Acad Orthop Surg. 2012;20:434–42. https://doi. org/10.5435/JAAOS-­20-­07-­434. Diwan S, Sayed D, Deer TR, Salomons A, Liang K.  An algorithmic approach to treating lumbar spinal stenosis: an evidenced-based approach. Pain Med. 2019;20:S23–31. https://doi.org/10.1093/pm/ pnz133. Fessler RG.  Surgery versus nonsurgery for lumbar spinal stenosis: an in-depth analysis of the 2016 Cochrane analysis, the studies included for analysis, and Cochrane methodology. J Neurosurg Spine. 2021:1–9. https://doi.org/10.3171/2021.1.SPINE201894. Guha D, Heary RF, Shamji MF. Iatrogenic spondylolisthesis following laminectomy for degenerative lumbar stenosis: systematic review and current concepts. Neurosurg Focus. 2015;39:E9. https://doi.org /10.3171/2015.7.FOCUS15259.

Ahorukomeye P, Saniei S, Pennacchio CA, Kuo A, Mlis ACS, Cheng CW, et al. Outcomes in surgical treatment for tandem spinal stenosis: systematic literature review. Spine J. 2022:S1529-9430(22)00791­4. https://doi.org/10.1016/j.spinee.2022.07.088. Austevoll IM, Hermansen E, Fagerland MW, Storheim K, Brox JI, Solberg T, et al. Decompression with or without fusion in degenerative lumbar spondylolisthesis. N Engl J Med. 2021;385:526–38. https:// doi.org/10.1056/NEJMoa2100990. Binder DK, Schmidt MH, Weinstein PR. Lumbar spinal stenosis. Semin Neurol. 2002;22:157–66. https://doi.org/10.1055/s-­2002-­36539. Bydon M, Macki M, Abt NB, Sciubba DM, Wolinsky JP, Witham TF, et al. Clinical and surgical outcomes after lumbar laminectomy: an analysis of 500 patients. Surg Neurol Int. 2015;6:S190–3. https:// doi.org/10.4103/2152-­7806.156578. Cinotti G, De Santis P, Nofroni I, Postacchini F. Stenosis of lumbar intervertebral foramen: anatomic study on predisposing factors. Spine. 2002;(Phila Pa 1976(27):223–9. https://doi.org/10.1097/00007632-­ 200202010-­00002.

Further Reading Kapetanakis S, Gkantsinikoudis N, Thomaidis T, Charitoudis G, Theodosiadis P.  The role of percutaneous transforaminal endoscopic surgery in lateral recess stenosis in elderly patients. Asian Spine J. 2019;13:638–47. https://doi.org/10.31616/asj.2018.0179. Katz JN, Zimmerman ZE, Mass H, Makhni MC. Diagnosis and management of lumbar spinal stenosis: a review. JAMA. 2022;327:1688– 99. https://doi.org/10.1001/jama.2022.5921. Kirker K, Masaracchio MF, Loghmani P, Torres-Panchame RE, Mattia M, States R. Management of lumbar spinal stenosis: a systematic review and meta-analysis of rehabilitation, surgical, injection, and medication interventions. Physiother Theory Pract. 2022:1–46. https://doi.org/10.1080/09593985.2021.2012860. Lafian AM, Torralba KD. Lumbar spinal stenosis in older adults. Rheum Dis Clin North Am. 2018;44:501–2. https://doi.org/10.1016/j. rdc.2018.03.008. Lai MKL, Cheung PWH, Cheung JPY. A systematic review of developmental lumbar spinal stenosis. Eur Spine J. 2020;29:2173–87. https://doi.org/10.1007/s00586-­020-­06524-­2. Lee SY, Kim TH, Oh JK, Lee SJ, Park MS. Lumbar stenosis: a recent update by review of literature. Asian Spine J. 2015;9:818–28. https://doi.org/10.4184/asj.2015.9.5.818. Lewandrowski KU, Yeung A, Lorio MP, Yang H, Ramírez León JF, Sánchez JAS, et al. Personalized interventional surgery of the lumbar spine: a perspective on minimally invasive and neuroendoscopic decompression for spinal stenosis. J Pers Med. 2023;13:710. https:// doi.org/10.3390/jpm13050710. Liu K, Liu P, Liu R, Wu X, Cai M. Steroid for epidural injection in spinal stenosis: a systematic review and meta-analysis. Drug Des Devel Ther. 2015;9:707–16. https://doi.org/10.2147/DDDT.S78070. Liu K, Zhu W, Shi J, Jia L, Shi G, Wang Y, Liu N. Foot drop caused by lumbar degenerative disease: clinical features, prognostic factors of surgical outcome and clinical stage. PLoS One. 2013;8:e80375. https://doi.org/10.1371/journal.pone.0080375. Lurie J, Tomkins-Lane C. Management of lumbar spinal stenosis. BMJ. 2016;352:h6234. https://doi.org/10.1136/bmj.h6234. Ma XL, Zhao XW, Ma JX, Li F, Wang Y, Lu B. Effectiveness of surgery versus conservative treatment for lumbar spinal stenosis: a system review and meta-analysis of randomized controlled trials. Int J Surg. 2017;44:329–38. https://doi.org/10.1016/j.ijsu.2017.07.032. Nechanicka N, Barsa P, Harsa P.  Psychosocial factors in patients indicated for lumbar spinal stenosis surgery. J Neurol Surg A Cent Eur Neurosurg. 2016;77:432–40. https://doi.org/10.1055/s-­0036-­1583179. Oshima Y, Watanabe N, Iizawa N, Majima T, Kawata M, Takai S. Knee-­ hip-­spine syndrome: improvement in preoperative abnormal posture following total knee arthroplasty. Adv Orthop. 2019;2019:8484938. https://doi.org/10.1155/2019/8484938.

475 Overley SC, Kim JS, Gogel BA, Merrill RK, Hecht AC. Tandem spinal stenosis: a systematic review. JBJS Rev. 2017;5:e2. https://doi. org/10.2106/JBJS.RVW.17.00007. Prather H, van Dillen L. Links between the hip and the lumbar spine (hip spine syndrome) as they relate to clinical decision making for patients with lumbopelvic pain. PM R. 2019;11:S64–72. https://doi. org/10.1002/pmrj.12187. Saeed F, Mukherjee S, Chaudhuri K, Kerry J, Ahuja S, Pal D. Prognostic indicators of surgical outcome in painful foot drop: a systematic review and meta-analysis. Eur Spine J. 2021;30:3278–88. https:// doi.org/10.1007/s00586-­021-­06936-­8. Schizas C, Theumann N, Burn A, Tansey R, Wardlaw D, Smith FW, et al. Qualitative grading of severity of lumbar spinal stenosis based on the morphology of the dural sac on magnetic resonance images. Spine (Phila Pa 1976). 2010;35:1919–24. https://doi.org/10.1097/ BRS.0b013e3181d359bd. Schroeder GD, Kurd MF, Vaccaro AR. Lumbar spinal stenosis: how is it classified? J Am Acad Orthop Surg. 2016;24:843–52. https://doi. org/10.5435/JAAOS-­D-­15-­00034. Shen J, Wang Q, Wang Y, Min N, Wang L, Wang F, et  al. Comparison between fusion and non-fusion surgery for lumbar spinal stenosis: a meta-analysis. Adv Ther. 2021;38:1404–14. https://doi. org/10.1007/s12325-­020-­01604-­7. Shimauchi-Ohtaki H, Minami M, Takahashi T, Kanematsu R, Honda F, Hanakita J.  Lumbar canal stenosis caused by marked bone overgrowth after decompression surgery. Case Rep Orthop. 2022;2022:9462399. https://doi.org/10.1155/2022/9462399. Splettstößer A, Khan MF, Zimmermann B, Vogl TJ, Ackermann H, Middendorp M, et  al. Correlation of lumbar lateral recess stenosis in magnetic resonance imaging and clinical symptoms. World J Radiol. 2017;9:223–9. https://doi.org/10.4329/wjr.v9.i5.223. Szpalski M, Gunzburg R.  Lumbar spinal stenosis in the elderly: an overview. Eur Spine J. 2003;12(Suppl 2):S170–5. https://doi. org/10.1007/s00586-­003-­0612-­1. Verbiest H.  A radicular syndrome from developmental narrowing of the lumbar vertebral canal. J Bone Joint Surg Br. 1954;36-B:230–7. https://doi.org/10.1302/0301-­620X.36B2.230. Verbiest H. Further experiences on the pathological influence of a developmental narrowness of the bony lumbar vertebral canal. J Bone Joint Surg Br. 1955;37-B:576–83. https://doi.org/10.1302/0301-­ 620X.37B4.576. Yamada T, Yoshii T, Yamamoto N, Hirai T, Inose H, Okawa A. Surgical outcomes for lumbar spinal canal stenosis with coexisting cervical stenosis (tandem spinal stenosis): a retrospective analysis of 565 cases. J Orthop Surg Res. 2018;13:60. https://doi.org/10.1186/ s13018-­018-­0765-­6.

Lumbar Spondylolysis

35.1 Generalities and Relevance Spondylolysis refers to a defect in the pars interarticularis (aka isthmus) of the neural vertebral arch between the superior and inferior articular facets of the same vertebra. The term is from the Greek words spondylos (vertebra) and lysis (defect). Spondylolysis can be unilateral or bilateral and most cases occur in the lower lumbar vertebrae. Bilateral pars interarticularis defects may induce an anterior vertebral body slippage in relation to the vertebra below, and then spondylolysis is called “spondylolisthesis” (c.f. Chap. 36 about Lumbar Spondylolisthesis). Two or more consecutive disc levels are rarely involved. Lumbar spondylolysis typically remains asymptomatic, but about 10% to 25% of cases manifest recurrent low-back pain that increases with activity and worsens by lumbar twisting or hyperextension. The lumbosacral radicular component is rare and does not go beyond the buttock or proximal lower extremities. Sciatic pain can be secondary to:

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• Lumbar discopathies or true intervertebral disc herniation at the same level or at the level above the spondylolysis • Dynamic sciatic pain due to segmental instability • Fibrocartilaginous proliferation at the level of the isthmus • Foraminal stenosis (Fig. 35.1) • Postural imbalance In addition, undiagnosed lumbar spondylolysis may result in failed back surgery syndrome. Spondylolysis was first described in 1858 by the English anatomist and surgeon George Murray Humphrey (1820– 1896). In 1975, the American spine surgeon Leon Lamont Wiltse (1913–2005) presented the concept of “fatigue fracture” in which most cases of isthmic spondylolysis were caused by repetitive load and stress rather than a single traumatic event. Lumbar spondylolysis may be congenital or acquired. Congenital defects develop mostly in individuals under the

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Fig. 35.1  Anatomic borders and different structures (a, b) that pass through the intervertebral foramina.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_35

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age of 10  years. While acquired types have two main mechanisms:

35  Lumbar Spondylolysis

Occasionally, pain discharges to the buttock and/or proximal lower extremities. However, severe radicular symptoms are rare and often associated with concomitant lumbar –– Repeated microtrauma, resulting in a stress injury and degenerative disorders. eventual fracture of the pars interarticularis (Stress fracUnlike cases with lumbar spondylolysis, patients with ture). In this form, a congenital “dysplastic” pars interar- spondylolisthesis are more likely to present true and comticularis is usually present (more frequent forms). plete sciatic pain with or without a neurologic deficit. –– Traumatic pars interarticularis defects result from high-­ However, the degree of radicular symptoms does not correvelocity hyperextension injury of the lumbar spine in a late with the degree of vertebral slippage. congenitally normal vertebra (less frequent forms). A spinal examination should seek for increased lumbar lordotic posture, tight hamstrings, limited trunk range of Many authors believed that both repetitive trauma and an motion (principally with extension), as well as pain and stiffinherent congenital or genetic weakness can make an indi- ness on the palpation of the pars fracture area. The positive vidual more susceptible to spondylolysis. Stork test is highly suggestive of a lumbar spondylolysis. Spondylolysis will decrease the segmental stability of the The maneuver consists of a single-leg hyperextension and lumbar spine, and increase the load exerted on the disc at the rotation of the spine which reproduces the patient’s pain. spondylolytic level and at the level above, accelerating disc The straight leg raise test should be performed when disdegeneration. In up to 65% of these individuals, spondyloly- cogenic sciatica is suspected. In addition, complete neurosis will progress to spondylolisthesis with sometimes signifi- logic and rheumatologic exams should be necessary. cant vertebral slipping. The nerve exiting below the pedicle Lumbar spondylolysis with or without slippage may also at that vertebral level is the most predisposed. Patients seem mask typical signs and symptoms of many other causes of to be most exposed to the progression of slippage during spinogenic or extra-spinogenic sciatica. growth spurts. Overall, the prevalence of spondylolysis is 4–6% in adolescents and young adults. Male adolescents involved in 35.3 Paraclinic Features sports have a higher prevalence compared to those not involved in sports. The mean age of diagnosis is 15 years of Lumbosacral anteroposterior and lateral standard radioage. Spondylolysis occurs in 8–15% of asymptomatic ado- graphs are inadequate for identifying the interarticularis part lescent athletes and up to 50% of symptomatic adolescent defect of a single vertebra (Fig.  35.2). The lesion is most athletes with concomitant low-back pain. typically visible in the oblique view which shows the classic There is a genetic predisposition with an increased inci- broken neck of the "Scotty dog" (Figs. 35.3 and 35.4). The dence seen in men, Alaskan Eskimo offspring, first-degree majority of spondylolysis is bilateral and interests only one descendants of patients with spondylolysis, concomitant vertebral level (mainly L5). Multilevel and high-vertebral pathologies such as spina bifida occulta, idiopathic scoliosis, lumbar spondylolysis are rare. Marfan syndrome, osteogenesis imperfecta, and Dynamic flexion-extension plain radiographs may be osteopetrosis. used in the evaluation of variable degrees of adjacent segmental instability. Computed tomography (CT) scan is much more accurate 35.2 Clinical Presentations in detecting spondylolysis than plain radiography (Figs. 35.5, 35.6, 35.7). However, magnetic resonance imaging (MRI) The majority of individuals with lumbar spondylolysis should be used as the first-line imaging modality in the pediremain asymptomatic, but about 20% of patients may pres- atric population due to radiation exposure from CT scan. ent with constitutive symptoms of insidious onset, recurrent Because plain radiography and even CT scan may miss low-back pain that increases with strenuous activity, aggra- stress fracture within the first 2 weeks of the injury, a bone vated by lumbar rotation and/or hyperextension, and scan (radionuclide imaging) is the most sensitive modality, improves with relative rest. and best detects early pars interarticularis pars defect. Attention should be given to child and adolescent athletes On CT scan, axial and sagittal reconstructions on bone playing a sport that requires repetitive lumbar extension and windows can assess the pars interarticularis lesions and furrotation. The onset of pain may be either acute or insidious ther degenerative disorders (Figs. 35.5, 35.6, 35.7). The morover several weeks. phology, orientation, and width of the pars defect are helpful

35.3 Paraclinic Features Fig. 35.2 Lumbosacral anteroposterior (a, b) and lateral standard radiographs are inadequate for identifying the interarticularis part defect (arrows) of a single vertebra

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Fig. 35.3  Normal oblique lumbar radiography showing the classic “Scottie Dog Model of the lumbar spine” (a). Ear: superior articular process (1). Nose: transverse process (2). Eye: pedicle (3). Neck: pars interarticularis aka isthmus (4). Foreleg: inferior articular process (5). Body: lamina and spinous process (6). Hind leg: inferior articular pro-

cess (contralateral) (7). Tail: superior articular process (contralateral) (8). Illustration of a black Scottie dog (Scottish terrier) (b). The classic broken neck of the "Scotty dog" (arrows) on oblique lumbar radiography may help to directly visualize the pars interarticularis defect (aka isthmolysis) (c)

for preoperative planning. Some cases with important osseous sclerotic appearance and increased uptake on the bone scan may be confused with an osteoid osteoma (Fig. 35.8). MRI is excellent at detecting bone marrow edema associated with acute pars interarticularis stress injury as well

as detailing neural and soft tissue pathologies. However, MRI is somewhat limited in adequately detecting the osseous cortical integrity of incomplete fractures (Fig.  35.8). The attention should be on the axial and sagittal T2-weighted images, as these will illustrate any compression of neuro-

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35  Lumbar Spondylolysis

Fig. 35.4 Left-sided posterolateral oblique view of a lumbar vertebra showing different anatomic structures that make up “The Scotty Dog Model” of the lumbar spine (a, b). Ear: superior articular process (1). Nose: transverse process (2). Eye: pedicle (3). Neck: pars interarticularis aka isthmus (4). Foreleg: inferior articular process (5). Body: lamina and spinous process (6). Hind leg: inferior articular process (contralateral) (7). Tail: superior articular process (contralateral) (8). Illustration of a black Scottie dog (Scottish terrier) (b)

Fig. 35.5  Case 1. Bilateral spondylolysis of L5 (arrows) as shown on lumbosacral sagittal reconstructions CT scan (a, b)

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35.3 Paraclinic Features

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Fig. 35.6  Case 2. Bilateral spondylolysis of L5 (arrows) without listhesis as shown on axial (a, b) and sagittal reconstructions (c, d) CT scan

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Fig. 35.7  Case 3. Right-sided (arrows) and left-sided (arrowheads) L5 spondylolysis. Axial (a) and sagittal reconstructions CT scan (b, c)

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35  Lumbar Spondylolysis

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Fig. 35.8  Case 4. Right-sided isthmic stress fracture of L5 (arrows) in a young athletic woman as seen on axial (a), sagittal (b), and coronal (c) reconstructions CT scan on bone windows. Note the important osseous

Fig. 35.9  Case 5. L4-L5 central disc herniation in a young patient with bilateral sciatica. Note the posterior recoil of the spinous process of L5 (star). This patient had a bilateral isthmolysis of L4 on a CT scan. Lumbosacral sagittal (a) and axial (b) T2-weighted MRI

a

logic elements (Figs. 35.9, 35.10, 35.11). However, MRI is not always sufficient to recognize a nondisplaced spondylolysis with certainty. For this reason, we have previously descripted the “continuous double-hump sign” as a simple valuable tool to aid in the diagnosis of lumbar spondylolysis (presence of the posterior epidural fat, between the posterior dura mater and the spinous process of the

c

sclerotic appearance on the left isthmic area mimicking an osteoid osteoma (arrowhead)

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corresponding lumbar vertebra) (Figs. 35.12, 35.13, 35.14, 35.15, 35.16). Besides the spondylolysis, other types of pathology in the lumbosacral spine should receive particular consideration during the neuroimaging assessment, in particular lumbar disc herniations, facet joint arthrosis, spinal canal, and foraminal stenosis, and osteophytosis.

35.3 Paraclinic Features Fig. 35.10  Case 6. L4-L5 central herniated disc (arrows) as shown in sagittal (a, b) and axial (c) T2-weighted MRI. Note the dysplastic vertebral body of L5 (stars)

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Fig. 35.11  Case 7. Large (giant) migrated L4-L5 disc herniation with sequestrated disc fragment (arrows) as seen on sagittal (a) and axial (b) postgadolinium T1- and sagittal (c) and axial (d) T2-weighted MRI. Note the pars interarticularis defect of L4 (arrowheads) (b, d)

35.3 Paraclinic Features

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Fig. 35.12  Case 8. The “continuous double-hump sign” (presence of the posterior epidural fat, between the posterior dura mater and the spinous process of the corresponding lumbar vertebra) (arrow) on lumbo-

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sacral sagittal T1-weighted MRI (a) in a patient with bilateral isthmolysis of L5 (arrowheads). Sagittal T1-weighted MRI (a–c)

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Fig. 35.13  Case 1. The “continuous double-hump sign” (arrow) on lumbosacral sagittal T1-weighted MRI (a) in a patient with bilateral isthmolysis of L5 (arrowheads). Sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c)

486 Fig. 35.14  Case 3. The “continuous double-hump sign” (oval line) on lumbosacral sagittal T1-weighted MRI (a) in a patient with bilateral isthmolysis of L5. Note the right-sided L5-S1 foraminal narrowing (arrows) as shown on axial T2-weighted MRI (b, c)

35  Lumbar Spondylolysis

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35.3 Paraclinic Features

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Fig. 35.15  Case 9. The “continuous double-hump sign” (arrowhead) and bilateral isthmolysis of L5 (arrows) as seen on lumbosacral sagittal T1-weighted MRI (a–c)

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Fig. 35.16  Case 9. Bilateral L5 isthmolysis (arrows) as seen on lumbosacral sagittal T2-weighted MRI. Sagittal (a) and axial (b) T2-weighted MRI. Parasagittal T2-weighted MRI (c, d)

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35  Lumbar Spondylolysis

35.4 Treatment Options and Prognosis

Overall, surgery is necessary in less than 10% of cases of lumbar spondylolysis. Some surgeons may recommend a direct local anesthetic block of the pars interarticularis under CT scan guidance before any surgical procedures. Technically, there are two main approaches for surgery:

Initial treatment of patients with spondylolysis is mainly conservative and aims to relieve pain and facilitate osseous healing at the defect. Conservative management includes bracing, activity restriction, pharmacologic therapy (analgesics, nonsteroidal anti-inflammatory drugs, and muscle (a) Direct pars interarticularis repair using Buck's cortical relaxants), and physical therapy supports. screw technique, Morscher hook-screw technique, or A spinal brace requires a thoracolumbosacral orthosis for any method using a combination of hooks, screws, or a period of 3–6 months with no sports activities. In addition cables to bracing, an organized physical therapy program is recom ( b) Posterolateral fusion using various devices with or withmended including stretching, strengthening, and posture-­ out autologous bone grafting (Figs. 35.17, 35.18, 35.19, modifying exercises. 35.20, 35.21, 35.22) Surgical intervention for lumbar spondylolysis is generally reserved for the following conditions: With the development of endoscopic techniques and advanced intraoperative fluoroscopy, many surgeons per–– Failure to respond to conservative treatment form percutaneous minimally invasive direct spondylosis –– Progression of vertebral slippage repair with good results. –– Intractable pain limiting daily functions If needed, some additional surgical procedures may be –– Development of neurological deficits added in conjunction with concomitant lesions such as –– Segmental instability associated with pain

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Fig. 35.17  Case 10. This 54-year-old woman was previously operated on at another department for a lumbar spinal stenosis. Four years later, she presented with left-sided sciatica. Lumbosacral MRI found an L3-L4 and L4-L5 disc herniation on the left side (arrows). CT scan

found a bilateral two-level isthmolysis on L4 and L5 (arrows). Sagittal T2- (a) and T1-weighted MRI (b), as well as axial T2-weighted MRI (c, d) and sagittal reconstruction CT scan (e)

35.4 Treatment Options and Prognosis

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decompressive laminectomy (spinal stenosis), herniectomy with or without discectomy (intervertebral lumbar disc herniation), foraminotomy (foraminal stenosis) (Figs.  35.17, 35.18, 35.19, 35.20, 35.21, 35.22). Potential surgical complications are rare but should be known including a failed fusion (pseudarthrosis), infections, chronic persistent pain, neurological deteriorations, progression of vertebral slippage, hardware failure, and failed back surgery syndrome. The prognosis in patients with spondylolysis is usually excellent. Asymptomatic individuals require no specific treatments or any changes in their daily or athletic activities. Even patients who present with symptomatic spondylolysis usually have a very favorable prognosis. More than 92% of the adolescent athletes managed conservatively were able to return to competitions and about 90% of those treated surgically. Psychological and social factors may affect the rehabilitation of injured athletes. Consequently, it is important to provide them with social support and personal assistance when needed.

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Fig. 35.18  Case 10. Intraoperative views after posterior dural decompression (stars), left-sided L3-L4-L5 foraminotomy (arrows) and pedicle screw fixation (a, b) Fig. 35.19  Case 10. Postoperative anteroposterior (a) and lateral (b) plain radiographs showing the position of the posterior L3-L4-L5 pedicle screw-rod system

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Fig. 35.20  Case 11. L4-L5 central disc herniation (arrowheads) in a 23-year-old man with bilateral sciatica. Lumbosacral sagittal (a) and axial (b–d) CT scan. This patient had a bilateral isthmolysis of L5 (arrows) on CT scan

35.4 Treatment Options and Prognosis

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Fig. 35.21  Case 11. Superior (a), inferior (b), and lateral (c) views of the L5 posterior arch

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Fig. 35.22  Case 11. Postoperative CT scan showing the L4-S1 posterior fixation system as seen on sagittal reconstructions (a, b) and axial (c, d) CT scan

Further Reading Akhaddar A.  Letter to the editor regarding "Symptomatic Unilateral Pediculolysis Associated with Contralateral Spondylolysis and Spondylolisthesis in Adults-Case Report and Review of Literature". World Neurosurg. 2020;143:635–7. https://doi.org/10.1016/j. wneu.2020.08.121. Akhaddar A, Boucetta M. Unsuspected spondylolysis in patients with lumbar disc herniation on MRI: the usefulness of posterior epidural fat. Neurochirurgie. 2012;58:346–52. https://doi.org/10.1016/j.neuchi.2012.05.004. Cheung KK, Dhawan RT, Wilson LF, Peirce NS, Rajeswaran G. Pars interarticularis injury in elite athletes—the role of imaging in diagnosis and management. Eur J Radiol. 2018;108:28–42. https://doi. org/10.1016/j.ejrad.2018.08.029. Chung CC, Shimer AL.  Lumbosacral spondylolysis and spondylolisthesis. Clin Sports Med. 2021;40:471–90. https://doi.org/10.1016/j. csm.2021.03.004. Darnis A, Launay O, Perrin G, Barrey C. Surgical management of multilevel lumbar spondylolysis: a case report and review of the literature. Orthop Traumatol Surg Res. 2014;100:347–51. https://doi. org/10.1016/j.otsr.2013.12.021. Debnath UK.  Lumbar spondylolysis—current concepts review. J Clin Orthop Trauma. 2021;21:101535. https://doi.org/10.1016/j. jcot.2021.101535. Deutman R, Diercks RL, de Jong TE, van Woerden HH. Isthmic lumbar spondylolisthesis with sciatica: the role of the disc. Eur Spine J. 1995;4:136–8. https://doi.org/10.1007/BF00298235.

Goetzinger S, Courtney S, Yee K, Welz M, Kalani M, Neal M. Spondylolysis in young athletes: an overview emphasizing nonoperative management. J Sports Med (Hindawi Publ Corp). 2020;2020:9235958. https://doi.org/10.1155/2020/9235958. Hu SS, Tribus CB, Diab M, Ghanayem AJ. Spondylolisthesis and spondylolysis. J Bone Joint Surg Am. 2008;90:656–71. Humphry GM.  A treatise on the human skeleton. Cambridge, UK: Macmillan & Co.; 1858. p. 143n. Kim KS, Chin DK, Park JY.  Herniated nucleus pulposus in isthmic spondylolisthesis: higher incidence of foraminal and extraforaminal types. Acta Neurochir (Wien). 2009;151:1445–50. https://doi. org/10.1007/s00701-­009-­0411-­5. Kim KS, Kim YW, Kwon HD.  Unilateral spondylolysis combined with contralateral lumbar pediculolysis in a military parachutist. J Spinal Disord Tech. 2006;19:65–7. https://doi.org/10.1097/01. bsd.0000161230.87271.f3. Kim YT, Lee H, Lee CS, Lee DH, Hwang CJ, Ahn TS. Direct repair of the pars interarticularis defect in spondylolysis. J Spinal Disord Tech. 2012; https://doi.org/10.1097/BSD.0b013e31827069e4. Lawrence KJ, Elser T, Stromberg R.  Lumbar spondylolysis in the adolescent athlete. Phys Ther Sport. 2016;20:56–60. https://doi. org/10.1016/j.ptsp.2016.04.003. Leone A, Cianfoni A, Cerase A, Magarelli N, Bonomo L. Lumbar spondylolysis: a review. Skeletal Radiol. 2011;40:683–700. https://doi. org/10.1007/s00256-­010-­0942-­0. Mushtaq R, Porrino J, Guzmán Pérez-Carrillo GJ. Imaging of spondylolysis: the evolving role of magnetic resonance imaging. PM R. 2018;10:675–80. https://doi.org/10.1016/j.pmrj.2018.02.001.

Further Reading Nordström D, Santavirta S, Seitsalo S, Hukkanen M, Polak JM, Nordsletten L, et al. Symptomatic lumbar spondylolysis. Neuroimmunologic studies. Spine (Phila Pa 1976). 1994;19:2752–8. https://doi. org/10.1097/00007632-­199412150-­00003. Ono T, Sakamoto A, Jono O, Shimizu A. Osteoid osteoma can occur at the pars interarticularis of the lumbar spine, leading to misdiagnosis of lumbar spondylolysis. Am J Case Rep. 2018;19:207–13. https:// doi.org/10.12659/ajcr.907438. Oshima Y, Inanami H, Iwai H, Koga H, Takano Y, Oshina M, et  al. Is microendoscopic discectomy effective for patients with concomitant lumbar disc herniation and spondylolysis? Global Spine J. 2020;10:700–5. https://doi. org/10.1177/2192568219868970. Sakai T, Sairyo K, Suzue N, Kosaka H, Yasui N. Incidence and etiology of lumbar spondylolysis: review of the literature. J Orthop Sci. 2010;15:281–8. https://doi.org/10.1007/s00776-­010-­1454-­4.

493 Tanveer F, Arslan SA, Darain H, Ahmad A, Gilani SA, Hanif A. Prevailing treatment methods for lumbar spondylolysis: a systematic review. Medicine (Baltimore). 2021;100:e28319. https://doi. org/10.1097/MD.0000000000028319. Tarpada SP, Kim D, Levine NL, Morris MT, Cho W. Comparing surgical treatments for spondylolysis: review on current research. Clin Spine Surg. 2021;34:276–85. https://doi.org/10.1097/ BSD.0000000000001115. Tofte JN, CarlLee TL, Holte AJ, Sitton SE, Weinstein SL.  Imaging pediatric spondylolysis: a systematic review. Spine (Phila Pa 1976). 2017;42:777–82. https://doi.org/10.1097/BRS.0000000000001912. Wiltse LL, Widell EH Jr, Jackson DW. Fatigue fracture: the basic lesion is isthmic spondylolisthesis. J Bone Joint Surg Am. 1975;57:17–22. Zhu JG, Qi DZ, Tan J. Repair of pars defect in a patient accompanied with disc herniation by a modified Buck's. Eur Rev Med Pharmacol Sci. 2012;16:1859–65.

Lumbar Spondylolisthesis

36.1 Generalities and Relevance Spondylolisthesis refers to a slippage (displacement) of one vertebral body compared to another. Overall, this displacement could be anterior (anterolisthesis) or posterior (retrolisthesis) with respect to the inferior adjacent vertebral body. However, in practice, the term “spondylolisthesis” is used to design an “anterolisthesis.” Lateral displacement is called laterolisthesis. The term derives from the Greek words spondylos (vertebra) and olisthesis (slippage). Spondylolisthesis was first described by the Belgian obstetrician George Herbiniaux (1740–1811) in 1782. He reported an osseous prominence of the anterior part of the

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sacrum as a factor of mechanical obstruction to vaginal delivery in some patients. However, Killian is the one who coined the term “spondylolisthesis” in 1854. The American orthopedic surgeon Henry William Meyerding (1884–1969) is best known for his spondylolisthesis classification system published in 1932. The first case of degenerative spondylolisthesis was reported by the German surgeon Herbert Junghanns (1902–1986) in 1930 whereas the first post-­ traumatic lumbar spondylolisthesis was described by the English orthopedic surgeon Reginald Watson-Jones (1902– 1972) in the 1940s. The severity of spondylolisthesis is graded from I through V based on the degree of slippage of one vertebral body relative to the adjacent vertebral body (Figs.  36.1, 36.2, 36.3)

Fig. 36.1  Degree of slippage of one vertebral body relative to the adjacent one. The severity of lumbar spondylolisthesis is graded from I to V

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_36

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Fig. 36.2  Lateral plain radiographs (a, b, d) and sagittal reconstruction CT scan (c) showing variable grades of lumbar spondylolisthesis: grade I (a), grade II (b), grade III (c), and grade IV (d)

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Fig. 36.3  Case 1. Sagittal T1- (a) and T2-weighted MRI (b) as well as axial T2-weighted MRI (c–e) showing grade I L4-L5 degenerative spondylolisthesis. Note the central and bilateral foraminal stenosis on the axial view (d)

36.1 Generalities and Relevance

[Grade I: 100% (aka spondyloptosis)]. This pathologic condition has six main etiologies (Table 36.1); however, the majority of cases are degenerative (Figs.  36.3, 36.4, 36.5) or isthmic (Figs.  36.6, 36.7, 36.8, 36.9, 36.10, 36.11, 36.12, 36.13, 36.14, 36.15, 36.17, 36.18, 36.19) occurring in the lower lumbar spine mainly on L5-S1 level for isthmic spondylolisthesis and L4-L5 level for degenerative spondylolisthesis. Traumatic spondylolisthesis is more unusual and fracture forms can be classified as follows: • • • • • •

Type 1 injury : facet dislocations Type 2 : facet fractures Type 3 : pars fractures Type 4 : fusion mass fractures Type 5 : pedicle fractures Type 6 : complex fractures with vertebral body involvement

Some risk factors for spondylolisthesis have been suggested such as first-degree descendants of patients with spondylolisthesis, native Alaskan Eskimo heritage, obesity, idiopathic scoliosis, or spina bifida occulta at S1 vertebral level. Lumbar spondylolisthesis is asymptomatic in most cases. However, when symptoms happen, they usually develop from either mechanical cause or lumbar spinal stenosis. The

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lumbosacral nerve exiting below the pedicle at that vertebral level is the most vulnerable. It seems that patients with isthmic spondylolisthesis are most exposed to the progression of slippage during growth spurts. On the contrary, older patients with degenerative spondylolisthesis are less likely to progress over the years. Sciatic pain may result from: • Lumbar discopathies and/or pseudodisc herniation at the same level as the spondylolisthesis • True lumbar disc herniation at the level above the spondylolisthesis (seen in up to 20% of patients) • Dynamic sciatic pain due to spinal intersegmental instability • Fibrocartilaginous proliferation at the level of the isthmus • Foraminal or extraforaminal impingement • Lumbosacral spinal stenosis due to intraspinal space narrowing with or without degenerative disorders • Bone spurs • Postural imbalance • Nerve injury Slippage progression is possible with time; however, worsening of the spondylolisthesis becomes less probable when the intervertebral disc has lost more than 80% of its original height and when vertebral endplate osteophytes have developed.

Table 36.1  Various etiologies of lumbar spondylolisthesis Etiology Degenerative Isthmic

Traumatic

Dysplastic

Pathologic Postsurgical/ iatrogenic

Description – Secondary to spinal degenerative changes without any defect in the pars interarticularis (Figs. 36.3, 36.4, 36.5) – Facet joint remodeling, intervertebral disc degeneration, and ligamentum flavum weakness may result in vertebra slippage – This form is more likely to occur in older adults, particularly in women older than fifty years – Caused by a defect in the pars interarticularis (aka spondylolysis or isthmolysis) (Figs. 36.6, 36.7, 36.8, 36.9, 36.10, 36.11, 36.12, 36.13, 36.14, 36.15, 36.17, 36.18, 36.19) but it can also be seen with an elongated par – The origin of isthmic spondylolisthesis is undetermined, but more likely secondary to repeated microtrauma, especially in the pediatric population related to sports. (c.f. Chap. 35 about Lumbar Spondylolysis) – The prevalence of spondylolysis is 4–6% in adolescents and young adults – Male adolescents involved in sports have a higher prevalence compared to those not involved in sports – This rare form results from high-velocity hyperextension injury of the lumbar spine in a congenitally normal vertebra – There is often a fracture of the pars interarticularis or the facet joint structure (bilateral pedicle fractures are rare) – The mean age at injury was 30 years, with the majority being men. The most common cause was road traffic accidents – There is a male predominance with a mean age at the injury of 65-years old – Extraspinal injuries were present in 2/3 of cases – Results from congenital abnormalities of the upper S1 facets or inferior L5 facets – In this form, the facet joints are more sagittally oriented than the classic frontal orientation – Dysplastic spondylolisthesis is more common in the pediatric population, with females more commonly affected than males Secondary to systemic causes (bone or connective tissue disorders) or focal lesions (either infection or tumor) – Iatrogenic instability caused by surgical complications – More frequent in cases operated on for lumbar spinal stenosis or stenosis with concomitant spondylolisthesis – There is no gender predominance with a mean patient age of 65-years old

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Fig. 36.4  Case 2. Grade I L4-L5 degenerative spondylolisthesis with L4-L5 disc herniation (arrowheads) as seen on sagittal (a, b) and axial (c) T2-weighted MRI. Note the bilateral facet joint degenerative changes (arrows) and the global L2-L5 spinal stenosis

36.1 Generalities and Relevance

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Fig. 36.5  Case 3. Grade I L4-L5 degenerative spondylolisthesis (arrows) with a concomitant disc herniation (arrowhead) as shown on sagittal T2-weighted MRI (a) and CT scan (b) as well as on axial T2-weighted MRI (c) and axial CT scan (d, e)

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Fig. 36.6  Case 4. Sagittal T1- (a, c) and T2-weighted MRI (b, d) showing grade II L5-S1 spondylolisthesis (arrows). Note the defect in the pars interarticularis (aka isthmolysis) (arrowheads) and the foraminal L5 nerve impingement (dotted circles)

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Fig. 36.7  Case 5. Lateral plain radiography (a), sagittal T1- (b), and T2-weighted MRI (c) showing a grade II L4-L5 spondylolisthesis. Note the L4-L5 lumbar spinal stenosis and pseudodisc herniation at the same level as the spondylolisthesis (arrows)

36.1 Generalities and Relevance

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Fig. 36.8  Case 5. Grade II L4-L5 spondylolisthesis as shown on sagittal reconstructions (a, b) and axial (c, d) CT scan. Note the bilateral L4 and L5 isthmolysis (arrows)

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Fig. 36.9  Case 6. Grade I L5-S1 isthmic spondylolisthesis as shown on sagittal T2-weighted MRI (a) and on sagittal reconstructions (b–d) CT scan. Note the bilateral two-level isthmolysis on L4 and L5 (arrows)

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Fig. 36.10  Case 7. Grade I L5-S1 spondylolisthesis with adjacent pseudolumbar disc herniation (arrowheads) as shown on sagittal T1- (a), T2(b), and axial T2-weighted MRI (c). Note the dysplastic L5 spinous process (arrows)

36.1 Generalities and Relevance

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Fig. 36.11  Case 7. Grade I L5-S1 isthmic spondylolisthesis as shown on sagittal parenchymal (a) and bone (b) CT scan as well as on axial CT scan (c). Note the dysplastic L5 spinous process (arrowheads) and the bilateral pars interarticularis defect of L5 (arrows)

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Fig. 36.12  Case 8. Bilateral pars interarticularis defect of L5 (arrows) as seen on lumbosacral sagittal reconstructions (a–c)

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Fig. 36.13  Case 8. Pars interarticularis defect of L5 (arrows) as seen on sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c)

36.1 Generalities and Relevance

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Fig. 36.14  Case 9. Grade III L5-S1 spondylolisthesis (arrows) with bilateral isthmolysis of L5 (arrowheads). Sagittal parenchymal (a) and bone (b) CT scan as well as on axial CT scan (c, d). Note the central spinal stenosis (dotted circles)

Fig. 36.15  Case 9. Grade III L5-S1 isthmic spondylolisthesis (arrows) as shown on sagittal T1- (a) and T2-weighted MRI (b)

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Fig. 36.16  Case 10. Grade II L4-L5 spondylolisthesis (arrows) as shown on lateral plain radiography (a), sagittal T1- (b), and T2-weighted MRI (c)

36.1 Generalities and Relevance

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Fig. 36.17  Case 10. Grade II L4-L5 isthmic spondylolisthesis (arrowhead) as shown on sagittal reconstructions (a, b) and axial (c) CT scan. Note the bilateral L4 isthmolysis (arrows)

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Fig. 36.18  Case 11. Grade II L4-L5 isthmic spondylolisthesis (double arrows) as seen on lumbosacral lateral plain radiography (a), sagittal reconstructions (b, c), and axial CT scan (d). Note the bilateral defect of the L4 pars interarticularis (arrows)

36.2 Clinical Presentations Fig. 36.19  Case 11. Lumbosacral MRI in the same patient as in Fig. 36.17. L4-L5 isthmic spondylolisthesis (arrows) as seen on sagittal T1- (a) and T2-weighted MRI (b)

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36.2 Clinical Presentations Diagnostic strategy for patients with lumbar spondylolisthesis starts with a history and physical evaluation. Overall, symptoms may be associated either with spinal stenosis causing lumboradicular syndrome or with mechanical low-back pain. Symptoms often worsened with spinal extension and activity, while spinal flexion and rest quickly improve symptoms. Any combination of low-back pain, hamstring spasm, neurogenic claudication, and lumbosacral radiculopathy can be encountered in patients with lumbar spondylolisthesis and especially among those suffering degenerative spondylolisthesis. The majority of individuals with isthmic spondylolisthesis remain asymptomatic, often discovered incidentally on radiographs. However, about 20 to 25% of patients may present with constitutive symptoms of insidious onset, recurrent low-back pain that increases with strenuous activity, aggravated by lumbar rotation and/or hyperextension, and improves with relative rest. Attention should be given to child and adolescent athletes playing a sport that requires repetitive lumbar extension and rotation. The onset of pain may be either acute or insidious over several weeks. Unlike cases with degenerative spondylolisthesis, patients with ­isthmic spondylolisthesis are less likely to present true and complete sciatic pain with or without a neurologic deficit.

b

Furthermore, central stenosis and symptoms of neurogenic claudication are rarely seen in cases with isthmic spondylolisthesis because the anterior vertebral translation increases the space available in the central spinal canal. Other symptoms may include difficulty walking, tingling, and numbness. Coughing and sneezing can increase the pain. Some patients may also present a “slipping sensation” when moving into an upright position. There are also some difficulties sitting down and trying to stand up. Nocturnal pain may also occur and is usually about malignancy. Patients with septic fever, localized pain that is worse at night, and spinal deformity could present spondylodiscitis or vertebral osteomyelitis. Whereas acute injury to the posterior elements of the lumbar spine caused by high-energy trauma will suggest a traumatic lumbar spondylolisthesis. Neurologic deficits may include motor and sensory weakness and are most common in the distribution of the exiting nerve roots. Partial or complete cauda equina syndrome is possible. The spinal examination should seek for increased lumbar lordotic posture, tight hamstrings, limited trunk range of motion (principally with extension), as well as pain and stiffness on the palpation of the pars fracture area. The positive Stork test is highly suggestive of lumbar spondylolysis. The maneuver consists of a single-leg hyperextension and rotation of the spine which reproduces the patient’s pain.

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The straight leg raise test should be performed when discogenic sciatica is suspected. In addition, complete neurologic, rheumatologic, and general exams should be necessary.

36.3 Paraclinic Features Spinal imaging is used to confirm a clinical diagnosis, characterize the cause of spondylolisthesis (c.f. Table 36.1), provide the degree of anterior vertebral slipping, show the compressive lesions, and assess the dynamic spinal instability. Furthermore, imaging features may help decisions regarding surgery and preoperative planning. Generally, there is no association between clinical symptom changes and spondylolisthesis radiographic progression. Standing lumbosacral anteroposterior and lateral standard radiographs are the standard for the initial diagnosis of spondylolisthesis (Fig. 36.20). Oblique radiographs may help to directly visualize the pars interarticularis. Regarding isthmic spondylolisthesis, the lesion is most typically visible in the oblique view which shows the classic broken neck on the “Scotty dog” (Fig. 36.21). The majority of spondylolysis is bilateral and interests only one vertebral level (mainly L5). Fig. 36.20  Case 12. Anteroposterior (a) and lateral (b) plain radiographs showing a grade I L4-L5 isthmic spondylolisthesis. Note the pars interarticularis defect (arrows) and the L4 spinous process slippage (brace)

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According to Meyerding’s radiographic classification, the majority of spondylolisthesis cases will represent grade I or II.  Dynamic flexion-extension plain radiographs may be used in the evaluation of variable degrees of adjacent segmental instability (Figs. 36.22, 36.23, 36.24). Computed tomography (CT) scan of the spine is much more accurate for diagnosing spondylolisthesis. The listhesis can be better visualized on sagittal reconstructions on bone windows as compared to axial CT imaging (Figs. 36.8, 36.9, 36.11, 36.12, 36.14, 36.17, 36.18, and 36.25). However, magnetic resonance imaging (MRI) should be used as the first-line imaging modality in the pediatric population due to radiation exposure from CT scan. MRI is excellent at detecting neural and soft tissue pathologies. However, MRI is somewhat limited in adequately detecting the osseous cortical integrity of incomplete fractures. The attention should be on the axial and sagittal T2-weighted images, as these will illustrate any compression of neurologic elements (Figs. 36.4, 36.5, 36.6, 36.7, 36.15, 36.16, 36.19, 36.26, and 36.29). Preoperative CT scan combined with MRI can be used in complex and severe cases to further define the anatomy of the region of interest, and assess associated disorders such as lumbar disc lesions, facet joint arthrosis, spinal canal, and

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36.3 Paraclinic Features

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Fig. 36.21  Normal oblique lumbar radiography showing the classic “Scottie Dog Model of the lumbar spine” (a). Ear: superior articular process (1). Nose: transverse process (2). Eye: pedicle (3). Neck: pars interarticularis aka isthmus (4). Foreleg: inferior articular process (5). Body: lamina and spinous process (6). Hind leg: inferior articular proFig. 36.22  Case 2. L4-L5 degenerative spondylolisthesis. Lateral dynamic flexion-extension plain radiographs (a, b) showing mild adjacent segmental instability (arrows)

a

cess (contralateral) (7). Tail: superior articular process (contralateral) (8). Illustration of a black Scottie dog (Scottish terrier) (b). The classic broken neck of the "Scotty dog" (arrows) on oblique lumbar radiography may help to directly visualize the pars interarticularis defect (aka isthmolysis) (c)

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512 Fig. 36.23  Case 12. Lateral dynamic flexion-extension plain radiographs (a, b) showing mild L4-L5 segmental instability (double arrows). Note the defect of the pars interarticularis (isthmolysis) (arrows)

Fig. 36.24  Case 13. Lateral dynamic flexion-extension plain radiographs (a, b) showing no segmental instability (double arrows)

36  Lumbar Spondylolisthesis

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36.3 Paraclinic Features

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Fig. 36.25  Case 13. Grade II L5-S1 isthmic spondylolisthesis (arrowhead) with bilateral isthmolysis of L5 (arrows) as seen on sagittal (a–c) and axial (d) CT scan

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Fig. 36.26  Case 14. Lumbosacral MRI showing mild vertebral slippage but an L4-L5 foraminal disc herniation (arrows). Sagittal (a, b) and axial (c) T2-weighted MRI. Note the defect of the pars interarticularis (isthmolysis) (arrowheads)

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foraminal stenosis, osteophytosis, vertebral neoplasms or osteomyelitis. To determine and predict vertebral slipping progression as well as to plan future treatment, further factors are also essential including the cause of spondylolisthesis, lumbopelvic measurements, sacral structures, and global spinal alignment.

36.4 Treatment Options and Prognosis The ultimate goal of treatment of a patient with lumbar spondylolisthesis is to: • • • • • •

Relieve pain Restore neural function Perform nervous decompression Stabilize any spinal instability Prevent neurologic deterioration Control causative factors if possible

Initial treatment of patients with spondylolisthesis is mainly conservative and consists of bracing, activity restriction, bed rest, pharmacologic therapy (analgesics, nonsteroidal anti-inflammatory drugs, and muscle relaxants), and physical therapy programs. If lumbosacral radicular symptoms predominate, transforaminal epidural corticosteroid injections may lead to temporary relief. Surgical intervention depends on many factors as shown above; however, surgery is generally reserved for the following conditions: • Failure to respond to conservative treatment (minimum of 3 months) • Progression of vertebral slippage • Intractable pain limiting daily functions • Development of neurological deficits • Segmental instability associated with pain Overall, surgery is necessary in less than 20% of cases of lumbar spondylolisthesis. The urgency of treatment is dictated largely by the presence of severe neurologic symptoms such as muscle weakness of the lower extremities and cauda equina syndrome. No definitive standards exist for surgical treatment. The surgical procedure includes a varying combination of decompression, reduction if possible, fusion with or without instrumentation, or interbody fusion (Figs.  36.27, 36.28, 36.29, 36.30, 36.31, 36.32, 36.33, 36.34, 36.35). Technically, there are three main approaches for surgery: anterior, posterior, or posterolateral. If possible, some surgeons recommend a reduction of the spondylolisthesis to decrease foraminal narrowing, improve spinopelvic sagittal alignment, and decrease the possibility

36  Lumbar Spondylolisthesis

of upcoming additional degenerative spinal change. However, this reduction can be more difficult and hazardous in higher grades and impacted lumbar spondylolisthesis (Figs. 36.14 and 36.15). Regarding lumbar traumatic spondylolisthesis, less severe (Types I to III) injuries and those with low-grade listhesis only require posterior instrumentation and fusion. Otherwise, if the injury involves the anterior column and/or pedicles (Types 4 to 6), or has a high-grade listhesis, posterior instrumentation, and fusion involving additional levels superiorly or inferiorly are required for stability with possible anterior interbody fusion. Surgical complications are unusual but should be known including a failed fusion (pseudarthrosis), infections, chronic persistent pain, neurological deteriorations, progression of vertebral slippage, hardware failure, and the failed back surgery syndrome (c.f. Chap. 13 about Surgical Complications of Discogenic Sciatica). With the development of endoscopic techniques and advanced intraoperative fluoroscopy, many surgeons perform percutaneous minimally invasive direct spondylolisthesis repair with good results. If needed, some additional surgical procedures may be added in conjunction with concomitant lesions related to vertebral tumors, spondylodiscitis, or other causative factors. Improvement in neurological symptoms, ambulation, and pain is expected with successful operative treatment except for patients with complete neurological injury or the presence of nerve root disruption. Overall, the outcome in patients with spondylolysis is usually good. Asymptomatic individuals require no specific treatments or any changes in their daily activities. Even patients who present with symptomatic lumbar spondylolisthesis usually have a very favorable prognosis. However, the general prognosis is limited by the nature of the lesions as well as the underlying disease. Psychological and social factors may affect the rehabilitation of injured young athletes. Consequently, it is important to provide them with social support and personal assistance when needed.

Fig. 36.27  Case 2. Intraoperative view after L2-L4 laminectomy and foraminotomy as well as posterior fusion with screws and rods

36.4 Treatment Options and Prognosis

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Fig. 36.28  Case 2. Postoperative CT scan showing the L3-L5 posterior fixation system as seen on sagittal (a) and coronal (b) reconstructions CT scan as well as on axial CT scan (c–e)

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Fig. 36.29  Case 12. Grade I L4-L5 isthmic spondylolisthesis as seen on sagittal T1- (a) and T2-weighted MRI (b, c). Note the concomitant pseudolumbar disc herniation (arrow)

36.4 Treatment Options and Prognosis

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Fig. 36.30  Case 12. Intraoperative views via a posterior approach (a–d). Position of the pedicle screws on L4 and L5 (b). One-piece ablation of the L4 posterior arch (c, d)

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Fig. 36.31  Case 12. Lateral (a) and anteroposterior (b) views of the L4 posterior arch. Note the bilateral pars interarticularis defect (arrows) and the inferior facet joints (stars)

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Fig. 36.32  Case 12. Intraoperative views via a posterior approach (a, b). Bilateral L4-L5 foraminotomy (arrows) (a). Position of the posterior screw-rod fixation system following decompression and reduction (b)

Fig. 36.33  Case 12. Postoperative anteroposterior (a) and lateral (b) plain radiographs showing the position of the posterior L4-L5 pedicle screw-rod system

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Further Reading

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Fig. 36.34  Case 12. Postoperative axial CT scan (a, b) showing position of the pedicle screws on L4 (a) and L5 (b)

Fig. 36.35  Case 3. Operative view after L4 posterior decompression, L4-L5 herniectomy/discectomy, and bilateral foraminotomy. Note the pedicle screws

Further Reading Abdel-Fattah AR, Bell F, Boden L, Ferry J, McCormick C, Ross M, et  al. To fuse or not to fuse: the elderly patient with lumbar stenosis and low-grade spondylolisthesis. Systematic review and meta-analysis of randomised controlled trials. Surgeon. 2022:S1479-­ 666X(22)00034-8. https://doi.org/10.1016/j.surge.2022.02.008. Aihara T, Takahashi K, Yamagata M, Moriya H.  Fracture-dislocation of the fifth lumbar vertebra. A new classification. J Bone Joint Surg Br. 1998;80:840–5. https://doi.org/10.1302/0301-­620x.80b5.8657. Akhaddar A, Boucetta M. Unsuspected spondylolysis in patients with lumbar disc herniation on MRI: the usefulness of posterior epidural fat. Neurochirurgie. 2012;58:346–52. https://doi.org/10.1016/j.neuchi.2012.05.004. Akkawi I, Zmerly H.  Degenerative spondylolisthesis: a narrative review. Acta Biomed. 2022;92:e2021313. https://doi.org/10.23750/ abm.v92i6.10526.

Alqarni AM, Schneiders AG, Cook CE, Hendrick PA. Clinical tests to diagnose lumbar spondylolysis and spondylolisthesis: a systematic review. Phys Ther Sport. 2015;16:268–75. https://doi.org/10.1016/j. ptsp.2014.12.005. Alomari S, Judy B, Sacino AN, Porras JL, Tang A, Sciubba D, et al. Isthmic spondylolisthesis in adults… A review of the current literature. J Clin Neurosci. 2022;101:124–30. https://doi.org/10.1016/j. jocn.2022.04.042. Bhalla A, Bono CM. Isthmic lumbar spondylolisthesis. Neurosurg Clin N Am. 2019;30:283–90. https://doi.org/10.1016/j.nec.2019.02.001. Bydon M, Alvi MA, Goyal A. Degenerative lumbar spondylolisthesis: definition, natural history, conservative management, and surgical treatment. Neurosurg Clin N Am. 2019;30:299–304. https://doi. org/10.1016/j.nec.2019.02.003. Chung CC, Shimer AL.  Lumbosacral spondylolysis and spondylolisthesis. Clin Sports Med. 2021;40:471–90. https://doi.org/10.1016/j. csm.2021.03.004. Dantas F, Dantas FLR, Botelho RV. Effect of interbody fusion compared with posterolateral fusion on lumbar degenerative spondylolisthesis: a systematic review and meta-analysis. Spine J. 2022;22:756– 68. https://doi.org/10.1016/j.spinee.2021.12.001. Deutman R, Diercks RL, de Jong TE, van Woerden HH. Isthmic lumbar spondylolisthesis with sciatica: the role of the disc. Eur Spine J. 1995;4:136–8. https://doi.org/10.1007/BF00298235. Gabel BC, Curtis E, Gonda D, Ciacci J.  Traumatic L5 posterolateral spondyloptosis: a case report and review of the literature. Cureus. 2015;7:e277. https://doi.org/10.7759/cureus.277. Guglielmino A, Sorbello M, Murabito P, Naimo J, Palumbo A, Lo Giudice E, et al. A case of lumbar sciatica in a patient with spondylolysis and spondylolysthesis and underlying misdiagnosed brucellar discitis. Minerva Anestesiol. 2007;73:307–12. Guha D, Heary RF, Shamji MF. Iatrogenic spondylolisthesis following laminectomy for degenerative lumbar stenosis: systematic review and current concepts. Neurosurg Focus. 2015;39:E9. https://doi.org /10.3171/2015.7.FOCUS15259. Guigui P, Ferrero E.  Surgical treatment of degenerative spondylolisthesis. Orthop Traumatol Surg Res. 2017;103:S11–20. https://doi. org/10.1016/j.otsr.2016.06.022. Hajjioui A, Khazzani H, Sbihi S, Bahiri R, Benchekroune B, Hajjaj-­ Hassouni N. Spondylolisthesis on bilateral pedicle stress fracture in

520 the lumbar spine: a case study. Ann Phys Rehabil Med. 2011;54:53– 8. https://doi.org/10.1016/j.rehab.2010.12.001. Hussain I, Kirnaz S, Wibawa G, Wipplinger C, Härtl R. Minimally invasive approaches for surgical treatment of lumbar spondylolisthesis. Neurosurg Clin N Am. 2019;30:305–12. https://doi.org/10.1016/j. nec.2019.02.004. Karsy M, Bisson EF. Surgical versus nonsurgical treatment of lumbar spondylolisthesis. Neurosurg Clin N Am. 2019;30:333–40. https:// doi.org/10.1016/j.nec.2019.02.007. Kim KS, Chin DK, Park JY.  Herniated nucleus pulposus in isthmic spondylolisthesis: higher incidence of foraminal and extraforaminal types. Acta Neurochir (Wien). 2009;151:1445–50. https://doi. org/10.1007/s00701-­009-­0411-­5. Li Y, Wu Z, Guo D, You H, Fan X.  A comprehensive comparison of posterior lumbar interbody fusion versus posterolateral fusion for the treatment of isthmic and degenerative spondylolisthesis: A meta-analysis of prospective studies. Clin Neurol Neurosurg. 2020;188:105594. https://doi.org/10.1016/j. clineuro.2019.105594. Meyerding HW.  Spondylolisthesis. Surg Gynecol Obstet. 1932;54:371–7. Murray MR, Skovrlj B, Qureshi SA.  Surgical treatment of isthmic spondylolisthesis. Clin Spine Surg. 2016;29:1–5. https://doi. org/10.1097/BSD.0000000000000358. Nikaido T, Konno SI.  Usefulness of lateral lumbar interbody fusion combined with indirect decompression for degenerative lumbar spondylolisthesis: a systematic review. Medicina (Kaunas). 2022;58:492. https://doi.org/10.3390/medicina58040492. Ramhmdani S, Xia Y, Xu R, Kosztowski T, Sciubba D, Witham T, et  al. Iatrogenic spondylolisthesis following open lumbar laminectomy: case series and review of the literature. World Neurosurg. 2018;113:e383–90. https://doi.org/10.1016/j. wneu.2018.02.039. Samuel AM, Moore HG, Cunningham ME. Treatment for degenerative lumbar spondylolisthesis: current concepts and new evidence. Curr Rev Musculoskelet Med. 2017;10:521–9. https://doi.org/10.1007/ s12178-­017-­9442-­3.

36  Lumbar Spondylolisthesis Schulte TL, Ringel F, Quante M, Eicker SO, Muche-Borowski C, Kothe R. Surgery for adult spondylolisthesis: a systematic review of the evidence. Eur Spine J. 2016;25:2359–67. https://doi.org/10.1007/ s00586-­015-­4177-­6. Takahashi T, Hanakita J, Ohtake Y, Funakoshi Y, Oichi Y, Kawaoka T, et  al. Current status of lumbar interbody fusion for degenerative spondylolisthesis. Neurol Med Chir (Tokyo). 2016;56:476–84. https://doi.org/10.2176/nmc.ra.2015-­0350. Van Isseldyk F, Liu Y, Kim JH, Correa C, Quillo-Olvera J, Kim JS. Full-­ endoscopic foraminotomy in low-grade degenerative and isthmic spondylolisthesis: a patient-specific tailored approach. Eur Spine J. 2023; https://doi.org/10.1007/s00586-­023-­07737-­x. Ver MLP, Dimar JR 2nd, Carreon LY.  Traumatic lumbar spondylolisthesis: a systematic review and case series. Global Spine J. 2019;9:767–82. https://doi.org/10.1177/2192568218801882. Vialle R, Charosky S, Rillardon L, Levassor N, Court C.  Traumatic dislocation of the lumbosacral junction diagnosis, anatomical classification and surgical strategy. Injury. 2007;38:169–81. https://doi. org/10.1016/j.injury.2006.06.015. Violas P, Lucas G.  L5S1 spondylolisthesis in children and adolescents. Orthop Traumatol Surg Res. 2016;102:S141–7. https://doi. org/10.1016/j.otsr.2015.03.021. Watson-Jones R. Fractures and other bone and joint injuries. 2nd ed. Baltimore, MD: Williams & Wilkins; 1941. Wiltse LL, Newman PH, Macnab I. Classification of spondylolisis and spondylolisthesis. Clin Orthop Relat Res. 1976:23–9. Yamaki VN, Morais BA, Brock RS, Paiva WS, de Andrade AF, Teixeira MJ.  Traumatic lumbosacral spondyloptosis in a pediatric patient: case report and literature review. Pediatr Neurosurg. 2018;53:263– 9. https://doi.org/10.1159/000488766. Yoshihara H.  Pathomechanisms and predisposing factors for degenerative lumbar spondylolisthesis: a narrative review. JBJS Rev. 2020;8:e2000068. https://doi.org/10.2106/JBJS.RVW.20.00068. Zhang J, Liu TF, Shan H, Wan ZY, Wang Z, Viswanath O, et al. Decompression using minimally invasive surgery for lumbar spinal stenosis associated with degenerative spondylolisthesis: a review. Pain Ther. 2021;10:941–59. https://doi.org/10.1007/s40122-­021-­00293-­6.

Lumbar Degenerative Scoliosis

37.1 Generalities and Relevance Sometimes lumbar structural scoliosis can cause lumbosacral radicular pain in the lower extremities, especially in adults. These patients may have coronal and sagittal deformities. When this happens, sciatica often results from foraminal stenosis with compression of its corresponding nerve root at the apex of the open end of the scoliosis curve. Hippocrates of Kos [460–377 BC] first recognized spinal deformities. He showed that the forward flexion of the spine changes with age and the work of the earth. In the second century AD, Claudius Galenus or Galen [129–216 AD], another Greek physician, described spinal deformities and curvatures and invented the terms “scoliosis,” “lordosis,” and “kyphosis” and he tried to treat them. The majority of the cases with misalignment of the lumbosacral spine are related to degenerative scoliosis in older patients (aging spine). Sciatica is rarely related to other forms of structural scoliosis (idiopathic, congenital, traumatic, neoplastic, infectious, or neurologic) unless scoliosis coexists with other causes of lumbosacral radiculopathy. This condition should be differentiated from the scoliotic list (aka sciatic scoliosis) which is nonstructural scoliosis secondary to discogenic lumbosacral nerve root irritation. The direction of sciatic scoliosis is not associated with the topographic location of nerve root compression but was related to the side of lumbar disc herniation (LDH). When the painful stimulus (LDH) is removed, most of the sciatic scoliotic list disappeared. The majority of sciatic scoliosis has been reported in adolescents and young adults while lumbar degenerative scoliosis is observed in elderly patients. Lumbar degenerative scoliosis can cause sciatica in four different ways or any combination of them: • • • •

Lumbar discopathies Postural imbalance Foraminal or extraforaminal stenosis Facet (zygapophyseal) joint arthritis

37

The main cause of this radiating pain in degenerative scoliosis is foraminal or extraforaminal nerve root compromise. Most degenerative lumbar scoliosis is mild to moderate (Cobb angle less than 40°) including 4 to 5 lumbar vertebral segments, but this condition is frequently associated with rotatory subluxation and lateral listhesis, and complicated with other lumbosacral degenerative affections. Then managing this form of adult scoliosis is usually complex and relatively difficult. Twenty percent of the patients with lumbar spinal stenosis had scoliosis and 90% of the patients with lumbar degenerative scoliosis had spinal stenosis. There is often a significant preponderance of men. For some authors, lateral stenosis was probably mostly due to degenerative phenomena (disc, vertebral endplate, ligamentum flavum, facet joint) which generated both scoliosis and stenosis with their specific and common symptoms. Concomitant degenerative lumbosacral spondylolisthesis is not rare (up to 25% of cases). In addition, the majority of degenerative lumbosacral spondylolisthesis is associated with central stenosis.

37.2 Clinical presentations The majority of symptomatic patients present with worsening low-back pain, progressive spinal deformity, and/or neurological symptoms (especially radicular pain, radiculopathy, or neurogenic claudication). Unlike traditional lumbar central canal stenosis, lumbosacral radicular pain seems to be more common than neurogenic claudication. Neurological deficits are rare and include sensory and/or motor deficits with or without reflex abnormalities. Besides lumbar stenosis symptoms, some patients complain of spinal imbalance symptoms mainly represented by axial pain and the incapacity to stand upright. Sometimes, the radical pain might hide the mechanical axial pain. The

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spinal examination should assess for pelvic retroversion and lumbar sagittal imbalance. The majority of patients have limited lumbar mobility but the Lasègue test is inconstantly positive. Lateral and foraminal stenosis (site of neural compression) is more often observed (up to 80% of cases) in the concavity of the lumbosacral curve of scoliosis. In some cases, separating lumbosacral radiculopathy from sciatic peripheral mononeuropathy on clinical grounds can be difficult. Therefore, in such cases electrodiagnostic studies are decisive. Many cases of adult lumbar degenerative scoliosis remain asymptomatic and scoliosis will be found only incidentally on spinal imaging.

37.3 Imaging Features Lumbar degenerative scoliosis can be assessed by plain radiographs, computed tomography (CT) scan, and magnetic resonance (MR) imaging (Figs. 37.1, 37.2, 37.3, 37.4, 37.5, 37.6, 37.7, 37.8, 37.9, 37.10, 37.11, 37.12). Lumbosacral anteroposterior and lateral standard radiographs are usually the first imaging evaluation for lumbar degenerative scoliosis (Figs. 37.1, 37.6a, 37.8a, and 37.10).

Fig. 37.1  Case 1. Coronal deviation of the lumbar spine (Cobb angle of 26°) as seen on plain radiographs (a, b)

a

Plain lumbosacral X-rays are useful for detecting vertebral defects, spondylosis, spinal misalignment (including spondylolisthesis), and instability (dynamic X-rays). Adjacent segment degeneration and loss of lordosis are common anomalies seen on plain radiography. Additional dynamic plain radiography including flexion, extension views, and even oblique views, can be required if there is a potential preoperative instability. Some other concomitant spinal disorders (e.g., osteoporosis) and degenerative changes can be best seen on CT scan with bone windows and reconstructed 3D images (Figs. 37.3, 37.8c, and 37.12). MR imaging remains the main imaging method for identifying symptomatic nerve root compromise in degenerative scoliosis. The imaging protocol should include axial, sagittal, and coronal images (Figs. 37.2, 37.5, 37.6b, c, 37.7, 37.9, and 37.11). Spinal MR imaging is helpful in visualizing lateral osteophyte, asymmetric bulging disc, pseudoarticulation, and altered alignment (e.g., lateral listhesis, and axial vertebral rotation angle). MR neurography is a new promising technique in helping to clearly determine nerve root entrapment by combining high-resolution images and uniform fat-suppressed T2-weighted images.

b

37.3 Imaging Features Fig. 37.2  Case 1. Lumbar degenerative scoliosis with concomitant L4-L5 disc herniation on the left side (arrows). Lumbosacral sagittal (a) and axial (b, c) T2-weighted MRI

Fig. 37.3  Case 2. Lumbosacral degenerative scoliosis as seen on CT scan (a–c). There is a coronal deviation of the lumbar spine with concomitant various degenerative changes: listhesis, lateral osteophyte, asymmetric bulging disc, pseudoarticulation, central and foraminal stenosis, zygapophyseal facet joint hypertrophy, and ligamentum flavum thickening

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Fig. 37.4  Case 2. Lumbosacral degenerative scoliosis as seen on MR imaging. There is various degenerative changes especially L4-L5 disc herniation (arrows) and spinal stenosis. Sagittal T1- (a) and T2-weighted MRI (b) as well as axial T2-weighted MRI (c, d) Fig. 37.5  Case 2. Coronal deviation of the lumbar spine (Cobb angle of 27°) with degenerative changes as seen on coronal T2-weighted MRI (a, b)

37.3 Imaging Features

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Fig. 37.6  Case 3. Lumbar degenerative scoliosis (Cobb angle of 24°) as seen on plain radiographs (a). There is a concomitant lumbar spinal stenosis, degenerative spondylolisthesis, and multisegmental discopathies (arrows). Sagittal T1- (b) and T2-weighted MRI (c)

Fig. 37.7  Case 3. Axial T2-weighted MRI (a–c) showing spinal canal narrowing, foraminal and extraforaminal stenosis (yellow arrows), and facet joint degenerative subluxation (red arrow)

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37  Lumbar Degenerative Scoliosis

Fig. 37.8  Case 4. Lumbar degenerative scoliosis (Cobb angle of 25°) as seen on plain radiographs (a) and coronal T2-weighted MRI (b). Note lumbar degenerative changes on sagittal CT scan with osteophytosis and zygapophyseal facet joint hypertrophy (arrows) (c)

Fig. 37.9  Case 4. Lumbosacral degenerative scoliosis as seen on sagittal (a, b) and axial (c, d) T2-weighted MRI. There are concomitant various degenerative changes: L4-L5 listhesis, L4-L5 disc herniation

(arrowheads), asymmetric bulging disc with foraminal stenosis (arrows), and zygapophyseal facet joint hypertrophy

37.3 Imaging Features

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Fig. 37.10  Case 5. Lumbar degenerative scoliosis (Cobb angle of 24°) as seen on anteroposterior (a) and lateral (b) plain radiographs

Fig. 37.11  Case 5. Lumbosacral degenerative scoliosis as seen on sagittal T2-weighted MRI (a, b) and on STIR sequences (c, d) T2-weighted MRI. There are concomitant multiple and various degenerative changes. Note the L3-L5 foraminal stenosis (arrows)

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Fig. 37.12  Case 5. Lumbosacral degenerative scoliosis as seen on coronal (a) and sagittal (b, c) reconstructions CT scan (b, c). There is a coronal deviation of the lumbar spine with concomitant various degenerative changes. Note the significant L3-L4 foraminal stenosis (arrow)

Often central stenosis occurs at the junctional level between the lumbar and lumbosacral scoliotic curves. While foraminal and lateral stenosis is most usually seen in the concavity of the distal lumbosacral curve. If needed, provocation tests using transforaminal selective nerve root blocks are achieved for identifying the exact symptomatic level. Concordance between clinical findings and spinal imaging results is essential before any surgical treatment. To prevent wrong-level lumbosacral spine surgery, it is imperative to correlate CT scan and/or MR imaging with preoperative and intraoperative radiographs.

37.4 Treatment Options and Prognosis Conservative treatment (activity modification, pharmacologic therapy, and physical therapy programs) may be effective in some patients with symptomatic lumbar degenerative scoliosis, but when the symptoms are uncontrollable and exacerbate progressively, surgical intervention should be considered. The key to surgical treatment for symptomatic degenerative lumbar scoliosis is to relieve lumbosacral radicular pain and correct/stabilize the spinal column. Modalities of surgical treatment include nerve root decompression, laminectomy decompression and fusion with pedicle fixation, and combined anterior-posterior decompression with spinal fixation. The stenosis-generated radicular pain will resolve by decompression with or without short fusion (Fig. 37.13). The primary imbalance-related pain is treated by correction surgery and long fusion. However, the perfect planned treatment of spinal stenosis and the correction of scoliosis might

Fig. 37.13  Case 5. Intraoperative appearance of the thecal sac (stars) after its decompression by L4-L1 bilateral laminectomy

not be always performed because of the general health status of the elderly population. For some authors, the treatment should be individualized according to the patient’s age, general and economic factors, the severity of the deformity, and other coexisting lumbar degenerative disorders. Complications associated with surgical treatment include the risks of any spine surgery in older populations such as neurovascular injury, dural tear, cerebrospinal fluid fistula, thromboembolism, infection, anesthesia complication, persistent pain, pseudoarthrosis, internal fixation failure, and spinal deformity progression. Patients with great coronal and/or sagittal deformities are at high risk of neurologic compromise during pedicle screw placement and corrective procedures (c.f. Chap. 13 about Surgical Complications). Most patients (about 80% of cases) presented with symptomatic lumbar scoliosis had excellent to good results after the surgical procedure; however, some fair or poor results were reported (up to 20% of cases). As with other traditional forms of lumbar spinal stenosis, patients with motor neurological deficits are more resistant to improvement. The fusion rate was about 90% in patients with lumbar fixation. Overall, important global coronal malalignment is clearly associated with poor patient outcomes.

Further Reading

Further Reading Akhaddar A, Arabi H.  Isolated painless scoliosis in lumbar disc herniation. Surg Neurol Int. 2020;11:159. https://doi.org/10.25259/ SNI_287_2020. Akhaddar A, Gourinda H, El Alami FZ, El Madhi T, Miri A. Scoliosis and diastematomyelia: four cases and a review of the literature. Rev Chir Orthop Reparatrice Appar Mot. 2000;86:300–5. Ferrero E, Khalifé M, Marie-Hardy L, Regnard N, Feydy A, De Loubresse CG, et  al. Do curve characteristics influence stenosis location and occurrence of radicular pain in adult degenerative scoliosis? Spine Deform. 2019;7:472–80. https://doi.org/10.1016/j. jspd.2018.09.010. Grass JP, Dockendorff IB, Soto VA, Araya PH, Henriquez CM. Progressive scoliosis with vertebral rotation after lumbar intervertebral disc herniation in a 10-year-old girl. Spine (Phila Pa 1976). 1993;18:336– 8. https://doi.org/10.1097/00007632-­199303000-­00005. Hawasli AH, Chang J, Yarbrough CK, Steger-May K, Lenke LG, Dorward IG.  Interpedicular height as a predictor of radicular pain in adult degenerative scoliosis. Spine J. 2016;16:1070–8. https://doi. org/10.1016/j.spinee.2016.04.017. Kim HJ, Chun HJ, Kang KT, Lee HM, Kim HS, Moon ES, et  al. A validated finite element analysis of nerve root stress in degenerative lumbar scoliosis. Med Biol Eng Comput. 2009;47:599–605. https:// doi.org/10.1007/s11517-­009-­0463-­y. Krishnan KM, Newey ML.  Lumbar scoliosis associated with a disc herniation in an adult. Rheumatology (Oxford). 2001;40:1427–8. https://doi.org/10.1093/rheumatology/40.12.1427. Lee SK, Jung JY. Degenerative lumbar scoliosis: added value of coronal images to routine lumbar MRI for nerve root compromise. Eur Radiol. 2020;30:2270–9. https://doi.org/10.1007/s00330-­019-­ 06584-­z.

529 Liu W, Chen XS, Jia LS, Song DW. The clinical features and surgical treatment of degenerative lumbar scoliosis: a review of 112 patients. Orthop Surg. 2009;1:176–83. https://doi.org/10.1111/j.1757-­7861.2009.00030.x. Ploumis A, Transfeldt EE, Gilbert TJ Jr, Mehbod AA, Dykes DC, Perra JE.  Degenerative lumbar scoliosis: radiographic correlation of lateral rotatory olisthesis with neural canal dimensions. Spine (Phila Pa 1976). 2006(31):2353–8. https://doi.org/10.1097/01. brs.0000240206.00747.cb. Pugely AJ, Ries Z, Gnanapragasam G, Gao Y, Nash R, Mendoza-Lattes SA. Curve characteristics and foraminal dimensions in patients with adult scoliosis and radiculopathy. Clin Spine Surg. 2017;30:E111– 8. https://doi.org/10.1097/BSD.0b013e3182aab1e3. Seitsalo S, Osterman K, Poussa M.  Scoliosis associated with lumbar spondylolisthesis. A clinical survey of 190 young patients. Spine (Phila Pa 1976). 1988;13:899–904. https://doi. org/10.1097/00007632-­198808000-­00005. Suk KS, Lee HM, Moon SH, Kim NH. Lumbosacral scoliotic list by lumbar disc herniation. Spine (Phila Pa 1976). 2001;26:667–71. https://doi.org/10.1097/00007632-­200103150-­00023. Tribus CB.  Degenerative lumbar scoliosis: evaluation and management. J Am Acad Orthop Surg. 2003;11:174–83. https://doi. org/10.5435/00124635-­200305000-­00004. Wang G, Cui X, Jiang Z, Li T, Liu X, Sun J. Evaluation and surgical management of adult degenerative scoliosis associated with lumbar stenosis. Medicine (Baltimore). 2016;95:e3394. https://doi. org/10.1097/MD.0000000000003394. Zhao Y, Qi L, Ding C, Quan S, Xu B, Yu Z, Li C.  Characteristics of Sciatic Scoliotic list in lumbar disc herniation. Global Spine J. 2022:21925682221126123. https://doi. org/10.1177/21925682221126123.

Lumbosacral Extraforaminal Stenosis (Far-Out Syndrome)

38.1 Generalities and Relevance Lumbosacral extraforaminal stenosis (LSES) (aka extraforaminal entrapment or lateral exit-zone stenosis) is known as the compression of the spinal nerve root (mainly L5) at the lumbosacral junction outside the lateral border of the pedicle. This condition induces principally sciatic pain with or without neurological deficits as well as neurogenic claudication. LSES is a rare disorder, making both clinical and imaging diagnoses difficult. In addition, this unusual spinal entity frequently results in failed back surgery syndrome. LSES was first reported by Danforth and Wilson in 1925. They observed compression of the L5 nerve by osteophytes at the lateral margin of the L5 and S1 vertebral bodies and the ligaments at the lumbosacral junction in a cadaveric study. In 1982, Nathan et  al. described the notion of the “lumbosacral tunnel” and they found that the L5 nerve could be entrapped inside this tunnel formed by the L5 vertebral body, the sacral ala, and the lumbosacral ligament. In 1984, the American spine surgeon Leon Lamont Wiltse (1913–2005) presented the concept of “Far-out Syndrome” as an entrapment of the L5 nerve root between the transverse process of the L5 vertebra and the sacral ala seen in elderly patients with degenerative lumbar scoliosis and younger patients with isthmic spondylolisthesis. Lumbosacral extraforaminal stenosis encompasses a large spectrum of compressive pathological conditions including those of “Far-out-Syndrome” and others related to vertebral, discal, foraminal, or extraforaminal lesions (Table 38.1).

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Table 38.1  Main causes of lumbosacral extraforaminal stenosis Anatomical structure involved Intervertebral disc

Description Discogenic: often far lateral disc herniation (aka extraforaminal LDH) with subsequent exiting nerve root compression Spondylolisthesis (with at least a 20% slip)

Vertebral isthmus (pars interarticularis) Foraminal area Foraminal stenosis with or without osteophytosis (bone spurs) Extraforaminal – Nerve root may be compressed between area the L5 transverse process and the sacral ala (Figs. 38.1 and 38.2) – Degenerative lumbar scoliosis – Osteophytes at L5 or S1 vertebral body (Fig. 38.3) – Lateral part of the L5–S1 facet joint – Lumbosacral ligament

For many authors, the association between congenital lumbosacral transitional vertebra (LSTV) and lower back/ sciatic pain characterizes Bertolloti’s syndrome rather than LSES (c.f. Chap. 57 about Bertolotti’s Syndrome). Consequently, preexisting lumbosacral transitional anatomy was not systematically included in the lumbosacral extraforaminal stenosis group. Because there are no standardized or validated criteria to define or diagnose LSES, no true consensus exists regarding its prevalence or general epidemiology. However, this condition is much less frequent than foraminal and intraspinal stenosis.

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Fig. 38.1  Case 1. Right-sided far-out syndrome at L5-S1. The L5 nerve root is compressed between the L5 transverse process and the sacral ala. There is also a concomitant disc herniation (arrows) com-

38  Lumbosacral Extraforaminal Stenosis (Far-Out Syndrome)

pressing both L5 and S1 nerve roots (arrowheads) as seen on axial T2-weighted MRI (a–c). Sagittal T1- (d) and T2-weighted (e) MRI

38.1 Generalities and Relevance

Fig. 38.2  Case 1. This right-sided far-out syndrome is better seen on CT scan (bone windows) (a–d). There is a bony spur formation from the “pseudoarticulation” into the root foramen. The right L5 nerve root

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(arrowheads) is compressed between the posterior-inferior-lateral part of the L5 vertebral body and the sacral ala (arrows)

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Fig. 38.3  Case 2. Left-sided far-out syndrome at L3-L4 (arrows). Note the extraforaminal stenosis (bracket) compressing the nerve root (arrowhead) as seen on coronal (a) and axial (b, c) CT scan

38.2 Clinical Presentations The majority of symptomatic patients with LSES present with low-back pain and unilateral sciatic pain with or without neurogenic claudication. Neurological deficits such as motor loss (mainly in the extensor hallucis longus muscle) and sensory disturbance at the L5 region are unusual. Unless there is a concomitant lumbar intraspinal stenosis, to the best of our knowledge, no patient presented with cauda equina syndrome (CES). Interestingly, more than 70% of patients with LSES show a positive Kemp sign (aka quadrant test or extension-rotation test), which is attributable to a narrowing of the extraforaminal area by forced dorsolateral extension and rotation of the lower back. However, this test can also be positive with any other nondegenerative extraforaminal lesions such as schwannoma or even facet joint pathology (e.g., osteoarthritis). Scoliosis may be found to be associated. A workup of low-back pain beginning with palpation, active and passive range of motion, and the straight leg raise test should be performed. In some cases, electrodiagnostic studies are decisive for separating lumbosacral radiculopathy from sciatic peripheral mononeuropathy or lumbosacral plexopathy.

Many other concomitant symptoms related to intraspinal stenosis, lumbar disc herniation, lumbar facet joint syndrome, or potential rheumatologic disease should be considered in clinical presentations. LSES may also mask typical signs and symptoms of many other causes of spinogenic or extra-spinogenic sciatica.

38.3 Paraclinic Features Spinal imaging diagnosis of LSES is often difficult because the area of interest is typically a "hidden zone." Lumbosacral anteroposterior and lateral standard radiographs are usually sufficient for identifying skeletal abnormality. Some authors recommend the Ferguson view (20 degrees caudocephalic anteroposterior). Most symptomatic patients show mild to moderate degenerative lumbar scoliosis. The curve convexity is identical to the symptomatic side. Disc height loss is a common finding at L5-S1 intervertebral level and L5 vertebral body inclines toward the symptomatic side. Axial and coronal CT scan on bone and parenchymatous windows can assess the compressive bony factors related to

38.4 Treatment Options and Prognosis

osteophytes, hypertrophy of the S1 superior process, sacral ala, and bone formation tissue (Figs. 38.2 and 38.3). Besides the LSES, certain associated spinal lesions should receive particular attention during neuroimaging assessment, in particular, lumbar disc herniations, facet joint arthrosis, spinal canal, and foraminal stenosis, osteophytosis, spondylolysis or spondylolisthesis as well as sacroiliac joint disorders. Conventional magnetic resonance imaging (MRI) demonstrates any abnormality in the intraspinal canal and can help to evaluate the degree of foraminal and extraforaminal nerve impingement (Fig.  38.1). However, traditional plans and sequences might not detect the condition. Some authors recommend diffuse tensor images and oblique coronal images. Oblique images are taken perpendicular to the intervertebral foramen with respect to the foraminal spinal nerve angle. In addition, the constructive interference in steady state sequence (CISS) has been reported to be helpful for detecting the loss of surrounding perineural fat and compression of the nerve root outside the foraminal zone. It is important to correlate CT scan and/or MRI with preoperative and intraoperative radiographs. Effective communication between the surgeon and the radiologist is essential regarding the precise location of the compressive lesions. A selective L5 nerve root block (e.g., bupivacaine and corticosteroid) under computed tomography (CT) guidance can be used as a diagnostic tool to define the origin of pain in a patient with LSES. Pain decreased in many cases following this percutaneous block infiltration but it appears that the injection did not provide long-lasting relief.

38.4 Treatment Options and Prognosis Treatment of patients with LSES ranges from conservative, pharmacological, and nonsurgical, to surgical. Conservative management includes activity modification, pharmacologic therapy (analgesics, nonsteroidal anti-inflammatory drugs, and muscle relaxants), and physical therapy interventions. Posture-modifying exercises can improve symptoms by improving muscle strength, coordination, and flexibility. Direct local anesthetic (e.g., bupivacaine) and corticosteroid injection (e.g., triamcinolone acetate) in the extraforaminal area under CT scan guidance produces successful relief of pain but does not offer long-term relief. Wiltse et al. in the 1980s recommended a unilateral posterior lumbosacral paraspinal approach to the alar transverse process for extraforaminal nerve decompression (Fig. 38.4). Wiltse highlighted the great importance of carrying nerve decompression far enough laterally. By Wiltse’s approach, fusion is often not required because the medial part of the

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Fig. 38.4  Illustration showing the unilateral posterolateral (extracanal) approach via paramedian muscle-s plitting technique (Transmusclar Wiltse approach) (arrow) exposing the extraforaminal area

L5-S1 facet joint is often conserved. Nowadays, various surgical approaches and techniques have been used including anterior, posterior, and posterolateral approaches, microsurgical conventional method, microendoscopic technique, and minimally invasive paramedian tubular-based resection procedures with or without fusion. Any concomitant foraminal or intraspinal lesion should be considered. Unrecognized LSES is a potential cause of failed back surgery syndrome. Surgical access to L5-S1 extraforaminal area is often difficult, unlike at other higher lumbar levels. This is mainly due, but not limited, to a depth surgical field, inclination of sacral ala, and bleeding from the vessels around the L5 spinal nerve. Therefore, a particular understanding of the regional anatomy is essential prior to adopting any surgical procedure. Surgical intervention should be considered for patients with severe L5 radiculopathy that failed to respond to conservative management including the use of NSAIDs, a selective nerve root block, and potentially a brace. Dysesthesias have been reported to be among the most important postoperative patient complaint in 5% to 30% of cases. The cause of the dysesthesias may be attributed to the manipulation of the dorsal root ganglion, thermal injury using cautery, and even the avulsion of the dorsal ramus of the spinal nerve. Some authors reported adjacent intervertebral segmental disease, especially in patients who had a spinal fusion procedure. Most patients presented with LSES had good results after the surgery without recurrence; however, some fair or poor results were reported in up to 20% largely due to insufficient surgical decompression.

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Further Reading Abe E, Sato K, Shimada Y, Okada K, Yan K, Mizutani Y.  Anterior decompression of foraminal stenosis below a lumbosacral transitional vertebra. A case report. Spine (Phila Pa 1976). 1997;22:823– 6. https://doi.org/10.1097/00007632-­199704010-­00023. Choi YK.  Lumbar foraminal neuropathy: an update on non-­surgical management. Korean J Pain. 2019;32:147–59. https://doi. org/10.3344/kjp.2019.32.3.147. Danforth MS, Wilson PD. The anatomy of the lumbo-sacral region in relation to sciatic pain. J Bone Joint Surg Am. 1925;7:109–60. Hashimoto M, Watanabe O, Hirano H. Extraforaminal stenosis in the lumbosacral spine. Efficacy of MR imaging in the coronal plane. Acta Radiol. 1996;37:610–3. https://doi.org/10.1177/02841851960 373P238. Heo DH, Sharma S, Park CK. Endoscopic treatment of extraforaminal entrapment of L5 nerve root (far-out syndrome) by unilateral biportal endoscopic approach: technical report and preliminary clinical results. Neurospine. 2019;16:130–7. https://doi.org/10.14245/ ns.1938026.013. Ichihara K, Taguchi T, Hashida T, Ochi Y, Murakami T, Kawai S.  The treatment of far-out foraminal stenosis below a lumbosacral transitional vertebra: a report of two cases. J Spinal Disord Tech. 2004;17:154–7. https://doi.org/10.1097/00024720-­ 200404000-­00013. Ikuta K, Kitamura T, Masuda K, Hotta K, Senba H, Shidahara S. Minimally invasive transtubular endoscopic decompression for L5 radiculopathy induced by lumbosacral extraforaminal lesions. Asian Spine J. 2018;12:246–55. https://doi.org/10.4184/asj.2018.12.2.246. Ise S, Abe K, Orita S, Ishikawa T, Inage K, Yamauchi K, et al. Surgical treatment for far-out syndrome associated with abnormal fusion of the L5 vertebral corpus and L4 hemivertebra: a case report. BMC Res Notes. 2016;9:329. https://doi.org/10.1186/s13104-­016-­ 2123-­2. Iwasaki H, Yoshida M, Yamada H, Hashizume H, Minamide A, Nakagawa Y, et al. A new electrophysiological method for the diagnosis of extraforaminal stenosis at L5-s1. Asian Spine J. 2014;8:145–9. https://doi.org/10.4184/asj.2014.8.2.145. Iwasaki M, Akiyama M, Koyanagi I, Niiya Y, Ihara T, Houkin K. Double crush of L5 spinal nerve root due to L4/5 lateral recess stenosis and bony spur formation of lumbosacral transitional vertebra pseudoarticulation: a case report and review. NMC Case Rep J. 2017;4:121–5. https://doi.org/10.2176/nmccrj.cr.2016-­0308. Jones TL 2nd, Hisey MS.  L5 radiculopathy caused by L5 nerve root entrapment by an L5-S1 anterior osteophyte. Int J Spine Surg. 2012;6:174–7. https://doi.org/10.1016/j.ijsp.2012.05.001. Kanematsu R, Hanakita J, Takahashi T, Minami M, Tomita Y, Honda F.  Extraforaminal entrapment of the fifth lumbar spinal nerve by nearthrosis in patients with lumbosacral transitional vertebrae. Eur Spine J. 2020;29:2215–21. https://doi.org/10.1007/s00586-­020-­ 06460-­1. Kikuchi K, Abe E, Miyakoshi N, Kobayashi T, Abe T, Hongo M, Shimada Y.  Anterior decompression for far-out syndrome below a transitional vertebra: a report of two cases. Spine J. 2013;13:e21–5. https://doi.org/10.1016/j.spinee.2013.02.033. Kim HS, Singh R, Adsul NM, Oh SW, Noh JH, Jang IT.  Management of root-level double crush: case report with technical notes on contralateral interlaminar foraminotomy with full endoscopic uniportal approach. World Neurosurg. 2019;122:505–7. https://doi. org/10.1016/j.wneu.2018.11.110. Kim JY, Kim HS, Jeon JB, Lee JH, Park JH, Jang IT. The novel technique of uniportal endoscopic interlaminar contralateral approach

38  Lumbosacral Extraforaminal Stenosis (Far-Out Syndrome) for coexisting L5-S1 lateral recess, foraminal, and extraforaminal stenosis and its clinical outcomes. J Clin Med. 2021;10:1364. https://doi.org/10.3390/jcm10071364. Kim K, Isu T, Matsumoto R, Miyamoto M, Isobe M.  A case of far-­ out syndrome: case report and review of the literature. No Shinkei Geka. 2006;34:313–7. Kitamura M, Eguchi Y, Inoue G, Orita S, Takaso M, Ochiai N, et al. A case of symptomatic extra-foraminal lumbosacral stenosis ("far-out syndrome") diagnosed by diffusion tensor imaging. Spine (Phila Pa 1976). 2012;37:E854–7. https://doi.org/10.1097/ BRS.0b013e318249537f. Lee S, Kang JH, Srikantha U, Jang IT, Oh SH. Extraforaminal compression of the L-5 nerve root at the lumbosacral junction: clinical analysis, decompression technique, and outcome. J Neurosurg Spine. 2014;20:371–9. https://doi.org/10.3171/2013.12.SPINE12629. Matsumoto M, Chiba K, Nojiri K, Ishikawa M, Toyama Y, Nishikawa Y.  Extraforaminal entrapment of the fifth lumbar spinal nerve by osteophytes of the lumbosacral spine: anatomic study and a report of four cases. Spine (Phila Pa 1976). 2002;27:E169–73. https://doi. org/10.1097/00007632-­200203150-­00020. Matsumoto M, Watanabe K, Ishii K, Tsuji T, Takaishi H, Nakamura M, et  al. Posterior decompression surgery for extraforaminal entrapment of the fifth lumbar spinal nerve at the lumbosacral junction. J Neurosurg Spine. 2010;12:72–81. https://doi.org/10.3171/2009.7 .SPINE09344. Nathan H, Weizenbluth M, Halperin N.  The lumbosacral ligament (LSL), with special emphasis on the “lumbosacral tunnel” and the entrapment of the 5th lumbar nerve. Int Orthop. 1982;6:197–202. https://doi.org/10.1007/BF00267730. Park MK, Son SK, Park WW, Choi SH, Jung DY, Kim DH.  Unilateral biportal endoscopy for decompression of extraforaminal stenosis at the lumbosacral junction: surgical techniques and clinical outcomes. Neurospine. 2021;18:871–9. https://doi.org/10.14245/ ns.2142146.073. Park YK, Kim JH, Chung HS, Suh JK.  Microsurgical midline approach for the decompression of extraforaminal stenosis in L5-S1. J Neurosurg. 2003;98:264–70. https://doi.org/10.3171/ spi.2003.98.3.0264. Sasaki M, Aoki M, Matsumoto K, Tsuruzono K, Akiyama C, Yoshimine T. Middle-term surgical outcomes of microscopic posterior decompression for far-out syndrome. J Neurol Surg A Cent Eur Neurosurg. 2014;75:79–83. https://doi.org/10.1055/s-­0032-­1327443. Takeuchi M, Wakao N, Kamiya M, Hirasawa A, Osuka K, Joko M, et  al. Lumbar extraforaminal entrapment: performance characteristics of detecting the foraminal spinal angle using oblique coronal MRI.  A multicenter study. Spine J. 2015;15:895–900. https://doi. org/10.1016/j.spinee.2015.02.011. Wiltse LL, Guyer RD, Spencer CW, Glenn WV, Porter IS.  Alar transverse process impingement of the L5 spinal nerve: the far-­ out syndrome. Spine (Phila Pa 1976). 1984;9:31–41. https://doi. org/10.1097/00007632-­198401000-­00008. Wiltse LL, Spencer CW. New uses and refinements of the paraspinal approach to the lumbar spine. Spine (Phila Pa 1976). 1988;13:696– 706. Wu PH, Kim HS, Jang IT. How I do it? Uniportal full endoscopic contralateral approach for lumbar foraminal stenosis with double crush syndrome. Acta Neurochir (Wien). 2020;162:305–10. https://doi. org/10.1007/s00701-­019-­04157-­z. Yang CC, Yeh KT, Liu KC, Wu WT.  Ameliorated full-endoscopic transforaminal decompression for L5-S1 foraminal and extraforaminal stenosis. Clin Spine Surg. 2021;34:197–205. https://doi. org/10.1097/BSD.0000000000001137.

Lumbosacral Vertebral Tumors

39.1 Generalities and Relevance A wide variety of benign and malignant neoplasms can involve the lower spine and induce low-back pain and lumbosacral radicular symptoms with or without neurological deficits (Fig. 39.1). Lumbosacral spinal tumors (LSTum) have various etiologies (Table 39.1); however, the majority of cases are malignant and related to metastatic cancer of the thyroid, breast, kidney, and prostate. Nearly 10% of patients with spinal metastases present without identified primary tumors. Pure epidural nonvertebral tumors will be discussed in Chap. 40 of the present book. Differentiating between benign and malignant spinal tumors is fundamental for diagnosing and treating the patient, especially in those complaining of sciatic pain. The majority of primary tumors are solitary but metastatic lesions are multiple. Spinal metastases usually involve anterior vertebral elements (vertebral body) with or without the pedicles; however, isolated vertebral neural arch involvement is rare.

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Globally, patients with systemic involvement have a less favorable outcome. Sciatica related to LSTum may result from one or more following mechanisms: • • • • • • • •

Direct neural compression due to epidural expansion Tumor nerve root infiltration Central or foraminal stenosis Pathologic fracture (c.f. Chap. 66) Intervertebral instability Spinal deformity Secondary spondylolisthesis Epidural hematoma

The pediatric and young adult populations have a high proportion of benign LSTum whereas metastatic tumors are much more frequent in higher age groups (in middle-aged and elderly patients). About two-thirds of all bone metastases are located in the spine and 10% of newly diagnosed cancers have already vertebral metastases. Table 39.1  Main different tumors involving the lumbosacral spine Malignant – Secondary malignant tumors (aka metastases): mainly from the thyroid, breast, kidney, prostate, and lung (Figs. 39.2, 39.3, 39.4, 39.5, 39.6, 39.7, 39.8, 39.9, 39.10, 39.11, 39.12) – Primary malignant neoplasm of bone (e.g., osteosarcoma, chondrosarcoma, chordoma, Ewing sarcoma, and primitive neuroectodermal tumor) (Figs. 39.13, 39.14, 39.15) – Bone marrow neoplasm (e.g., multiple myeloma, solitary plasmacytoma, lymphoma, leukemia) (Figs. 39.16, 39.17, 39.18, 39.19, 39.20, 39.21) Benign – Osteoid osteoma, osteoblastoma (Fig. 39.22) – Aneurysmal bone cyst (Fig. 39.23) – Osteochondroma – Giant cell tumors Others – Aggressive hemangioma (Figs. 39.24 and 39.25) – Eosinophilic granuloma (c.f. Chap. 51)

Fig. 39.1  Illustration of a lumbar vertebroepidural tumor compressing the thecal sac and its contents as seen in axial and sagittal sections

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_39

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39.2 Clinical Presentations Patients with LSTum may present with various clinical presentations, including spinal, neurologic, and extraspinal manifestations. Anamnestic data on preexisting disease could be very helpful to identify the expected cause of symptoms. Tumors may become symptomatic due to vertebral pain, pathological compression fractures, or extension into the spinal canal with radicular nerve compression and ensuing neurological deficits. Nonmechanical pain in the lower back with or without radicular symptoms is the most frequent complaint of both benign and malignant spinal tumors. The pain may increase with physical activity and can be worse at night and when lying down. Local or radicular pain is often initially attributed to lumbosacral degenerative disease and may be present for weeks or months. Overall, clinical data regarding the onset of low-­ back pain, presence or absence of lower limb weakness, and acute or progressive neurological symptoms may give only little benefit in differentiating between the different causes of LSTum. However, it seems that patients with malignant LSTum tend to have more rapid gradual symptoms than those with benign forms. In addition, fatigue and weight loss should point toward malignancy.

39  Lumbosacral Vertebral Tumors

The physical exam may show localized pain and tenderness, spinal stiffness and postural changes, spinal deformity or angulation, and decreased range of motion, with or without neurologic deficits. Bilateral lumbosacral radicular pain with or without neurogenic claudication is correlated to large involvement with bilateral extension. Cauda equina syndrome (CES) is not rare and are often related to severe compressive lesion. Many other concomitant symptoms related to underlying etiologies or systemic diseases should be considered in clinical presentations. In the majority of benign cases, the general condition remains conserved. Some vertebral tumors are found incidentally when imaging is performed for other reasons.

39.3 Paraclinic Features Given the high difference in patient management, the main objective of the radiologist is to distinguish benign from malignant tumors and even to suggest the most likely tumor type. Various imaging studies may be used such as computed tomography (CT) scan, magnetic resonance imaging (MRI), and bone scintigraphy (Figs.  39.2, 39.3, 39.4, 39.5, 39.6,

Fig. 39.2  Case 1. L5 secondary malignant tumor from papillary thyroid carcinoma (arrows) with epidural extension (arrowheads). Sagittal postgadolinium T1- (a) and T2-weighted MRI (b) as well as on axial postgadolinium T1- (c) and T2-weighted MRI (d)

39.3 Paraclinic Features

39.7, 39.8, 39.9, 39.10, 39.11, 39.12, 39.13, 39.14, 39.15, 39.16, 39.17, 39.18, 39.19, 39.20, 39.21, 39.22, 39.23, 39.24, 39.25). An LSTum can be identified based on the patient’s age, the exact location of the tumor within the vertebra, CT scan analysis of the tumor bony matrix, the presence of a soft tissue invasion and/or reaction, and MRI signal features. Plain radiography shows some difficulties in differentiating causative lesions due to the complex anatomy of the lum-

Fig. 39.3  Case 1. Microscopic image showing vertebral localization of classic papillary thyroid carcinoma. The tumor is formed by branching papillary structures with fibrovascular cores. The trabecular bone is marked by the black star. The tumor cells show nuclear enlargement, overlapping, grooves, and clear chromatin (Hematoxylin and eosin stain, original magnification ×200). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

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bosacral spine and overlying gas and soft tissue structures. Spinal metastases may be osteolytic, sclerotic, or mixed. On CT scan, sharply circumscribed lesions with a sclerotic rim indicate a benign slow-growing tumor, whereas a moth-eaten or permeative pattern usually means a malignant rapidly growing neoplasm. Cortical integrity and pathologic fractures should also be evaluated. CT scan is better than MRI in the detection of tumoral osteoid matrix formation. MRI helps identify the lesion and particularly considers paravertebral and intracanalar extension with or without radicular compression. MRI is also sensitive in the evaluation of bone marrow infiltration in extramedullary hematopoiesis. For example, aggressive vertebral hemangioma appears as an expansile lytic lesion associated with a “polka dot” or “spotted” pattern on axial CT scan and a “corduroy” or “jail bar” shape on sagittal or coronal CT scan imaging. Bone scintigraphy is relatively unspecific and not always conclusive but allows visualization of all the skeletal systems in a single plane. Sometimes, the final diagnosis of LSTum is challenging and the tumors may be confused with other possible diseases in the lumbosacral region including: • • • •

Pure epidural tumors Extensive degenerative lesions Osteoporotic compression fracture Congenital lesions (arachnoid cyst, meningocele, lipoma, dermoid, epidermoid cysts) • Osteogenesis imperfect • Osteomalacia • Paget’s Disease

Fig. 39.4  Case 2. Sacral metastatic prostatic adenocarcinoma (stars) in a 65-year-old patient with bilateral sciatica and cauda equina syndrome. Pelvic axial CT scan (a) and postgadolinium T1-weighted MRI (b)

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Fig. 39.5  Case 2. Sagittal fast spine echo (a), postgadolinium T1- (b), and T2-weighted MRI (c) showing the sacral localization of prostatic adenocarcinoma (stars). Note the thoracolumbosacral vertebral involvement

• Vertebral osteomyelitis or spondylodiscitis • Vascular lesions and chronic epidural hematomas • Some rheumatologic diseases such as gouty tophus, pigmented villonodular synovitis, and rheumatoid nodules • Giant Schmörl’s node • Therapy effects (e.g., postradiotherapy) Spinal imaging is essential for planning the trajectory of any percutaneous procedure such as spinal biopsy

(Fig. 39.18), vertebroplasty, or vertebral body augmentation technique. Biologic findings could help in differentiating between benign and malignant LSTum and may be sometimes appropriate for the final diagnosis. Sometimes, a percutaneous vertebral biopsy may be necessary during the course of the diagnostic workup in order to identify the causative tumor before continuing a more extensive evaluation and/or planning a final treatment.

39.3 Paraclinic Features

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Fig. 39.6  Case 3. L5 and S1 vertebral localization of prostatic acinar adenocarcinoma (arrows) as seen on sagittal reconstruction CT scan (a), STIR sequence (b), and PET scan (c)

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Fig. 39.7  Case 3. L5 vertebral localization of prostatic acinar adenocarcinoma with bony invasion as seen on axial CT scan on both parenchymatous (a) and bony windows (b)

Fig. 39.8  Case 3. Microscopic image showing vertebral localization of prostatic acinar adenocarcinoma (Gleason 4+3=7). The tumor cells are arranged in glandular and cribriform structures (arrows) (Hematoxylin and eosin stain, original magnification ×100). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

39.3 Paraclinic Features

Fig. 39.9  Case 4. L5 vertebral localization of pulmonary adenocarcinoma (stars) with epidural extension (arrows) as seen on sagittal reconstruction CT scan (a), postgadolinium T1- (b), and T2-weighted MRI

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(c) as well as on axial CT scan (d), postgadolinium T1- (e), and T2-weighted MRI (f)

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Fig. 39.10  Case 5. Sacral localization of pulmonary carcinoma (stars) with epidural extension (arrows) in a 65-year-old man with bilateral sciatica and cauda equina syndrome. Axial postgadolinium T1- (a) and

Fig. 39.11  Case 5. Microscopic image showing vertebral localization of moderately differentiated pulmonary adenocarcinoma. The trabecular bone is marked by the black star. The tumor cells are arranged in cystic glandular structures (arrows) (Hematoxylin and eosin stain, original magnification ×100). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

39  Lumbosacral Vertebral Tumors

T2- (b) as well as on sagittal T2-weighted MRI (c). Axial pelvic CT scan with contrast injection (d, e)

39.3 Paraclinic Features

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a

b

d

e

Fig. 39.12  Case 6. L2 and L3 vertebral localization of squamous cell carcinoma (stars) as seen on sagittal reconstruction (a, b) and axial (c) CT scan. Note the L3-L4 posterior joint invasion with foraminal extension on the left side (arrow). Microscopic image showing vertebral localization of moderately differentiated squamous cell carcinoma (d)

c

(Hematoxylin and eosin stain, original magnification ×200). The tumor is composed of large polygonal tumor cells with hyperchromatic, anisocaryotic nuclei and figures of mitosis. The cancer cells were positive for P40 (e) (Immunohistochemistry, original magnification ×200). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

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Fig. 39.13  Case 7. L4-S1 vertebroepidural Ewing sarcoma (stars) in a 17-year-old young man as seen on sagittal (a) and coronal (b) postgadolinium T1-weighted MRI and on sagittal T2-weighted MRI (c)

39.3 Paraclinic Features Fig. 39.14  Case 7. L5 Ewing sarcoma (arrows) with a moth-eaten pattern as seen on sagittal (a) and coronal (b) reconstruction CT scan as well as on axial CT scan (c, d)

Fig. 39.15  Case 7. Operative view of the sarcoma (stars) after posterior laminectomy (a). Thecal sac appearance following bilateral tumor resection (b)

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Fig. 39.16  Case 8. S1 vertebral localization of solitary plasmacytoma with pathologic fracture (arrow) as seen on axial (a), sagittal (b), and coronal (c, d) reconstructions CT scan

39.3 Paraclinic Features Fig. 39.17  Case 8. S1 vertebral localization of solitary plasmacytoma (stars) with epidural (arrows), sacroiliac joint, and pelvic involvement as seen on axial (a) and coronal (b) postgadolinium T1- and sagittal T2-weighted MRI (c)

Fig. 39.18  Case 8. Pelvic axial CT scan for planning the trajectory of the percutaneous procedure for spinal biopsy (arrow) of the sacral tumor (solitary plasmacytoma)

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Fig. 39.19  Case 9. S1-S2 solitary plasmacytoma involving both anterior and posterior parts of the vertebras with epidural (arrows), sacroiliac joint, and pelvic extension as seen on sagittal T1-weighted before

39  Lumbosacral Vertebral Tumors

(a) and after (b) gadolinium injection and on T2-weighted MRI (c). Axial postgadolinium T1- (d, e) and T2-weighted MRI (f)

39.3 Paraclinic Features

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Fig. 39.20  Case 9. Appearance of the sacral solitary plasmacytoma on axial (a, b) and sagittal (c, d) FDG-PET scan

Fig. 39.21  Case 9. Microscopic image showing histological with hematoxylin and eosin stain (HE) and immunohistochemical features of solitary plasmacytoma of the sacrum. There are sheets of neoplastic mature and plasma cells with abundant basophilic cytoplasm and round

eccentric nuclei (a) (HE stain, original magnification ×200). The trabecular bone is marked by the black star. The tumors cells were positive for CD138 (b) (Immunohistochemistry, original magnification ×200). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

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Fig. 39.22  Case 10. Osteoblastoma of the sacrum (arrows) in a 15-year-old man with sacral pain and pseudosciatic pain on the left side. CT scan shows a hypoattenuating area with central calcifications

39  Lumbosacral Vertebral Tumors

and surrounding sclerosis. Axial CT scan on parenchymal (a) and bone (b) windows as well as on coronal (c) and sagittal reconstructions (d). (Courtesy of Pr. Nabil Hammoune.)

39.3 Paraclinic Features

Fig. 39.23  Case 11. Large sacral aneurysmal bone cyst (dotted circles) with intracanalar and pelvic involvement in a 12-year-old girl. There is a typical MRI appearance: heterogenous fluid-fluid levels on both T1-

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and T2-weighted MRI. Note the septations separating the cysts. Pelvic axial T1-weighted MRI with (a) and without (b) gadolinium injection as well as on axial (c) and sagittal (d) T2-weighted MRI

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Fig. 39.24  Case 12. L3 vertebral aggressive hemangioma with epidural involvement (arrows) as seen on sagittal T1-weighted MRI before (a) and after gadolinium injection (b) as well as on T2-weighted MRI (c)

39.3 Paraclinic Features

Fig. 39.25  Case 12. L3 vertebroepidural aggressive hemangioma (arrows) as seen on axial CT scan (a), postgadolinium T1- (b), and T2-weighted MRI (c). Microscopic image of the vertebral hemangioma. There are vascular structures of variable size, thickened walls,

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blood-engorged lumens, and endothelial cells without atypia (d). Note the reactive new bone formation (black star) (d) (Hematoxylin and eosin stain, original magnification ×100). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

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39.4 Treatment Options and Prognosis Treatment of LSTum-inducing sciatic pain is not well established and depends on many factors including but not limited to the histopathologic nature of the tumor, its aggression and extension, spinal stability, underlying diseases, patient’s general condition, and degree of neurological disorders. Oncologists, neuroradiologists, and neuropathologists may assist in the formal diagnosis, optimal management, and monitoring. Also, clinicians should always consider spinal growth and the timing of spinal maturity when managing the pediatric spine. The aim of treatment is to: • • • •

Relieve pain Maintaining axial spine motion and functional ability Prevent the progression of the disease Avoid spinal complications

Medication, conservative measures, physical therapy programs, bracing, surgery, radiotherapy, hormone therapy, and chemotherapy have been offered. A number of open surgical approaches have been proposed whether they are anterior, posterior, posterolateral, or mixed approaches depending on the location and the size of the damage. However, when surgery is indicated, most patients underwent decompression and short fusion surgery with rigid pedicle screw fixation and bone graft via a posterior lumbar approach. Treating clinicians have to take into account that many patients present advanced age, spinal fragility, poor bone quality, and other potential comorbidities. Furthermore, the rate of postoperative complications related to the instrumentation is not insignificant in the elderly. Sometimes, less invasive surgery may be indicated. Neurophysiologic monitoring during surgery and the use of navigational tools are crucial to reduce the occurrence of new neurologic deficits or neurologic worsening. A vertebroplasty via a percutaneous transpedicular approach can be considered in some cases with a vertebral compression fracture. This minimally invasive procedure aims to restore height to the collapsed lumbar vertebral body, reduce kyphosis, and improve the patient’s pain and function. Regarding the sacrum, sacroplasty is a variation of vertebroplasty, in which cement is injected into the sacrum to improve its structural integrity and alleviate symptoms. Sacroplasty was first introduced as a treatment for pelvic lesions resulting from metastasis with a good outcome. However, the long-term results of sacroplasty remain unknown. Overall, surgery may be considered when there is a failure of radiation therapy, unknown diagnosis, pathologic fracture, and/or spinal instability, or when there is significant com-

39  Lumbosacral Vertebral Tumors

pression of the nerve roots. Sometimes, hypervascular tumors or aggressive hemangioma may need spinal angiography and additional preoperative embolization (within 24 h) prior to surgical resection. Etiological treatment should be undertaken afterward whether the tumor is benign or malignant. Regarding their origins, malignancies should be correctly managed by chemotherapy, surgery, and/or radiation therapy. Complications are especially related to prolonged bed rest (e.g., pneumonia, deep venous thrombosis with the associated risk of pulmonary embolism), heavy comorbidity, and spinal instrumentation. The prognosis is variable depending on the concomitant disease, tumor nature and aggressiveness, initial neurological disorders, treatment response, delay of treatment, and patient’s general condition. The prognosis is better for young patients with benign LSTum and for those without severe and longtime neurologic impairment. Progressive clinical deterioration is common in patients with malignant LSTum and life-threatening consequences. Whatever the results, careful clinical and paraclinical follow-up should be needed.

Further Reading Abril Martín JC, Calvo Crespo E, Alvarez Galovich L, Castillo Benítez-­ Cano F, Fernández-Yruegas D, Vallejo Galbete JC, et al. Malignant lumbosciatic syndrome. Report of 21 cases with vertebral metastases. Rev Clin Esp. 1993;193:131–5. Aledavood SA, Amirabadi A, Memar B.  Non surgical treatment of sacral osteosarcoma. Iran J Cancer Prev. 2012;5:46–9. Bagley CA, Gokaslan ZL. Cauda equina syndrome caused by primary and metastatic neoplasms. Neurosurg Focus. 2004;16:e3. https:// doi.org/10.3171/foc.2004.16.6.3. Brat HG, Renton P, Sandison A, Cannon S.  Chondromyxoid fibroma of the sacrum. Eur Radiol. 1999;9:1800–3. https://doi.org/10.1007/ s003300050925. Byung-June J, Seung-Eun C, Sang-Ho L, Hyeop JS, Suk PS. Solitary lumbar osteochondroma causing sciatic pain. Joint Bone Spine. 2007;74:400–1. https://doi.org/10.1016/j.jbspin.2006.04.010. Chatterjee S, Bodhey NK, Gupta AK, Periakaruppan A. Chordoma of the lumbar spine presenting as sciatica and treated with vertebroplasty. Cardiovasc Intervent Radiol. 2010;33:1278–81. https://doi. org/10.1007/s00270-­009-­9701-­9. Chu EC, Trager RJ, Chen ATC. Conservative management of low-back pain related to an unresectable aggressive sacral hemangioma: a case report. Am J Case Rep. 2022;23:e936984. https://doi.org/10.12659/ AJCR.936984. Chung OM, Yip SF, Ngan KC, Ng WF. Chondroblastoma of the lumbar spine with cauda equina syndrome. Spinal Cord. 2003;41:359–64. https://doi.org/10.1038/sj.sc.3101458. Cicala D, Briganti F, Casale L, Rossi C, Cagini L, Cesarano E, et al. Atraumatic vertebral compression fractures: differential diagnosis between benign osteoporotic and malignant fractures by MRI. Musculoskelet Surg. 2013;97:S169–79. https://doi.org/10.1007/s12306-­ 013-­0277-­9. Conrad MD, Schonauer C, Pelissou-Guyotat I, Morel C, Madarassy G, Deruty R.  Recurrent lumbosacral metastases from intracra-

Further Reading nial meningioma. Report of a case and review of the literature. Acta Neurochir (Wien). 2001;143:935–7. https://doi.org/10.1007/ s007010170024. Cortet B, Cotten A, Deprez X, Deramond H, Lejeune JP, Leclerc X, et  al. Value of vertebroplasty combined with surgical decompression in the treatment of aggressive spinal angioma. Apropos of 3 cases. Rev Rhum Ed Fr. 1994;61:16–22. Dalle Ore CL, Lau D, Davis JL, Safaee MM, Ames CP. Rare case of a recurrent juvenile ossifying fibroma of the lumbosacral spine. J Neurosurg Spine. 2018;28:647–53. https://doi.org/10.3171/2017.10. SPINE17947. de Moraes FB, Cardoso AL, Tristão NA, Pimenta WE Jr, Daher S, de Souza CS, et  al. Primary liposarcoma of the lumbar spine: case report. Rev Bras Ortop. 2015;47:124–9. https://doi.org/10.1016/ S2255-­4971(15)30356-­6. Fiumara E, Scarabino T, Guglielmi G, Bisceglia M, D'Angelo V. Osteochondroma of the L-5 vertebra: a rare cause of sciatic pain. Case report. J Neurosurg. 1999;91:219–22. https://doi.org/10.3171/ spi.1999.91.2.0219. Gaetani P, Tancioni F, Merlo P, Villani L, Spanu G, Baena RR.  Spinal chondroma of the lumbar tract: case report. Surg Neurol. 1996;46:534–9. https://doi.org/10.1016/s0090-­3019(96)00226-­1. Gallia GL, Sciubba DM, Bydon A, Suk I, Wolinsky JP, Gokaslan ZL, et al. Total L-5 spondylectomy and reconstruction of the lumbosacral junction. Technical note. J Neurosurg Spine. 2007;7:103–11. https://doi.org/10.3171/SPI-­07/07/103. Giner J, Isla A, Cubedo R, Tejerina E.  Primary epidural lumbar ewing sarcoma: case report and review of the literature. Spine (Phila Pa 1976). 2016;41:E375–8. https://doi.org/10.1097/ BRS.0000000000001246. Greco F, De Palma L, Toniolo R. Surgical lumbar sciatica of non-disk origin: vertebral osteoid osteoma and osteoblastoma. Arch Putti Chir Organi Mov. 1983;33:371–80. Honeyman SI, Warr W, Curran OE, Demetriades AK. Paraganglioma of the lumbar spine: a case report and literature review. Neurochirurgie. 2019;65:387–92. https://doi.org/10.1016/j.neuchi.2019.05.010. Kerekes D, Goodwin CR, Ahmed AK, Verlaan JJ, Bettegowda C, Abu-­ Bonsrah N, et al. Local and distant recurrence in resected sacral chor-

557 domas: a systematic review and pooled cohort analysis. Global Spine J. 2019;9:191–201. https://doi.org/10.1177/2192568217741114. Kurugoglu S, Adaletli I, Mihmanli I, Kanberoglu K. Lumbosacral osseous tumors in children. Eur J Radiol. 2008;65:257–69. https://doi. org/10.1016/j.ejrad.2007.03.030. Ohtori S, Yamagata M, Hanaoka E, Suzuki H, Takahashi K, Sameda H, et al. Osteochondroma in the lumbar spinal canal causing sciatic pain: report of two cases. J Orthop Sci. 2003;8:112–5. https://doi. org/10.1007/s007760300019. Payer M.  Neurological manifestation of sacral tumors. Neurosurg Focus. 2003;15:E1. https://doi.org/10.3171/foc.2003.15.2.1. Sarmiento JM, Chan JL, Cohen JD, Mukherjee D, Chu RM. L5 osteoid osteoma treated with partial laminectomy and cement augmentation. Cureus. 2019;11:e4239. https://doi.org/10.7759/cureus.4239. Shamhoot EA, Balaha AM, Ganna AA.  Role of combined vertebroplasty and spinal decompression in the management of aggressive vertebral hemangiomas. Asian J Neurosurg. 2020;15:919–25. https://doi.org/10.4103/ajns.AJNS_291_20. Steib JP, Pierchon F, Farcy JP, Lang G, Christmann D, Gnassia JP.  Epithelioid sarcoma of the spine: a case report. Spine (Phila Pa 1976). 1996;21:634–8. https://doi.org/10.1097/00007632-­ 199603010-­00019. Tekaya AB, Moalla M, Salah MB, Saidane O, Tekaya R, Hadhri K, et al. Spinal osteoid osteoma revealed by radiculopathy: case report and literature review. Int J Spine Surg. 2021;14:S26–32. https://doi. org/10.14444/7161. Yoshioka H, Tsuneto S, Kashiwagi T. Pain control with morphine for vertebral metastases and sciatica in advanced cancer patients. J Palliat Care. 1994;10:10–3. Van den Brande R, Mj Cornips E, Peeters M, Ost P, Billiet C, Van de Kelft E.  Epidemiology of spinal metastases, metastatic epidural spinal cord compression and pathologic vertebral compression fractures in patients with solid tumors: a systematic review. J Bone Oncol. 2022;35:100446. https://doi.org/10.1016/j.jbo.2022.100446. Wang GQ, Kang YJ, Lv GH, Li YW, Wang B. Osteoid osteoma leading to sciatica. Spine J. 2016;16:e315. https://doi.org/10.1016/j. spinee.2015.11.038.

Epidural Nonvertebral Tumors

40.1 Generalities and Relevance The majority of spinal tumors arise from the vertebral bone. If the tumor continues to grow, it can invade the epidural space, becomes vertebroepidural, and causes neurologic damage. Though more infrequent, some tumors can originate from the epidural space itself (Fig.  40.1). Pure spinal epidural tumors constitute a distinct clinic-pathologic group of spinal tumors that requires specific management completely different from those of other vertebroepidural and intradural tumors (c.f. Chaps. 39 and 42 about Lumbosacral Vertebral Tumors and Intradural Lumbosacral Tumors, respectively). Epidural nonvertebral tumors (ENVT) are unusual accounting for less than 10% of all spinal tumors, mainly represented by thoracic and cervical epidural tumors. Lumbosacral epidural space is rarely involved, representing less than 20% of all ENVT.  Simultaneous involvement of multiple spinal areas is not rare.

40

Tumors developing into the spinal epidural space have a wide range of etiologies and variable degrees of malignancy; however, more than 90% of lesions are metastatic. Primary tumors involving the epidural space are rare. Table 40.1 represents the most frequent causes of lumbosacral radiculopathies related to extradural nonvertebral origin tumors previously reported in the literature (Table 40.1). The majority of ENVT are located intraspinal and affect neurologic function by compressing or invading one or more of the cauda equina roots. Vertebral invasions are unusual reducing the risk of pathologic fractures or spinal instability. Less frequently, some benign extradural tumors may have both intraspinal and extraspinal extensions, connected through a widening intervertebral foramen, and are known as “dumbbell” or “hourglass” tumors. Patients with lumbosacral ENVT can present with back pain radiating to the legs, motor, and sensory dysfunction of the lower extremities, bladder and/or bowel dysfunction, sexual dysfunction, perineal anesthesia, and even complete cauda equina syndrome (CES). Spinal epidural metastases occur mostly in middle-aged and elderly patients without gender predominance whereas primary benign epidural tumors occur in a younger population. Table 40.1  Most frequent extradural nonvertebral tumors causing lumbosacral radiculopathies previously reported in the literature Metastases (secondary tumors) Primary tumors

Fig. 40.1  Illustration of a lumbar epidural tumor without osseous involvement compressing the thecal sac and its contents as seen in axial (left) and sagittal (right) sections

Extramedullary hematopoiesis Others

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_40

Lung, breast, gastrointestinal, prostate, melanoma, and lymphoma (Fig. 40.2) Benign: Schwannoma, meningioma, lipoma, angiolipoma (Figs. 40.3, 40.4, 40.5) Malignant: Primitive neuroectodermal tumors (e.g., extraskeletal Ewing sarcoma), ganglioglioma, rhabdoid tumor, granulocytic sarcoma (chloroma), neuroblastoma (Figs. 40.6, 40.7, 40.8) Lymphoma (mainly non-Hodgkin’s lymphoma), leukemia, myelofibrosis, thalassemia (Figs. 40.9, 40.10, 40.11, 40.12) Angioma (Fig. 40.13)

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40  Epidural Nonvertebral Tumors

Fig. 40.2  Case 1. L3-L4 anterior epidural metastasis (arrows) as seen on sagittal (a), coronal (b), and axial (c) myelo-CT scan in a 70-year-old man with bilateral sciatica

Fig. 40.3  Case 2. Giant L2-L5 epidural schwannoma (stars) as seen on sagittal T1-weighted MRI before (a) and after gadolinium injection (b) as well as on T2-weighted image (c). Note the L4 posterior vertebral body erosion

40.4  Treatment Options and Prognosis

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Fig. 40.4  Case 2. Axial postgadolinium T1-weighted MRI (a, b) showing the large epidural schwannoma (stars) with cauda equina compression, vertebral body erosion, and right neural foramen extension (arrow)

Fig. 40.5  Case 2. Giant epidural schwannoma (stars) with vertebral erosion. Lumbosacral bony CT scan on axial (a, b) and sagittal reconstruction (c) showing secondary bone changes especially posterior vertebral body erosion

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40  Epidural Nonvertebral Tumors

Fig. 40.6  Case 3. Sacral epidural Ewing sarcoma (stars) with posterior paravertebral extension (arrows) as seen on sagittal T2- (a), axial T1before (b), and after gadolinium injection (c) as well as on axial T2-weighted MRI (d)

Further Reading

Fig. 40.7  Case 3. Sacral epidural Ewing sarcoma (star). Intraoperative view following posterior laminectomy showing the compressive epidural tumor (stars) (a). Operative view following tumor resection and the appearance of normal thecal sac (arrow) (b)

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40  Epidural Nonvertebral Tumors

Fig. 40.8  Case 4. L4-S1 lumbosacral posterolateral epidural neuroblastoma with posterior paravertebral extension on the left side (stars) as seen on axial (a–c) and sagittal reconstruction myelo-CT scan (d)

Further Reading

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Fig. 40.9  Case 5. Extensive lumbosacral epidural MALT lymphoma (arrows) in a 39-year-old patient with acute lumbalgia with bilateral sciatic pain. Sagittal T1-weighted MRI before (a) and after (b) gadolinium injection as well as on T2-weighted MRI (c)

Fig. 40.10  Case 5. Epidural MALT lymphoma (arrows) as seen on axial postgadolinium T1- (a) and T2-weighted MRI (b)

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Fig. 40.11  Case 5. Photomicrograph image showing histological with hematoxylin and eosin stain (HE) and immunohistochemical features of extra-nodal marginal zone B cell lymphoma (MALT lymphoma). The tumor is composed by sheets of neoplastic small lymphocytes with irregular nuclear contours and inconspicuous nucleoli (centrocyte-like)

40  Epidural Nonvertebral Tumors

(a) (HE stain, original magnification ×200). Immunohistochemistry findings (original magnification ×200): positivity for CD20 (b), positivity for Bcl2 (c), and positivity for Ki-67 (proliferation index estimated at 25%) (d). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

Further Reading

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Fig. 40.12  Case 6. S1-S2 anterior epidural lymphoma (double arrows) with diffuse vertebral bone marrow infiltration and presacral extension as seen on sagittal postgadolinium T1- (a) and T2-weighted MRI (b) as well as on axial postgadolinium T1- (c) and T2-weighted MRI (d)

Fig. 40.13  Case 7. L5-S1 lateral epidural angioma (stars) with posterior vertebral body erosion (scalloping) (arrows) and L5-S1 neural foraminal widening on the right side. Axial T1- before (a, b) and after (c, d) gadolinium injection as well as on sagittal postgadolinium T1-weighted MRI (e)

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40  Epidural Nonvertebral Tumors

Patients with suspected schwannoma or meningioma should be investigated for possible association with neurofibromatosis. A deep neurocutaneous examination will be needed. A careful full physical examination should be performed to search for other systemic concomitant lesions. In some cases, separating lumbosacral radiculopathy from lumbosacral plexopathy or peripheral neuropathy on clinical grounds can be difficult. Therefore, in such cases electrodiagnostic studies are decisive. In addition, patients with sphincter disorders might be evaluated with various combinations of urodynamic studies. Fig. 40.14  Operative view of an epidural lymphoma (arrows) after posterior laminectomy. Note the normal appearance of the dura (arrowheads)

40.2 Clinical Presentations The initial evaluation of patients with lumbosacral ENVT should include a detailed past medical history and clinical exam. History would include questions about recent underlying diseases and a history of malignancies or surgeries. Most patients with malignant tumors initially complain of pain. It may be focal in the lower back, radicular (often bilateral) along lower limbs, or referred. This nonspecific pain evolves in a subacute progressive manner and can be aggravated by physical activity or at night. As the tumor grows, patients will present paresthesia, leg weakness, and sphincter disorders. The presence of sensory disturbances is less common but the perianal area should be inspected accurately. Radicular pain may enhance during the Valsalva maneuver (forced expiration against a closed glottis). Paraplegia is not rare on initial clinical presentation. Indeed, lumbar and/or sacral radicular pain will quickly give way to paresthesia, urinary retention, bowel incontinence, saddle anesthesia, and variable motor and/or sensory deficits in the lower extremities developing a CES. The median time from the onset of symptoms to diagnosis is less than 2  months. While benign epidural tumors have more subtle and less severe manifestations. Regarding lower limb reflexes, ankle jerk, and knee jerk are absent with a negative Babinski reflex. Lasègue test can be positive. Neurologic signs and symptoms related to lumbosacral malignant ENVT rarely exist in isolation but are often associated with other nonneurologic symptoms linked with the underlying etiology. Generally, chills, night sweats, fatigue, and weight loss should point toward malignancy.

40.3 Paraclinic Features Magnetic resonance imaging (MRI) remains the best initial procedure for the assessment of cauda equina root compression. This imaging method might help to localize the site and extension of the epidural tumor and provide evidence for its nature. Additionally, MRI can provide more information about spinal and paraspinal soft tissue involvement. The usual exploration needs urgent sagittal and axial T1 and T2 sequences with or without T1 postgadolinium injection. For patients with contraindications to MRI (e.g., metallic implants), myelo-computed tomography (CT) is an alternative option (Figs. 40.2 and 40.8). Patients with bladder disorders might be evaluated with an abdominopelvic CT scan or ultrasound for detecting urinary retention and incomplete bladder emptying. Further extraspinal imaging studies as well as biological investigations may be indicated for specific cases in the search for the primary tumors or underlying diseases. Although unusual, a bony CT scan with anatomical reconstructions in sagittal and coronal planes may be useful for identifying secondary bone changes especially posterior vertebral body erosion (scalloping), neural foraminal widening, and spinal deformities (Fig. 40.5). A wide variety of MRI patterns may be observed depending on the histologic nature of the lesion, its extension, and the different stages of the disease. The MRI appearance of epidural metastasis mostly depends on the primitive tumor’s natural histology. Nevertheless, marked edema and homogeneous gadolinium enhancement are common findings. Sometimes, the vertebral body appears slightly hypointense on T1-weighted images (WI) and slightly hyperintense on T2-WI compared to normal bone marrow. Most epidural extramedullary hematopoiesis shows a diffuse and infiltrative epidural mass which is isointense on

40  Epidural Nonvertebral Tumors

T1-WI and isointense or slightly hyperintense on T2-WI. There is homogeneous enhancement following gadolinium administration. Diffuse bone marrow infiltration on the MRI associated with multiple extradural masses suggests the presence of a tumor with a hematological disorder. Lymphomatous tumors have a homogeneous, medium signal intensity mass extending over multiple vertebrae with possible paravertebral extension (Fig. 40.12). There is also a regular enhancement after gadolinium injection (Figs.  40.9, 40.10, and 40.12). Spinal epidural angiolipoma appears as a hyperintense lesion on T1-WI. Gadolinium enhancement is due to the vascularity of this neoplasm. Furthermore, fat suppression sequences may enhance areas of abnormal signal intensity within this fatty tumor. Epidural schwannomas are frequently associated with hemorrhage, intrinsic vascular changes, and cyst formations. On T1-weighted MRI, schwannomas are usually isointense welldefined rounded masses. They appear on T2WI as a hyperintense often with a mixed signal. There are strong enhancements after gadolinium injection (Figs. 40.3 and 40.4). Schwannomas can extend over two or more vertebral levels or may develop extraspinal through the neural foramen, forming the classic hourglass or dumbbell-shaped appearance. Spinal epidural meningiomas are rarer. They share similar MRI characteristics to classic intracranial meningiomas with broad-based dural attachment and dural tail sign following gadolinium administration. On spinal imaging, some ENVT may be confused with a wide spectrum of other epidural and even intradural lumbosacral lesions such as: • Degenerative lesions (free/sequestered disc fragment, synovial cyst, ligamentum flavum lesions) • Tarlov cysts • Spinal epidural hematomas • Vascular lesions (cavernous angioma, vascular malformations, varices) • Benign or malignant vertebroepidural tumors • Congenital lesions (arachnoid cyst, meningocele, lipoma, dermoid, epidermoid cysts) • Spinal epidural lipomatosis • Granulomatous lesions (tuberculoma, sarcoidosis) • Epidural abscesses • Some rheumatologic diseases (gouty tophus, pigmented villonodular synovitis, rheumatoid nodules) • Intradural tumoral or nontumoral lesions Furthermore, patients should be assessed by appropriate biologic and imaging studies to look for the primary tumor

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or for potential underlying disorders. Consultations with experts such as oncologists and hematologists can aid in diagnosis evaluation. In extramedullary hematopoiesis, bone marrow cytology and lymph node biopsy can provide the final diagnosis.

40.4 Treatment Options and Prognosis Management strategies for ENVT vary considerably, depending primarily on the nature of the tumor, its extension, neurologic and urologic impairment, and the patient’s general condition. Several options might be offered including conservative measures, medical treatments (e.g., pain management), partial or radical resections, and complementary chemotherapy and/or radiotherapy. Overall, cancer patients need multidisciplinary management. The majority of cases without neurological deficits or spinal instability may be managed conservatively. However, patients need to be followed up regularly because any rapid or severe neurological deterioration requires surgical decompression as soon as possible. Patients who present features of cauda equina compression need surgical intervention for tissue diagnosis and decompression. The majority of cases undergo a posterior laminectomy (Fig. 40.14). For malignant tumors, a maximal degree of resection is recommended with maximal preservation of neurologic structures. Care should be taken to minimize joint damage and the possibility of CSF leaks. Benign tumors require complete surgical resection. The surgical procedure can be enlarged laterally for the possibility of radical removal, especially with dumbbell-shaped benign tumors. Sometimes, an additional spinal fusion may be required if there is a potential preoperative instability and/or an iatrogenic instability because of the surgical procedure. Neurophysiologic monitoring during surgery and the use of navigational tools are crucial to reduce the occurrence of new neurologic deficits or neurologic worsening. Etiological treatment should be undertaken afterward whether the cause is primary or metastatic tumors (e.g., radiotherapy and/or chemotherapy). Further associated lesions should always be considered. Postoperative complications are especially related to prolonged bed rest (e.g., thromboembolic disorders, pressure ulcers, pneumonia, spasticity, neuropathic pain, depression), the complexity of surgical procedures, the nature and degree of invasion of the primary lesion, and sphincter disorders.

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Spinal epidural benign tumors with incomplete neurologic impairments tend to have better outcomes. Complications, recurrences, and mortality rates are high in patients who have a malignant epidural neoplasm.

Further Reading Akhaddar A, Gazzaz M, Derraz S, Rifi L, Amarti A, Aghzadi A, et al. Spinal epidural angiolipomas: a rare cause of spinal cord compression. A report of 8 cases and review of the literature. Neurochirurgie. 2000;46:523–33. Barz M, Aftahy K, Janssen I, Ryang YM, Prokop G, Combs SE, et al. Spinal manifestation of malignant primary (PLB) and secondary bone lymphoma (SLB). Curr Oncol. 2021;28:3891–9. https://doi. org/10.3390/curroncol28050332. Bustoros M, Thomas C, Frenster J, Modrek AS, Bayin NS, Snuderl M, et al. Adult primary spinal epidural extraosseous Ewing's sarcoma: a case report and review of the literature. Case Rep Neurol Med. 2016;2016:1217428. https://doi.org/10.1155/2016/1217428. Celli P, Trillò G, Ferrante L. Spinal extradural schwannoma. J Neurosurg Spine. 2005;2:447–56. https://doi.org/10.3171/spi.2005.2.4.0447. Cossu G, Barges-Coll J, Messerer M. Minimally invasive resection of a lumbar extradural schwannoma: how I do it. Acta Neurochir (Wien). 2019;161:2365–8. https://doi.org/10.1007/s00701-­019-­04057-­2. Erdem MB, Kale A, Yaman ME, Emmez H. A rare entity in the lumbar epidural region: T-cell lymphoblastic lymphoma. Int J Spine Surg. 2021;14:S52–6. https://doi.org/10.14444/7165. Fuster S, Castañeda S, Ferrer E, Wang J, Poblete J. Spontaneous chronic epidural hematoma of the lumbar spine mimicking an extradural spine tumour. Eur Spine J. 2013;22(Suppl 3):S337–40. https://doi. org/10.1007/s00586-­012-­2402-­0. Giner J, Isla A, Cubedo R, Tejerina E.  Primary epidural lumbar ewing sarcoma: case report and review of the literature. Spine (Phila Pa 1976). 2016;41:E375–8. https://doi.org/10.1097/ BRS.0000000000001246. Goh DH, Lee SH, Cho DC, Park SH, Hwang JH, Sung JK.  Chronic idiopathic myelofibrosis presenting as cauda equina compression due to extramedullary hematopoiesis: a case report. J Korean Med Sci. 2007;22:1090–3. https://doi.org/10.3346/jkms.2007.22.6.1090. Kang SH, Lee SM, Ha DH, Lee HJ. Extensive spinal extradural ganglioneuroma of the lumbar spine: mimicking lymphoma. Eur Spine J. 2018;27:520–5. https://doi.org/10.1007/s00586-­018-­5568-­2. Kim YS, Lee JK, Choi KY, Jang JW.  Spinal Burkitt's lymphoma mimicking dumbbell shape neurogenic tumor: a case report and review of the literature. Korean J Spine. 2015;12:221–4. https://doi. org/10.14245/kjs.2015.12.3.221. Kurucu N, Akyüz C, Varan A, Akçören Z, Aydin B, Yalçin B, et  al. Primary paraspinal and spinal epidural non-hodgkin lymphoma in childhood. J Pediatr Hematol Oncol. 2021;43:e395–400. https://doi. org/10.1097/MPH.0000000000001858. Mally R, Sharma M, Khan S, Velho V.  Primary lumbo-sacral spinal epidural non-Hodgkin's lymphoma: a case report and review of literature. Asian Spine J. 2011;5:192–5. https://doi.org/10.4184/ asj.2011.5.3.192.

40  Epidural Nonvertebral Tumors Musahl V, Rihn JA, Fumich FE, Kang JD. Sacral intraspinal extradural primitive neuroectodermal tumor. Spine J. 2008;8:1024–9. https:// doi.org/10.1016/j.spinee.2007.04.001. Nanassis K, Tsitsopoulos P, Marinopoulos D, Mintelis A, Tsitsopoulos P.  Lumbar spinal epidural angiolipoma. J Clin Neurosci. 2008;15(4):460–3. https://doi.org/10.1016/j.jocn.2006.11.021. O'Neill T, Grosch C, Eustace S, Bresnihan B. Sciatica caused by isolated non-Hodgkin's lymphoma of the spinal epidural space: a report of two cases. Br J Rheumatol. 1991;30:385–6. https://doi. org/10.1093/rheumatology/30.5.385. Ozdemir N, Usta G, Minoglu M, Erbay AM, Bezircioglu H, Tunakan M. Primary primitive neuroectodermal tumor of the lumbar extradural space. J Neurosurg Pediatr. 2008;2:215–21. https://doi. org/10.3171/PED/2008/2/9/215. Rocchi G, Caroli E, Frati A, Cimatti M, Savlati M.  Lumbar spinal angiolipomas: report of two cases and review of the literature. Spinal Cord. 2004;42:313–6. https://doi.org/10.1038/sj.sc.3101535. Seok JH, Park J, Kim SK, Choi JE, Kim CC.  Granulocytic sarcoma of the spine: MRI and clinical review. AJR Am J Roentgenol. 2010;194:485–9. https://doi.org/10.2214/AJR.09.3086. Slouma M, Rahmouni S, Dhahri R, Khayati Y, Zriba S, Amorri W, et al. Epidural myeloid sarcoma as the presenting symptom of chronic myeloid leukemia blast crisis. Clin Rheumatol. 2020;39:2453–9. https://doi.org/10.1007/s10067-­020-­05167-­4. Supik LF, Broom MJ. Epidural lipoma causing a myelographic block in a patient who had sciatica and lumbosacral spondylolisthesis. A case report. J Bone Joint Surg Am. 1991;73:1104–7. Suresh SC, Raju B, Jumah F, Nanda A. Lumbosacral extradural extramedullary hematopoiesis in thalassemia major causing spinal canal stenosis. Surg Neurol Int. 2020;11:331. https://doi.org/10.25259/ SNI_563_2020. Székely G, Miltényi Z, Mezey G, Simon Z, Gyarmati J, Gergely L Jr, et al. Epidural malignant lymphomas of the spine: collected experiences with epidural malignant lymphomas of the spinal canal and their treatment. Spinal Cord. 2008;46:278–81. https://doi. org/10.1038/sj.sc.3102124. Teo M, Zrinzo L, King A, Aspoas AR, David KM.  Giant extradural sacral meningioma. Acta Neurochir (Wien). 2010;152:485–8. https://doi.org/10.1007/s00701-­009-­0414-­2. Turel MK, Kerolus MG, O'Toole JE.  Minimally invasive “separation surgery” plus adjuvant stereotactic radiotherapy in the management of spinal epidural metastases. J Craniovertebr Junction Spine. 2017;8:119–26. https://doi.org/10.4103/jcvjs.JCVJS_13_17. Turgut M, Gökpinar D, Barutça S, Erkuş M. Lumbosacral metastatic extradural Merkel cell carcinoma causing nerve root compression— case report. Neurol Med Chir (Tokyo). 2002;42:78–80. https://doi. org/10.2176/nmc.42.78. Weissman MN, Lange R, Kelley C, Belgea K, Abel L.  Intraspinal epidural sarcoidosis: case report. Neurosurgery. 1996;39:179–81. https://doi.org/10.1097/00006123-­199607000-­00041. Wu HY, Xu WB, Lu LW, Li HH, Tian JS, Li JM, et al. Imaging features of spinal atypical teratoid rhabdoid tumors in children. Medicine (Baltimore). 2018;97:e13808. https://doi.org/10.1097/ MD.0000000000013808. Yáñez ML, Miller JJ, Batchelor TT. Diagnosis and treatment of epidural metastases. Cancer. 2017;123:1106–14. https://doi.org/10.1002/ cncr.30521.

Spinal Epidural Lipomatosis

41.1 Generalities and Relevance Spinal epidural lipomatosis is the result of abnormal accumulation of unencapsulated fat tissue within the epidural space of the spinal canal. This unusual disease may be asymptomatic while other severe forms impinge on the thecal sac in the lumbosacral area or cause spinal cord compression in the cervicothoracic region. The lumbar region is by far the most frequently involved. Epidural lipomatosis is typically associated with the long use of exogenous corticosteroid therapy. However, other underlying etiologies may exist such as: • • • •

Cushing’s syndrome Hypothyroidism Pituitary adenoma Scheuermann disease

Obesity may also be a causative condition. Sometimes, the exact cause is not known and the spinal epidural lipomatosis is then considered “idiopathic”. Adult men seem more usually affected than women.

41.2 Clinical Presentations Symptoms of spinal epidural lipomatosis are often nonspecific and maybe like other degenerative spinal conditions resulting in stenosis. In the lumbosacral area, most symptomatic patients present with a combination of pain, radicular symptoms, and paresthesia.

41

Uncommonly, some cases can present with more serious neurologic conditions such as cauda equina syndrome (CES) with leg weakness and bowel/bladder/sexual disturbances.

41.3 Imaging Features Magnetic resonance imaging (MRI) is the technique of choice to identify the location and extension of the adipose tissue in the extradural space, as well as the nerve root impingement. Typically, signal characteristics of the lipomatosis follow that of the fat on all sequences: high signal on both T1- and T2-weighted images without gadolinium enhancement. Also, the signal of the spinal epidural lesion is homogeneously suppressed on fat suppression sequences. On the lumbosacral spine, the thecal sac appears narrowed and often resembles a “triangle” or “Y”-shaped configuration on the axial MRI plane due to circumscribed fat compression (Figs. 41.1, 41.2, 41.3, 41.4, 41.5, 41.6). In the lumbar spine, some cases with spinal epidural lipomatosis may be confused with other epidural lesions such as: • Spinal epidural hematomas • Vascular lesions (cavernous angioma, vascular malformations, varices) • Benign or malignant vertebro-epidural tumors • Congenital lesions (arachnoid cyst, meningocele, lipoma, dermoid, epidermoid cysts)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_41

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Fig. 41.1  Sagittal T1- (a) and T2-weighted MRI (b), and axial T2-weighted MR images (c, d) showing excess fat seen in the lumbar epidural space (arrows). Therefore, the dural sac appears narrowed (dotted circles)

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Fig. 41.2  Lumbosacral spinal epidural lipomatosis (arrows) as seen on sagittal T1- (a) and T2-weighted MRI (b), and axial T2-weighted MR images (c, d). Note the circumferential impingement of the dural sac.

The sac shows “triangular” (c) and “Y”-(d) shaped configurations on axial sections

41.3  Imaging Features

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Fig. 41.3  Spinal epidural lipomatosis (arrows) in a diabetic patient with a concomitant lumbar central spinal stenosis and lumbar disc herniations. Sagittal T1- (a) and T2-weighted MRI (b), and axial T2-weighted MR images (c, d)

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Fig. 41.4  The same case as Figure 41.3 showing the degenerative lumbar spinal stenosis as seen on sagittal CT scan reconstructions (a, b)

574 Fig. 41.5  Idiopathic spinal epidural lipomatosis (arrows) in an obese patient with a concomitant lumbar disc herniation. Sagittal T1- (a) and T2-weighted MRI (b)

41  Spinal Epidural Lipomatosis

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Fig. 41.6  The same case as Figure 41.5 showing the accumulation of fat tissue within the epidural space of the lumbar spinal canal. Note the herniated disc on L4-L5 (arrow). Axial lumbar T2-weighted MR images (a–c)

41.4 Treatment Options and Prognosis Spinal epidural lipomatosis can be managed conservatively or surgically. However, on most occasions, no specific treatment is required. Conservative therapy includes stopping corticosteroids and a body weight loss regimen. While surgical therapy comprises an epidural fat decompression procedure via laminectomy or laminotomy. The patient’s conditions, neurologic signs and symptoms, the underlying etiology of lipomatosis, and topographic features all influence the treatment decisions. Conservative treatment seems more successful in obese patients with idiopathic spinal epidural lipomatosis. Overall,

surgical decompression is a reasonable option in patients with CES, those with paralyzing sciatica or other neurological impairment, or those who have failed conservative management.

Further Reading Ahmad S, Best T, Lansdown A, Hayhurst C, Smeeton F, Davies S, et al. Spinal epidural lipomatosis: a rare association of Cushing's disease. Endocrinol Diabetes Metab Case Rep. 2020;2020:20–0111. https:// doi.org/10.1530/EDM-­20-­0111. Akhaddar A, Ennouali H, Gazzaz M, Naama O, Boucetta M. Idiopathic spinal epidural lipomatosis without obesity: a case with relapsing and remitting course. Spinal Cord. 2008;46:243–4. https://doi. org/10.1038/sj.sc.3102099.

576 Al-Omari AA, Phukan RD, Leonard DA, Herzog TL, Wood KB, Bono CM.  Idiopathic spinal epidural lipomatosis in the lumbar spine. Orthopedics. 2016;39:163–8. https://doi. org/10.3928/01477447-­20160315-­04. Alomari S, Lubelski D, Khalifeh JM, Sacino AN, Theodore N, Witham T, et  al. Etiologies and outcomes of spinal epidural lipomatosis: systematic review of the literature and meta-analysis of reported cases. Clin Spine Surg. 2022;35:383–7. https://doi.org/10.1097/ BSD.0000000000001344. Holder EK, Raju R, Dundas MA, Husu EN, McCormick ZL. Is there an association between lumbosacral epidural lipomatosis and lumbosacral epidural steroid injections? A comprehensive narrative literature review. N Am Spine Soc J. 2022;9:100101. https://doi. org/10.1016/j.xnsj.2022.100101. Kim K, Mendelis J, Cho W.  Spinal epidural lipomatosis: a review of pathogenesis, characteristics, clinical presentation, and management. Global Spine J. 2019;9:658–65. https://doi. org/10.1177/2192568218793617. Kotilainen E, Hohenthal U, Karhu J, Kotilainen P.  Spinal epidural lipomatosis caused by corticosteroid treatment in ulcerative colitis. Eur J Intern Med. 2006;17:138–40. https://doi.org/10.1016/j. ejim.2005.08.011. Lim MJR, Zheng Y, Babla Singbal S, Makmur A, Yeo TT, Kumar N.  Clinical and radiological characteristics of spinal epidural lipomatosis: a retrospective review of 90 consecutive patients. J Clin Orthop Trauma. 2022;32:101988. https://doi.org/10.1016/j. jcot.2022.101988.

41  Spinal Epidural Lipomatosis Mosch MHW, de Jong LD, Hazebroek EJ, van Susante JLC. Lumbar epidural lipomatosis is increased in patients with morbid obesity and subsequently decreases after bariatric surgery. World Neurosurg. 2021:S1878-8750(21)01708-3. https://doi.org/10.1016/j. wneu.2021.11.007. Praver M, Kennedy BC, Ellis JA, D'Amico R, Mandigo CE. Severity of presentation is associated with time to recovery in spinal epidural lipomatosis. J Clin Neurosci. 2015;22:1244–9. https://doi. org/10.1016/j.jocn.2015.03.005. Spinnato P, Barakat M, Lotrecchiano L, Giusti D, Filonzi G, Spinelli D, et  al. MRI features and clinical significance of spinal epidural lipomatosis: all you should know. Curr Med Imaging. 2021; https:// doi.org/10.2174/1573405617666210824111305. Valcarenghi J, Bath O, Boghal H, Ruelle M, Lambert J.  Benefits of bariatric surgery on spinal epidural lipomatosis: case report and literature review. Eur J Orthop Surg Traumatol. 2018;28:1437–40. https://doi.org/10.1007/s00590-­018-­2206-­y. Walker PB, Sark C, Brennan G, Smith T, Sherman WF, Kaye AD. Spinal epidural lipomatosis: a comprehensive review. Orthop Rev (Pavia). 2021;13:25571. https://doi.org/10.52965/001c.25571. Yang K, Ji C, Luo D, Li K, Xu H.  Lumbar laminotomy and replantation for the treatment of lumbar spinal epidural lipomatosis: a case report. Medicine (Baltimore). 2021;100:e26795. https://doi. org/10.1097/MD.0000000000026795.

Intradural Lumbosacral Tumors

42.1 Generalities and Relevance Intradural lumbosacral tumors (IDLSTum) may arise from the nerve roots, the leptomeninges, or the filum terminale (Fig. 42.1). The 20 lumbo-sacro-coccygial nerve roots constitute the cauda equina (horse tail) that originates from the conus medullaris (the terminal end of the spinal cord). The cauda equina nerve roots exit the thecal sac at each level and move towards each lateral recess on each side. Therefore, the number of nerve roots declines as they spread caudally from 20 at L2/L3 vertebral level to 11 at L5/S1 vertebral level. The filum terminale (AKA filum terminalis) is a delicate thread form of connective tissue that extends inferiorly from the conus medullaris to the termination of the thecal sac at S2. Intradural tumors constitute approximately one-third of all spinal neoplasms. There is a wide variety of IDLSTum (Table 42.1), but the couple schwannoma and meningioma represent more than 90% of all these tumors. Given the topographic proximity between the cauda equina nerve roots and the conus medullaris, many signs and symptoms could be encountered in both cauda equina syndrome (CES) and conus medullary syndrome. Both syndromes can present with back pain radiating to the legs, motor and sensory dysfunction of the lower extremities, bladder and/or bowel dysfunction, sexual dysfunction, and perineal anesthesia. However, conus medullaris syndrome causes both upper and lower motor neuron disorders, whereas CES causes predominantly lower motor neuron disorders (Table 42.2). Regarding the pathophysiology of lumbosacral radicular neuropathies due to IDLSTum, functional damage and neurologic deficits could be caused by direct compression of the radicular structures, ischemic damage secondary to vascular compression, or chemical irritative effects.

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Patients with primary tumors are commonly young and healthy, while those with metastatic tumors are older and frequently have a history of malignancy. Low back and/or radicular pain is often originally attributed to classic lumbosacral degenerative diseases with a significant delay between the onset of symptoms and the final diagnosis. The majority of nerve sheath tumors (namely meningioma, schwannoma, and neurofibroma) may arise in a solitary and sporadic manner; however, the development of multiple tumors is not rare and can be part of a complex genetic condition well-known as neurofibromatosis Type 2. Some schwannomas may have both intraspinal and extraspinal extension, connected through a widening intervertebral foramen, and are known as “dumbbell” or “hourglass” tumors. These types of intradural tumors can be also intra/ extradural.

Fig. 42.1  Illustrative image showing lumbar intradural tumor (without osseous involvement) compressing the thecal sac and its content (mainly cauda equina nerve roots) as seen in axial (left) and sagittal (right) sections

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_42

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578 Table 42.1  The most frequent lumbosacral intradural tumors causing lumbosacral radiculopathies previously reported in the literature Benign tumors

Malignant tumors

–  Meningioma – Nerve sheath tumors (schwannoma and neurofibroma) (Figs. 42.2, 42.3, 42.4, 42.5, 42.6, 42.7, 42.8, 42.9, 42.10, 42.11) – Myxopapillary ependymoma (filum terminal) (Fig. 42.12) –  Ganglioglioma (Figs. 42.13, 42.14, 42.15, 42.16) –  Paraganglioma (Figs. 42.17, 42.18, 42.19, 42.20) –  Hemangioblastoma –  Lipoma – Leptomeningeal metastasis (mainly lung and breast carcinoma in adults and medulloblastomas in children) (Fig. 42.21) –  Lymphoma – Malignant ependymoma (Figs. 42.22, 42.23, 42.24, 42.25, 42.26) –  Carcinoid tumor –  Rhabdomyosarcoma –  Granulocytic sarcoma (myeloblastoma) –  Atypical teratoid/rhabdoid tumor

Table 42.2  The key difference between cauda equina syndrome from conus medullaris syndrome

Vertebral level Neurologic level Motor neurons Onset of symptoms Low back pain Radicular pain Motor loss

Reflexes Sensory deficit

Sphincter dysfunction Electromyogram Causes Outcome

Cauda equina syndrome L2-Sacrum Lumbosacral nerve roots

Conus medullaris syndrome T12-L2 Sacral cord segment (conus and epiconus) and nerve roots Lower motor neuron Combination of lower and upper motor neuron Gradual and unilateral Sudden and bilateral Less marked More severe Asymmetric, more marked, areflexia, atrophy, rare fasciculations Both ankle and knee jerks absent Saddle zone, unilateral, asymmetric, no sensory dissociation Late

More marked Mild to moderate Symmetric, less marked, hyperreflexia, rare atrophy, fasciculations Only ankle jerk absent

Multiple root levels and sphincters may be involved Various, mainly spinal degenerative, rarely intradural tumors More favorable than conus medullaris syndrome

Normal lower extremity, external anal sphincter involvement Various, mainly tumor and spinal trauma

Perianal zone, bilateral, symmetric, sensory dissociation Early

Less favorable than cauda equina syndrome

42.2 Clinical Presentations The initial evaluation of patients with IDLSTum should include a detailed past medical history and clinical exam. History would include questions about recent underlying diseases, medications, surgeries, neurofibromatosis, or malignancies. Patients present with signs and symptoms of nerve root compression. Common presentations include weakness, localized back pain, radicular pain, sensory deficits, occasional urinary difficulties, and gait ataxia. Motor deficits are not common at the onset of clinical presentation, but will appear later. Cases with complete CES are rare. However, the majority of patients have a relatively long and nonspecific disease course. Unlike vertebral and extradural tumors, radicular pain that is described as progressive, severe, burning, or dysesthetic characterizes intradural tumors. Pain is classically worse at night and exacerbated in the recumbent position. Sometimes, radicular pain may entirely disappear during the daytime. Weakness is often associated with hyporeflexia and atrophy along the radicular innervation of the affected lower limb. Babinski’s sign and the Lasègue test are often negative. Regarding sciatic pain, some patients may present atypical onset of isolated sciatica, whereas others may complain of rapid progression of acute sciatica to a CES within a few days. Topographically, the main differential diagnosis of CES regards the region of conus medullaris (Table 42.2). However, it seems that patients with malignant IDLSTum tend to have more rapid gradual symptoms than those with benign forms. In addition, fatigue and weight loss should point toward malignancy. In some cases, separating lumbosacral radiculopathy from lumbosacral plexopathy or lower limb peripheral neuropathy on clinical grounds can be difficult. Therefore, in such cases electrodiagnostic studies are decisive. In addition, patients with sphincter disorders can be assessed with various combinations of urodynamic studies (e.g., uroflowmetry and cystometry). Neurofibromatosis should be considered in pediatric patients with a nerve sheath tumor and in cases with further spinal or cranial tumors (particularly vestibular schwannomas and meningiomas), skin lesions (Lisch nodules, cutaneous neurofibromas, café-au-lait macules (Fig.  42.2)), or a parent with neurofibromatosis. In this context, additional ophthalmic, otologic, and dermatologic evaluation may be useful. Hemangioblastoma may occur in the context of Von Hippel-Lindau disease which is a neurocutaneous syndrome characterized by benign and malignant tumors in multiple organs such as cerebellar, retinal, renal, hepatic, pancreatic, or genital tract tumors.

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Fig. 42.2  Case 1. Multiple cutaneous café-au-lait macules on the posterior (a) anterior (b) surface of the trunk. On spinal MRI, this young patient had dural sac ectasia with multiple neurofibromatoses (arrow). Thoracolumbar spinal axial (c, d) MRI

42.3 Imaging Features Magnetic resonance imaging (MR) remains the best method of evaluation for intradural tumors including cauda equina tumors (Figs. 42.2, 42.3, 42.4, 42.5, 42.7, 42.10, 42.11, 42.12, 42.14, 42.15, 42.17, and 42.21, 42.22, 42.23). This imaging method might help to localize the site and potential extension of the tumor and provide evidence for its nature and its relationship with the cauda equina nerve roots. The classic exploration needs urgent sagittal and axial T1 and T2 sequences with or without T1 post-gadolinium injection. Gradient echo sequences help to visualize blood products and calcifications. Complete spinal and cranial imaging is recommended after the detection of some tumors such as ependymomas, medulloblastomas, and anaplasic astrocytomas. For patients with contraindications to MRI (e.g., metallic implants), a myelo-computed tomography (CT) is an alternative option. Patients with bladder disorders might be evaluated with an abdominopelvic CT scan or ultrasound for detecting urinary retention and incomplete bladder emptying. Further angiographic studies as well as biological investigations may be indicated for specific cases in the search for an etiology. Plain radiographs are useful in select cases with spinal deformities. Classically, nerve sheath tumors may present with intralesional calcifications and changes in vertebral bone including pedicle erosion, scalloping, and neuroforamina widening (Fig. 42.13). However, a CT scan is a more rel-

evant technic for imaging evaluation of the bony spine and calcified tumors. Furthermore, a CT scan is useful when larger tumors require combined surgical approaches or in cases with potential spinal instability. The MRI appearance will vary depending on the histology. The majority of meningiomas have a broad-based dural attachment with a dural tail sign (linear attachment pattern). Unlike most schwannomas, meningiomas do not have a hyposignal central area on T2-weighted image (WI). Nerve sheath tumors may have extradural neural foraminal widening with a dumbbell appearance. Schwannomas present as a marked hyperintense round lesion on T2WI with the heterogeneous cystic component when larger. Unlike neurofibromas (Figs.  42.2, 42.10, and 42.11) which are fusiform or plexiform and encase nerve roots, schwannomas are round and displace nerve roots (Figs.  42.3, 42.4, 42.5 and 42.7). Most neurofibromas are bilateral multilevel tumors. Leptomeningeal metastases show nerve root involvement with multifocal nodular enhancement (Fig.  42.21). Myxopapillary ependymomas are typically isointense on T1WI and hyperintense on T2WI with gadolinium enhancement. These tumors are characterized by sausage-shaped morphology and the “cap sign” which is a hypointense rim (hemosiderin secondary to previous bleeding) found at the extremities of the tumor on T2WI (Figs. 42.22 and 42.23). Paragangliomas have prominent flow voids. Intradural lipoma typically appears hyperintense on both T1WI and T2WI (fatty signal intensities) without gadolinium enhancement (Fig. 42.17).

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Fig. 42.3  Case 2. L4 intradural schwannoma (arrows) as seen on sagittal T1-weighted MRI before (a) and after (b) gadolinium injection as well as on T2-weighted (c) MRI

Sometimes, hypervascular tumors such as hemangioblastomas and paragangliomas or some large meningiomas may need spinal angiography and additional preoperative embolization (within 24 h) prior to surgical resection.

Topographically, IDLSTum should be differentiated from other intradural lumbosacral lesions (Table  42.3) as well as epidural lesions whether they are tumoral, traumatic, infectious, vascular, iatrogenic, inflammatory, granulomatous, or malformative.

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Fig. 42.4  Case 2. The intradural schwannoma is lateralized on the left with L4-L5 foraminal widening (arrows) as seen on axial T1-weighted MRI before (a) and after (b) gadolinium injection as well as on T2-weighted (c) MRI

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Fig. 42.5  Case 3. L1-L2 intradural benign schwannoma (arrows) as seen on sagittal post-gadolinium T1- (a) and T2-weighted (b) MRI as well as on axial T2-weighted MRI (c)

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Fig. 42.6  Case 3. Intraoperative view showing the intradural benign schwannoma (a). Tumor appearance following complete surgical resection (b)

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Fig. 42.7  Case 4. Multiple benign schwannomas of the cauda equina (arrows) as seen on sagittal T1-weighted MRI before (a) and after (b) gadolinium injection as well as on STIR sequence (c) and T2-weighted MRI (d)

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Fig. 42.8  Case 4. Intraoperative view after dura opening showing the intradural benign schwannomas (a). Tumors’ appearance following complete surgical resection (b)

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Fig. 42.9  Case 4. Microscopic image of the benign schwannomas showing spindle cell tumor proliferation organized in hypercellular Antoni A areas (star) and myxoid hypocellular Antoni B areas (circle) (a) (Hematoxylin and eosin stain, original magnification ×60). Tumor

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cells are elongated and wavy with reduced cytoplasm (b) (Hematoxylin and eosin stain, original magnification ×100). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

42.3  Imaging Features Fig. 42.10  Case 5. Multiple dural and intradural lumbosacral plexiform neurofibromas as seen on sagittal (a) and coronal (b) T1-weighted MRI as well as on sagittal (c) and coronal (d) T2-weighted MRI

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Fig. 42.11  Case 5. Multiple dural and intradural sacral plexiform neurofibromas as seen on axial T2-weighted MRI (a) and on STIR sequence (b) Fig. 42.12  Case 6. Multiple intradural lumbosacral myxopapillary ependymomas (arrows) in a 25-year-old man who presented with bilateral sciatica. Lumbosacral sagittal (a) and axial (b, c) post-­ gadolinium T1-weighted MRI

D

E

F

42.3  Imaging Features

587

E

D

F

Fig. 42.13  Case 7. L5-S1 intradural foraminal ganglioneuroma (arrows) as seen on axial (a) and sagittal reconstructions (b, c) CT scan with foraminal widening. (Courtesy of Pr. Hassan Baallal.)

D

E

F

Fig. 42.14  Case 7. The ganglioneuroma (arrows) as seen on axial T2-weighted MRI (a) and sagittal T1- (b) and T2-weighted MRI (c)

588

42  Intradural Lumbosacral Tumors

D

E

F

Fig. 42.15  Case 7. The ganglioneuroma (arrows) as seen on axial (a), sagittal (b), and coronal (c) post-gadolinium T1-weighted MRI

Fig. 42.16  Case 7. Microscopic image of the ganglioneuroma. There are a double-cell population. The first is composed of Schwann cells (black arrows) separated by loose myxoid stroma and the second is formed of mature ganglion cells (yellow arrows) (Hematoxylin and eosin stain, original magnification ×200). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

42.3  Imaging Features

D

589

E

F

G

H

Fig. 42.17  Case 8. Paraganglioma (arrows) of the filum terminalis as seen on sagittal post-gadolinium T1-weighted MRI (a), on STIR sequence (b), and on T2-weighted MRI (c). Axial post-gadolinium T1- (d) and T2-weighted MRI (e)

D

E

F

Fig. 42.18  Case 8. Intraoperative view after dura opening showing the intradural paraganglioma attached to the filum terminalis (arrow) (a). Tumor appearance following complete surgical resection (b, c)

590

42  Intradural Lumbosacral Tumors

D

Fig. 42.19  Case 8. Photomicrograph image of the paraganglioma showing the nest of tumor cells within a fibrovascular stroma, known as the Zellballen pattern (a) (Hematoxylin and eosin stain, original magnification ×60). Tumor cells are round to polygonal with abundant granu-

E

lar eosinophilic cytoplasm; the nuclei were uniformly round to oval and have moderate nuclear pleomorphism (b) (Hematoxylin and eosin stain, original magnification ×100). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

c

d

e

f

Fig. 42.20  Case 8. The tumor is positive for chromogranin-A (c), synaptophysin (d), and Cytokeratin (AE1/AE3) (e). Sustentacular cells are highlighted by their reactivity for S100 protein (f). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

42.3  Imaging Features

a

591

b

c

Fig. 42.21  Case 9. Multiple intradural cauda equina metastasis in a patient with a malignant tumor of the mandible. Sagittal post-gadolinium T1- (a) and T2-weighted (b) MRI as well as on STIR sequence (c)

592

a

42  Intradural Lumbosacral Tumors

b

c

Fig. 42.22  Case 10. Intradural L3-S2 malignant ependymomas (arrows) in a 22-year-old woman who presented with bilateral sciatica and mild cauda equina syndrome. Sagittal post-gadolinium T1- (a) and T2-weighted (b) MRI as well as on STIR sequence (c)

a

b

c

Fig. 42.23  Case 10. Intradural L3-S2 malignant ependymomas (arrows) as seen in axial post-gadolinium T1- (a) and T2-weighted (b, c) MRI

42.3  Imaging Features

593

a

b

c

Fig. 42.24  Case 10. Operative view after posterior laminectomy (a, b). Note the appearance of the tumor (intradural malignant ependymoma) through the dura layer (a, b). Tumor appearance (arrows) after dura opening (c)

Fig. 42.25  Case 10. Microscopic image of the malignant ependymoma (WHO grade 3). There are ependymal cells arranged in perivascular pseudorosettes (arrows) (Hematoxylin and eosin stain, original magnification ×60) (a). Tumor cells are ovoids with nuclei showing moderate cytonuclear atypia and mitosis (Hematoxylin and eosin stain, original magnification ×200) (b). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

a

b

594 Fig. 42.26  Case 10. Postoperative sagittal post-gadolinium T1- (a) and T2-weighted (b) MRI showing complete tumor resection

42  Intradural Lumbosacral Tumors

a

Table 42.3  The main intradural lumbosacral lesions mimicking intradural neoplasms Cavernoma, vascular malformations (AVM, AVF) Spontaneous (anticoagulation), post-traumatic Tuberculoma, sarcoidosis Bacterial abscess, fungal, viral, parasitic (schistosomiasis, cysticercosis, hydatidosis) Inflammation Arachnoiditis, Guillain-Barré syndrome Dysembryogenetic Lipoma, epidermoid cyst, dermoid cyst, teratoma, neurenteric cyst Arachnoid cysts Leptomeningeal cysts Degenerative Intradural lumbar disc herniation Iatrogenic Foreign bodies Vascular Hematoma Granulomatous Infection

b

42.4 Treatment Options and Prognosis Management strategies regarding IDLSTum vary significantly, depending primarily on the nature of the tumor and on its exact location. Several options might be offered including conservative measures, medical treatments, partial or radical resections, or just a biopsy. Surgical excision is the gold standard in the treatment of most intradural tumors sited in the lumbosacral region. However, further associated lesions or underlying conditions should always be considered. Preoperative radiography is needed to localize precisely the level of the tumor.

Further Reading

The aim of microsurgery for IDLSTum is to achieve a maximal degree of resection combined with maximal preservation of the functional integrity of neurologic structures. Subsequently, many surgeons recommend intraoperative electrophysiological monitoring of the lower limbs and sphincters to reduce iatrogenic morbidity. Traction on the spinal root should be avoided. If needed, the nerve root or rootlet from which the tumor develops can be sacrificed as the rootlet is generally sensory in origin. In meningioma, it’s necessary to cauterize the dura attachment. The majority of leptomeningeal metastases require only surgical decompression and a biopsy for histopathologic study. The dura should be closed in a hermetic manner to avoid any postoperative CSF fistula, pseudomeningocele, and potential meningitis. Some dumbbell-shaped tumors (manly schwannomas and neurofibromas) may require a posterior or posterolateral approach followed by an anterior approach either at the same surgical procedure or in a second-stage surgery. Sometimes, an additional spinal fusion may be required if there is a potential preoperative instability and/or an iatrogenic instability because of the surgical procedure. Complications are especially related to prolonged bed rest, the nature and extension of the tumor, the degree of neurologic impairment, and sphincter disorders. Neurophysiologic monitoring during surgery and the use of navigational tools are crucial to reduce the occurrence of new neurologic deficits or neurologic worsening. The best predictors of outcome are initial neurological presentation, the timing of diagnosis, rapidity of surgical decompression, nature of the lesion, and degree of surgical resection. Benign lesions, incomplete neurologic impairments, and complete surgical excision tend to have better outcomes. Recurrence is not rare. Residual radicular neuropathic pain needs appropriate medical therapy. Malignant tumors, especially metastatic ones, carry a poor prognosis which will require additional radio- and/or chemotherapy.

Further Reading Abul-Kasim K, Thurnher MM, McKeever P, Sundgren PC. Intradural spinal tumors: current classification and MRI features. Neuroradiology. 2008;50:301–14. https://doi.org/10.1007/s00234-­007-­0345-­7. Akhaddar A, Ajja A, Albouzidi A, Boucetta M. Cystic schwannoma of the cauda equina mimicking hemangioblastoma. Neurochirurgie. 2008;54:101–3. https://doi.org/10.1016/j.neuchi.2008.01.007. Ardon H, Plets C, Sciot R, Calenbergh FV. Paraganglioma of the cauda equina region: a report of three cases. Surg Neurol Int. 2011;2:96. https://doi.org/10.4103/2152-­7806.82989. Bagley CA, Gokaslan ZL. Cauda equina syndrome caused by primary and metastatic neoplasms. Neurosurg Focus. 2004;16:e3. https:// doi.org/10.3171/foc.2004.16.6.3. Barrena López C, De la Calle GB, Sarabia HR.  Intradural ganglioneuroma mimicking lumbar disc herniation: case report.

595 World Neurosurg. 2018;117:40–5. https://doi.org/10.1016/j. wneu.2018.05.225. Betchen S, Schwartz A, Black C, Post K. Intradural hemangiopericytoma of the lumbar spine: case report. Neurosurgery. 2002;50:654– 7. https://doi.org/10.1097/00006123-­200203000-­00045. Bonnal J, Pellegrin J, Cordani I. Sciatica caused by meningioma of the cauda equina. Mars Chir. 1952;4:46–50. Bradford R, Crockard HA, Isaacson PG. Primary rhabdomyosarcoma of the central nervous system: case report. Neurosurgery. 1985;17:101– 4. https://doi.org/10.1227/00006123-­198507000-­00019. Champeaux C, Drier A, Devaux B, Tauziède-Espariat A.  Malignant primary diffuse leptomeningeal gliomatosis with histone H3.3 K27M mutation. Neurochirurgie. 2018;64:198–202. https://doi. org/10.1016/j.neuchi.2017.12.007. Diabira S, Akhaddar A. Tumeurs rachidiennes intradurales (Intradural spinal tumors). Encycl Med Chir (EMC—Neurologie). Edition 2021. Chapter 17-275-A-10. Elsevier Masson. doi: https://doi. org/10.1016/S0246-­0378(21)83164-­4 Fujii K, Abe T, Koda M, Funayama T, Noguchi H, Miura K, et  al. Cauda equina schwannoma with concomitant intervertebral disc herniation: a case report and review of literature. J Clin Neurosci. 2019;62:229–31. https://doi.org/10.1016/j.jocn.2018.12.033. Gardiman MP, Fassan M, Orvieto E, Iaria L, Calderone M, Mardari R, et  al. A 14-year-old girl with multiple tumors. Brain Pathol. 2012;22:865–8. https://doi.org/10.1111/j.1750-­3639.2012.00639.x. Ghedira K, Matar N, Bouali S, Zehani A, Jemel H.  Acute paraplegia revealing a hemorrhagic cauda equina paragangliomas. Asian J Neurosurg. 2019;14:245–8. https://doi.org/10.4103/ajns. AJNS_206_17. El-Hajj VG, Pettersson Segerlind J, Burström G, Edström E, Elmi-­ Terander A. Current knowledge on spinal meningiomas: a systematic review protocol. BMJ Open. 2022;12:e061614. https://doi. org/10.1136/bmjopen-­2022-­061614. Herb E, Schwachenwald R, Nowak G, Müller H, Reusche E.  Acute bleeding into a filum terminale ependymoma. Neurosurg Rev. 1990;13:243–5. https://doi.org/10.1007/BF00313026. Holtzman RN, Jormark SC. Nondural-based lumbar clear cell meningioma. Case report. J Neurosurg. 1996;84:264–6. https://doi. org/10.3171/jns.1996.84.2.0264. Kalsi P, Hassan MF, Scoones D, Bradey N, Tizzard S.  An unusual case of ectopic prostate tissue in an intradural lipoma of the conus medullaris. Br J Neurosurg. 2011;25:757–8. https://doi.org/10.3109 /02688697.2010.544792. Kato T, George B, Mourier KL, Lot G, Gelbert F, Mikol J. Intraforaminal neurinoma in the lumbosacral region. Neurol Med Chir (Tokyo). 1993;33:86–91. https://doi.org/10.2176/nmc.33.86. Kim DY, Lee JK, Moon SJ, Kim SC, Kim CS. Intradural spinal metastasis to the cauda equina in renal cell carcinoma: a case report and review of the literature. Spine (Phila Pa 1976). 2009;34:E892–5. https://doi.org/10.1097/BRS.0b013e3181b34e6c. Koustais S, O’Halloran PJ, Hassan A, Brett F, Young S. Incidental primary intradural carcinoid tumor in a patient with lumbar radiculopathy. World Neurosurg. 2017;105:1042.e11–4. https://doi. org/10.1016/j.wneu.2017.06.179. Li L, Patel M, Nguyen HS, Doan N, Sharma A, Maiman D. Primary atypical teratoid/rhabdoid tumor of the spine in an adult patient. Surg Neurol Int. 2016;7:27. https://doi.org/10.4103/2152-­7806.178523. Loke TK, Ma HT, Ward SC, Chan CS, Metreweli C.  MRI of intraspinal nerve sheath tumours presenting with sciatica. Australas Radiol. 1995;39:228–32. https://doi.org/10.1111/j.1440-­1673.1995. tb00281.x. Maamri K, Hadj Taieb MA, Trifa A, Elkahla G, Njima M, Darmoul M. Spinal clear cell meningioma without dural attachment: a case report and literature review. Radiol Case Rep. 2022;17:1760–4. https://doi.org/10.1016/j.radcr.2022.02.052.

596 Masui F, Yokoyama R, Soshi S, Beppu Y, Asanuma K, Fujii K. A malignant peripheral nerve-sheath tumour responding to chemotherapy. J Bone Joint Surg Br. 2004;86:113–5. Miliaras GC, Kyritsis AP, Polyzoidis KS.  Cauda equina paraganglioma: a review. J Neurooncol. 2003;65:177–90. https://doi. org/10.1023/b:neon.0000003753.27452.20. Morita M, Osawa M, Naruse H, Nakamura H.  Primary NK/T-cell lymphoma of the cauda equina: a case report and literature review. Spine (Phila Pa 1976). 2009;34:E882–5. https://doi.org/10.1097/ BRS.0b013e3181b29de6. Mosch A, Kuiters RR, Kazzaz BA. Intradural granulocytic sarcoma: a rare cause of sciatic pain. Clin Neurol Neurosurg. 1991;93:341–4. https://doi.org/10.1016/0303-­8467(91)90103-­v. Nadkarni TD, Menon RK, Desasi KI, Goel A. Hemangioblastoma of the filum terminale. J Clin Neurosci. 2006;13:285–8. https://doi. org/10.1016/j.jocn.2005.02.025. Neromyliotis E, Kalyvas AV, Drosos E, Komaitis S, Bartziotas D, Skandalakis GP, et  al. Spinal atypical rhabdoid teratoid tumor in an adult woman: case report and review of the literature. World Neurosurg. 2019;128:196–9. https://doi.org/10.1016/j. wneu.2019.05.007. Ogbodo E, Kaliaperumal C, Keohane C, Bermingham N, Kaar G. Sciatica as a presenting feature of thyroid follicular adenocarcinoma in a 79-year-old woman. BMJ Case Rep. 2011;2011:bcr1020115014. https://doi.org/10.1136/bcr.10.2011.5014. Ottenhausen M, Ntoulias G, Bodhinayake I, Ruppert FH, Schreiber S, Förschler A, et al. Intradural spinal tumors in adults-update on management and outcome. Neurosurg Rev. 2019;42:371–88. https://doi. org/10.1007/s10143-­018-­0957-­x. Pagano A, Iaquinandi A, Fraioli MF, Bossone G, Carra N, Salvati M.  Cauda equina syndrome from intradural metastasis of a non-­

42  Intradural Lumbosacral Tumors neural tumor: case report and review of literature. Br J Neurosurg. 2021:1–8. https://doi.org/10.1080/02688697.2021.1958155. Postacchini F, Urso S, Tovaglia V.  Lumbosacral intradural tumours simulating disc disease. Int Orthop. 1981;5:283–9. https://doi. org/10.1007/BF00271084. Revuelta Barbero JM, Saab Mazzei A, Cotúa Quinteros C, de Reina L. Primary well differentiated neuroendocrine tumor of the filum terminale. Case report and literature review. Neurocirugia (Astur : Engl Ed). 2018;29:244–9. https://doi.org/10.1016/j.neucir.2017.11.002. Salman-Monte TC, Castro-Dominguez F, Villalba G, Capellades J, Monfort J. Atypical onset of sciatica in a patient with a filum terminale hemangioblastoma. Reumatol Clin (Engl Ed). 2018;14:115–8. https://doi.org/10.1016/j.reuma.2016.10.006. Strong C, Yanamadala V, Khanna A, Walcott BP, Nahed BV, Borges LF, Coumans JV. Surgical treatment options and management strategies of metastatic renal cell carcinoma to the lumbar spinal nerve roots. J Clin Neurosci. 2013;20:1546–9. https://doi.org/10.1016/j. jocn.2013.02.014. Than KD, Ghori AK, Wang AC, Pandey AS.  Metastatic malignant peripheral nerve sheath tumor of the cauda equina. J Clin Neurosci. 2011;18:844–6. https://doi.org/10.1016/j.jocn.2010.08.039. Yang C, Li G, Fang J, Wu L, Yang T, Deng X, Xu Y.  Clinical characteristics and surgical outcomes of primary spinal paragangliomas. J Neurooncol. 2015;122:539–47. https://doi.org/10.1007/ s11060-­015-­1742-­0. Yu D, Choi JH, Jeon I.  Giant intradural plexiform schwannoma of the lumbosacral spine—a case report and literature review. BMC Musculoskelet Disord. 2020;21:454. https://doi.org/10.1186/ s12891-­020-­03492-­y.

Conus Medullaris Lesions

43.1 Generalities and Relevance The conus medullaris or “conus terminalis” is the terminal end of the spinal cord, which typically occurs at the L1 vertebral level in the adult that corresponds to the sacral cord segment between S1 and S5. The lower end of the conus medullaris is called “epiconus”. After the spinal cord ends caudally, the spinal nerves continue to branch out diagonally, creating the cauda equina nerve roots (Figs. 43.1, 43.2). Topographically, proximity to the L5 intramedullary segment and involvement of the first sacral segments could explain some radicular symptoms which look like sciatic pain when the conus medullaris is damaged. The intramedullary conus represents a distinct entity of the spinal cord regarding its anatomical, clinical, and microsurgical features. Furthermore, conus medullaris syndrome may mimic clinically cauda equina syndrome (CES). Both syndromes can present with back pain radiating to the legs, motor and sensory dysfunction of the lower extremities, bladder and/or bowel dysfunction, sexual dysfunction, and perineal anesthesia. However, conus medullaris syndrome

43

causes both upper and lower motor neuron disorders, whereas CES causes predominantly lower motor neuron disorders. Also, conus medullaris syndrome results from various lesions, whether intramedullary, intradural, or extradural. In this chapter, we will focus mainly on intramedullary conus lesions. (c.f. refer to Chap. 42 about Intradural Lumbosacral Tumors and Chaps. 40 and 39 about Epidural Non-Vertebral Tumors and Lumbosacral Vertebral Tumors, respectively). Lumbosacral radicular symptoms related to conus medullary lesions (CML) should be distinguished from lumbosacral radicular symptoms related to spinal funicular lesions (c.f. Chap. 44 about Intraspinal Funicular Sciatica). Regarding the pathophysiology of conus medullaris syndrome, functional damage and neurologic deficits could be caused by direct compression of the nervous structures (medullar and/or radicular), ischemic damage secondary to vascular compression, or chemical irritative effects. In the United States, the incidence of conus medullaris syndrome is about 449 new cases per year. At the same time, we would see 1016 new cases of CES.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_43

597

598 Fig. 43.1  Normal sagittal view of the lumbosacral spine. Note the position of the conus medullaris (terminal end of the spinal cord), which typically occurs at the L1 vertebral level in the adult. After the spinal cord ends caudally, the spinal nerves continue to branch out diagonally, creating the cauda equina nerve roots

43  Conus Medullaris Lesions

T12 Conus medullaris L1 Thecal sac Lumbar spine

L2 Cauda equina roots

Anterior longitudinal ligament

L3

Interspinous ligament

L4 Posterior longitudinal ligament

Supraspinous ligament

L5 Intervertebral disc Sacrum

Coccyx

S1

Filum terminalis

43.2 Etiologies

599

a

b

Fig. 43.2  Operative view of the thoracolumbar thecal sac after laminectomy of T11-L2 (a). The appearance of the conus medullaris and the epiconus (arrowhead) after the opening of the dura (b). Note the cauda

equina nerve roots (arrows) and the position of the Adamkiewicz artery (AKA the great anterior radiculomedullary artery or arteria radicularis magna) (b)

43.2 Etiologies

Table 43.1 represents the most frequent causes of lumbosacral radiculopathies related to intramedullary conus lesions previously reported in the literature (Table 43.1). Topographically, these intramedullary conus lesions should be differentiated from other intradural extramedullary diseases as well as epidural lesions whether they are tumoral, traumatic, infectious, vascular, iatrogenic, inflammatory, granulomatous, or malformative.

Intraparenchymatous conus medullaris lesions have a wide range of etiologies; however, most lesions are neoplasms (Figs.  43.3, 43.4, 43.5, 43.6, 43.7, 43.8, 43.9, 43.10). Ependymomas are the most common intraconal tumor in adult patients, followed by astrocytomas and hemangioblastomas.

600

43  Conus Medullaris Lesions

a

b

c

d

Fig. 43.3  Case 1. Teratoma of the conus medullaris (arrows) in a 31-year-old man manifesting as an isolated right-sided sciatic pain. Lumbar sagittal T1- before (a) and after gadolinium injection (b), T2-weighted MRI (c), and on STIR sequence (d)

a

b

c

Fig. 43.4  Case 1. Operative views of the teratoma after dura opening (durotomy) (a) and during dissection of the lesion (b). Note the appearance of the teratoma and its contents after the complete removal of the lesion (c)

43.2 Etiologies

601

a

b

c

Fig. 43.5  Case 1. Postoperative lumbar MRI showing complete removal of the teratoma. Lumbar sagittal T1- before (a) and after gadolinium injection (b), and on T2-weighted MRI (c)

a

b

c

Fig. 43.6  Case 2. Ventriculus terminalis (AKA fifth ventricle) (arrows) as seen on sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c)

602

43  Conus Medullaris Lesions

a

b

c

d

Fig. 43.7  Case 3. Metastasis of the conus medullaris (arrows) in an adult man manifesting as an isolated bilateral lumbosacral radicular pain. Lumbar sagittal T1- before (a) and after gadolinium injection (b). Axial post-contrast T1-weighted MRI (c, d)

a

b

c

d

Fig. 43.8  Case 4. Conus medullaris hematomyelia (arrows). Lumbar sagittal T1- before (a) and after gadolinium injection (b), on STIR sequence (c), and on T2-weighted MRI (d)

43.2 Etiologies

a

603

b

c

d

Fig. 43.9  Case 5. Conus medullaris myelopathy (arrows) with intradural perimedullary dilated veins (arrowheads) as seen on sagittal T1- (a) and T2-weighted MRI (b). A spinal vascular malformation was highly suspected. Selective spinal angiography of the right T10 segmental

Fig. 43.10  Case 5. Operative view of the vascular malformation: engorged venous vessels on the posterior surface of the conus medullaris (arrows) following laminectomy and durotomy

artery demonstrated a right-sided dural fistula (arrows) (c). Postoperative spinal angiogram showing complete vascular exclusion of the dural fistula (arrows) (d)

43  Conus Medullaris Lesions

604 Table 43.1  The most common causes of sciatica related to intramedullary conus lesions reported in the literature

Table 43.2  The key difference between intramedullary conus lesions from cauda equina lesions

Tumors

– Glial tumors: ependymoma (myxopapillary), astrocytoma, glioblastoma multiform, ganglioglioma – Non-glial tumors: hemangioblastoma, primitive neuroectodermal tumor (e.g., medulloblastoma, neuroblastoma), lymphoma –  Primary melanoma – Metastasis (mainly lung and breast carcinoma) Vascular – Cavernoma, vascular malformations (AVM, AVF), amyloid angiopathy –  Ischemic Hematoma – Spontaneous (coagulopathies, anticoagulant drugs) –  Post-traumatic Granulomatous –  Tuberculoma –  Sarcoidosis Infection Bacterial abscess, fungal, viral, parasitic (schistosomiasis, cysticercosis, hydatidosis) Inflammation Myelitis Demyelination Multiple sclerosis Dysembryogenetic Lipoma, ventriculus terminalis, epidermoid cyst, dermoid cyst, teratoma Malformation Congenital malformation of the conus medullaris Idiopathic From unknown cause

Vertebral level Neurologic level Motor neurons Onset of symptoms Low back pain Radicular pain Motor loss

The initial evaluation of patients with CML should include a detailed past medical history and clinical exam. History would include questions about recent underlying diseases, medications, infections, injuries, and history of malignancies or surgeries. Most patients with intramedullary conus tumors initially complained of local lower back pain. This nonspecific pain evolves in a progressive subacute manner to a distinct unilateral or bilateral pseudoradicular lower limb pain (even sciatic pain). Normally, there are early bladder and bowel sphincter disorders. The presence of sensory disturbances in the perianal area has to be inspected accurately. Motor deficits are not common at the onset of clinical presentation, but will appear later. Regarding lower limb reflexes, only ankle jerk is absent and often associated with a Babinski sign. Lasègue test is rarely positive. Topographically, the main differential diagnosis of conus medullaris syndrome regards the region of cauda equina (Table 43.2). The symptoms and their duration may vary greatly before an imaging diagnosis of intraconal lesions is established. These characters vary greatly depending mainly on the nature of the involved lesion. Overall, clinical features are

Lower motor neuron

Gradual and unilateral

Sensory deficit

Perianal zone, bilateral, symmetric, sensory dissociation

Sphincter dysfunction Electromyogram

Early Normal lower extremity, external anal sphincter involvement Various, mainly tumor and spinal trauma Less favorable than cauda equina syndrome

Multiple root levels and sphincters may be involved Various, mainly spinal degenerative More favorable than conus medullaris syndrome

Reflexes

Outcome

More marked Mild to moderate Symmetric, less marked, hyperreflexia, rare atrophy, fasciculations Only ankle jerk absent

Cauda equina lesions L2-Sacrum Lumbosacral nerve roots

Less marked More severe Asymmetric, more marked, areflexia, atrophy, rare fasciculations Both ankle and knee jerks absent Saddle zone, unilateral, asymmetric, no sensory dissociation Late

Causes

43.3 Clinical Presentations

Conus medullaris lesions T12-L2 Sacral cord segment (conus and epiconus) and nerve roots Combination of lower and upper motor neuron Sudden and bilateral

neither specific nor sensitive for conus medullaris syndrome. However, some characters would guide the diagnosis. For example, conus medullaris syndrome is caused by traumatic injury or vascular etiologies present more acutely. Sciatic pain related to intraconal lesions rarely exists in isolation, but is often associated with other neurologic or non-­ neurologic symptoms linked with the underlying etiology and causative factors. Consequently, besides sciatica, other concomitant symptoms can include. Fever, chills, night sweats, fatigue, and weight loss should point toward ­malignancy or infection. Though uncommon, when patients present with sciatica but without obvious lumbosacral or spinal cause, it is important to consider intramedullary conus lesions. In some cases, separating lower-level myelopathy from lumbosacral plexopathy or lumbosacral radiculopathy on clinical grounds can be difficult. Therefore, in such cases electrodiagnostic studies are decisive. In addition, patients with sphincter disorders might be evaluated with various combinations of urodynamic studies (e.g., uroflowmetry and cystometry).

43.4  Imaging Features

Besides CES, the differential diagnosis of CML should include other syndromes or diseases with bilateral lower limb and/or perineal sensorimotor disorders such as:

605

administration may indicate intraconal non-neoplastic lesions, such as multiple sclerosis, spinal cord infarction, radiation myelopathy, or subacute necrotizing myelopathy, rather than conus medullaris tumors. • Lumbar and/or sacral plexopathy Both ependymomas (can be multiples) and astrocytomas • Peripheral neuropathies of the lower limbs appear heterogeneous due to cystic, hemorrhagic, and • More traditional causes of bilateral lumbosacral radicu- necrotic areas. On T1-weighted MRI, these tumors are usulopathy (e.g., LDH, LSS, SPL) ally isointense to hyperintense. They appear on T2WI, an • Causes of higher myelopathies (especially from the tho- iso- to hypointense. There are strong enhancements after racic level) gadolinium injection. However, in contrast to ependymomas, • Tethered cord syndrome astrocytomas are usually eccentric within the spinal cord and • HIV-related myelopathy have less well-defined limits due to their infiltrative growth • Transverse myelitis pattern. • Syringomyelia Hemangioblastomas, which can be associated with von • Amyotrophic lateral sclerosis Hippel Lindau syndrome, appear isointense to hypointense • Hereditary spastic paraplegia on T1WI and hyperintense on T2WI with homogeneous and • Hereditary sensorimotor neuropathy (Charcot-Marie-­ intense enhancement after gadolinium injection. There are Tooth, Dejerine-Sottas) flow voids within these hypervascular tumors. Important • Spinal progressive muscular atrophy cystic components and an over-proportional conus medul(Kennedy-Alter-Sung) laris enlargement in relation to the size of the tumor charac• Different types of myopathies terize hemangioblastomas. The MRI appearance of intraconal metastasis mostly depends on the primitive tumor’s natural histology. Nevertheless, marked edema and gadolinium enhancement 43.4 Imaging Features are common findings. Most tuberculomas appear as an iso-hypointense Magnetic resonance imaging (MR) remains the best method expanded lesion on T1WI sequences and iso-hyperintense of evaluation for conus medullary syndrome. This imaging lesion on T2WI sequences with a rim- to nodular-like post-­ method might help localize the intramedullary lesion's site gadolinium enhancement. Intramedullary conus abscess is and provide evidence for the etiology. The classic explora- characterized by strong capsule enhancement following gadtion needs urgent sagittal and axial T1 and T2 sequences olinium administration. Biologic parameters are also with or without T1 post-gadolinium injection. For patients suggestive. with contraindications to MRI (e.g., metallic implants), a Cavernomas have a classic “mulberry-like” shape or myelo-computed tomography (CT) is an alternative option. “popcorn” appearance with a slight enhancement following Patients with bladder disorders might be evaluated with an gadolinium injection. Cavernomatous lesion shows the typiabdominopelvic CT scan or ultrasound for detecting uri- cal patterns of heterogeneity with central hyperintense signary retention and incomplete bladder emptying. Further nals on both T1WI and T2WI, surrounded by a hypointense angiographic studies as well as biological investigations area on T2WI. On T2* sequence, there is a pathognomonic may be indicated for specific cases in the search for an hemosiderin ring. etiology. Regarding vascular malformations, mainly arteriovenous Sometimes, a bony CT scan may be useful for identifying fistula (AVF) and arteriovenous malformation (AVM), the secondary bone changes, especially posterior vertebral body diagnosis is achieved by using MRI and selective digital erosion (scalloping) and spinal deformities. angiography (Fig.  43.9). The dilated veins seem like low-­ In the face of suspicion of a CML, the main objective of intensity vessels on T1WI images and are difficult to show the radiologist is to distinguish tumoral from non-tumoral within the cerebrospinal fluid (CSF). In contrast, the low siglesions. The main imaging characteristics that are used to nal serpiginous vessels are easily recognized around the spidifferentiate these two main entities consist of pathological nal cord in the hyperintensity of the CSF on spinal cord expansion, gadolinium enhancement, and T2WI. Intramedullary, high signal intensity indicates venous tumoral cyst formation. congestion. Following gadolinium injection, the dilated A wide variety of MRI patterns may be observed depend- veins are enhanced. The association of dilated veins and high ing on the histologic nature of the lesion, its extension, and spinal cord signal rather points to an AVF. However, a nidus the different stages of the disease (Figs.  43.3, 43.6, 43.7, together with dilated veins is encountered in intraconal 43.8, 43.9). For example, ring enhancement after gadolinium AVM.

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Intramedullary conus lipoma typically appears hyperintense on both T1WI and T2WI without post-gadolinium enhancement. Both epidermoid and dermoid cysts might appear similarly on T1/T2-weighted images and rarely demonstrate post-gadolinium enhancement around the cystic margins. However, dermoid cysts are usually well-defined lobulated masses that have low attenuation from fat density and the cystic lesion appears hyperintense on T1WI. In addition, the signal intensity of dermoids follows that of fat, not CSF. In addition, some epidermoid and dermoid cysts can demonstrate calcifications that appear hypointense on both T1WI and T2WI within the cysts; however, these calcifications are better seen on CT-scan. However, the two cystic lesions present with differences visible on diffusion-weighted imaging (DWI): epidermoid cysts typically have an elevated signal on DWI due to the presence of fat and epithelial keratin inside the cyst; whereas arachnoid cysts have unrestricted diffusion and a low signal in imaging Teratoma presents as a heterogeneous solid and cystic masse with high lipid contents (Fig. 43.3). The association with congenital abnormalities is not rare.

43.5 Treatment Options and Prognosis Management strategies vary considerably, depending primarily on the nature of the lesion. Several options might be offered including conservative measures, medical treatments, partial or radical resections, or just a biopsy. The aim of microsurgery for intraconal tumors is to achieve a maximal degree of resection combined with maximal preservation of the functional integrity of spinal cord tracts. Consequently, many surgeons recommend intraoperative electrophysiological monitoring of the lower limbs and sphincters to reduce surgical morbidity. The dura should be closed in a hermetic manner to avoid a postoperative CSF fistula, pseudomeningocele, and potential meningitis. Etiological treatment should be undertaken afterward whether the cause is benign, malignant, infectious, or inflammatory. Further associated lesions should always be considered. Complications are especially related to prolonged bed rest (e.g., thromboembolic disorders, pressure ulcers, osteoporosis, heterotopic ossification, pneumonia, spasticity, neuropathic pain, depression), nature of the causative lesion, origin of underlying disease, and sphincter disorders. The best predictors of outcome are initial neurological presentation, the timing of diagnosis, the rapidity of surgical decompression, and the nature of the lesion. Benign lesions and incomplete neurologic impairments tend to have better outcomes.

43  Conus Medullaris Lesions

Further Reading Akhaddar A, el Hassani MY, Ghadouane M, Hommadi A, Chakir N, Jiddane M, Boukhrissi N.  Dermoid cyst of the conus medullaris revealed by chronic urinary retention. Contribution of imaging. J Neuroradiol. 1999;26:132–6. Artner J, Leucht F, Schulz C, Cakir B.  Sciatica and incomplete paraplegia after spontaneous haematoma of the spinal cord due to a cumarine-induced coagulopathy: case report. Open Orthop J. 2012;6:189–93. https://doi.org/10.2174/18743250012060101 89. Asahar SF, Malek KA, Zohdi WNWM, Peter AB. Chronic back pain in a young female patient: a case of ependymoma originating from the conus medullaris. Korean J Fam Med. 2020;41:68–72. https://doi. org/10.4082/kjfm.18.0157. Canbay S, Hasturk AE, Markoc F, Caglar S. Schwannoma of the conus medullaris: a rare case. Chin J Cancer. 2011;30:867–70. https://doi. org/10.5732/cjc.011.10213. Candy N, Young A, Devadass A, Dean A, McMillen J, Trivedi R. Dual lumbar bronchogenic and arachnoid cyst presenting with sciatica and left foot drop. Acta Neurochir (Wien). 2017;159:2029–32. https://doi.org/10.1007/s00701-­017-­3284-­z. Chotmongkol V, Wanitpongpun C, Phuttharak W, Khamsai S. Intramedullary conus medullaris tuberculoma: a case report and review of the literature. Infect Dis Rep. 2021;13:82–8. https://doi. org/10.3390/idr13010010. D'Angiolillo JC, Patel NV, Hernandez RN, Hanft S. Bilateral lumbar radiculopathy secondary to myxopapillary ependymoma: a case report. J Chiropr Med. 2021;20:170–5. https://doi.org/10.1016/j. jcm.2022.01.004. Ebner FH, Roser F, Acioly MA, Schoeber W, Tatagiba M. Intramedullary lesions of the conus medullaris: differential diagnosis and surgical management. Neurosurg Rev. 2009;32:287–300; discussion 300-1. https://doi.org/10.1007/s10143-­008-­0173-­1. el-Banhawy A, Elwan O, Taher Y.  Bilharzial granuloma of the conus medullaris and cauda equina. Paraplegia. 1972;10:172–80. https:// doi.org/10.1038/sc.1972.29. Er U, Yigitkanli K, Simsek S, Adabag A, Bavbek M.  Spinal intradural extramedullary cavernous angioma: case report and review of the literature. Spinal Cord. 2007;45:632–6. https://doi.org/10.1038/ sj.sc.3101990. Fujisawa H, Igarashi S, Koyama T. Acute cauda equina syndrome secondary to lumbar disc herniation mimicking pure conus medullaris syndrome—case report. Neurol Med Chir (Tokyo). 1998;38:429– 31. https://doi.org/10.2176/nmc.38.429. Haddad R, Hentzen C, Le Breton F, Sheikh Ismael S, Amarenco G.  Lumbosacral radicular pain during micturition, defecation or orgasm. Eur J Pain. 2019;23:1091–7. https://doi.org/10.1002/ ejp.1372. Han IH, Kuh SU, Chin DK, Kim KS, Jin BH, Cho YE.  Surgical treatment of primary spinal tumors in the conus medullaris. J Korean Neurosurg Soc. 2008;44:72–7. https://doi.org/10.3340/ jkns.2008.44.2.72. Hayashi F, Sakai T, Sairyo K, Hirohashi N, Higashino K, Katoh S, et al. Intramedullary schwannoma with calcification of the epiconus. Spine J. 2009;9:e19–23. https://doi.org/10.1016/j.spinee.2008.11.006. Hsu KC, Li TY, Chu HY, Chen LC, Chang ST, Wu YT. Conus medullaris metastasis in breast cancer: report of a case and a review of the literature. Surg Today. 2013;43:910–4. https://doi.org/10.1007/ s00595-­012-­0289-­3. Inoue T.  Pure conus medullaris syndrome without lower extremity involvement caused by intradural disc herniation at L1/2: a case report. Spine Surg Relat Res. 2018;3:392–5. https://doi. org/10.22603/ssrr.2018-­0032.

Further Reading Kalsi P, Hassan MF, Scoones D, Bradey N, Tizzard S.  An unusual case of ectopic prostate tissue in an intradural lipoma of the conus medullaris. Br J Neurosurg. 2011;25:757–8. https://doi.org/10.3109 /02688697.2010.544792. Kim JT, Bahk JH, Sung J.  Influence of age and sex on the position of the conus medullaris and Tuffier's line in adults. Anesthesiology. 2003;99:1359–63. https://doi. org/10.1097/00000542-­200312000-­00018. Naito K, Yamagata T, Nagahama A, Kawahara S, Ohata K, Takami T. Surgical management of solitary nerve sheath tumors originating around the epiconus or conus medullaris: a retrospective case analysis based on neurological function. Neurosurg Rev. 2018;41:275– 83. https://doi.org/10.1007/s10143-­017-­0851-­y. Podnar S.  Epidemiology of cauda equina and conus medullaris lesions. Muscle Nerve. 2007;35:529–31. https://doi.org/10.1002/ mus.20696. Prasad GL, Divya S.  A comprehensive review of adult onset spinal teratomas: analysis of factors related to outcomes and recurrences. Eur Spine J. 2020;29:221–37. https://doi.org/10.1007/ s00586-­019-­06037-­7. Saiful Azli MN, Abd Rahman IG, Md Salzihan MS. Ancient schwannoma of the conus medullaris. Med J Malaysia. 2007;62:256–8.

607 Steinberg JA, Gonda DD, Muller K, Ciacci JD. Endometriosis of the conus medullaris causing cyclic radiculopathy. J Neurosurg Spine. 2014;21:799–804. https://doi.org/10.3171/2014.7.SPINE14117. Toda H, Okamoto T, Nishida N, Yuba Y, Iwasaki K. Idiopathic hematomyelia as a rare cause of epiconus syndrome. Clin Neurol Neurosurg. 2014;125:75–7. https://doi.org/10.1016/j.clineuro.2014.07.023. Toribatake Y, Baba H, Kawahara N, Mizuno K, Tomita K.  The epiconus syndrome presenting with radicular-type neurological features. Spinal Cord. 1997;35:163–70. https://doi.org/10.1038/ sj.sc.3100369. Tsuchiya A, Akiyama H, Hasegawa Y.  Spinal sarcoidosis presenting with epiconus syndrome. Intern Med. 2014;53:2529–32. https://doi. org/10.2169/internalmedicine.53.1685. Weng YC, Chin SC, Wu YY, Kuo HC.  Clinical, neuroimaging, and nerve conduction characteristics of spontaneous Conus Medullaris infarction. BMC Neurol. 2019;19:328. https://doi.org/10.1186/ s12883-­019-­1566-­1. Wong JJ, Dufton J, Mior SA.  Spontaneous conus medullaris infarction in a 79 year-old female with cardiovascular risk factors: a case report. J Can Chiropr Assoc. 2012;56:58–65.

Intraspinal Funicular Sciatica

44.1 Generalities and Relevance Sciatic pain can be the major presenting symptom in some patients with spinal cord compression or other myelopathies. This unusual neurologic pain is named funicular or cordonal sciatica. For some authors, this pain is a true “sciatica”, while for others it is only a referred pain known as “sciatica-like leg pain”. Whatever the denomination, this is a false localizing presentation which may lead to missed or delayed diagnosis as well as a possible risk of unnecessary lumbosacral spinal surgery particularly when: • The pain is the major symptom • There are no other neurologic symptoms (pain alone) • There is a coexisting lumbosacral degenerative lesion. According to Larner, a “false localizing sign” can be defined as a confusing clinical condition in which the anatomical situation of the lesion causing neurologic symptoms is distant or remote from the anatomical site predicted by neurologic examination. This referred pain is also known as tract pain, cordonal pain, or “Funicular Pain”. The concept of “False localizing sign” was first proposed by the English neurologist James Stansfield Collier (1870– 1935) in 1904. He observed an additional “false localizing sign” in 12.4% of cases (20 from 161) with intracranial tumors studied clinically and pathologically. According to the position of the causative lesion, false localizing signs can be caused by intraspinal, intracranial [c.f. Chap. 111 about Intracranial Funicular Sciatica], or other lesions. The exact pathophysiology of funicular pain due to spinal cord compression is poorly understood. Classically, the pain is attributed to two main mechanisms: (a) Irritation of the ascending spinothalamic tract (b) Interruption of the pathways of pain modulation

44

Furthermore, concomitant lower limb motor weakness may be caused by irritation of the descending corticospinal tract. Besides the mechanical injury mentioned above, chemical inflammatory factors have been involved. The neurologic lesions can be secondary to: • • • •

Direct neurologic tract compression Spinal cord hypoxia or ischemia Venous obstruction A combination of more than one of these three previous mechanisms.

Only a few cases of sciatica as a false localizing sign were reported in the literature, mainly in patients with cervical cord compression and less frequently with thoracic myelopathy. This rare phenomenon may present in pediatric and adult populations without distinct gender predilection.

44.2 Clinical Presentations Unlike radicular pain, funicular pain is continuous, not exacerbated by root stretching, diffuse/vague and poorly localized, non-dermatomal distribution, deep, contralateral to spinal cord compression, and not correlated with physical findings. However, the neurogenic pain is mostly bilateral. In some cases, the straight leg raising test result can be positive even without spinal root stretching. Increased deep tendon reflexes and possible Babinski sign or ankle clonus may have an important diagnosed value for spinal cord myelopathy than the lumbosacral radiculopathy. It is therefore very important that a detailed clinical examination is performed by a neurologist and/or neurosurgeon looking for possible ataxia, pyramidal syndrome, or decreased thermal sensitivity. To prevent wrong or delayed diagnosis in addition to correctly identifying the cause of the symptoms, some methods

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_44

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were successful such as cervical epidural blocks and electrophysiological procedures (spinal cord-evoked potentials, motor-evoked potentials, and somatosensory-evoked potentials).

44.3 Imaging Features Cases with no traditional lumbosacral radicular pattern should always alert to a possible cause of myelopathy at a higher spinal level. When suspected, neuroimaging investigations, especially magnetic resonance imaging, should be used for identifying a possible cause of sciatic pain at a higher level. MRI is now the primary imaging modality that may indicate the exact topography of the lesions, their exact margins,

a

and inner structures, as well as their relationships with adjacent structures. The majority of patients with sciatica as a false localizing sign may be associated with one of the following diseases: –– Tumors (intramedullary, intradural, or epidural) (Figs. 44.1, 44.2, 44.3, 44.4) –– Multiple sclerosis (Fig. 44.5) –– Spinal cord injury –– Spinal intradural hemorrhage –– Cervical spondylosis –– Cervical or thoracic disc herniation (Figs. 44.6, 44.7, 44.8) Spinal epidural blocks, as a diagnostic tool for funicular pain, may be useful by giving relief of sciatica-like leg pain.

b

d

c

e

Fig. 44.1  Case 1. T11-T12 epidural B cells lymphoma (Mucosa-­ 65-year-old man. Sagittal (a, b) and axial (c) post-gadolinium associated lymphoid tissue AKA MALT lymphoma) (arrows) manifest- T1-weighted MRI as well as sagittal (d) and axial (e) T2-weighted ing as bilateral sciatic pain without any other neurologic symptoms in a MRI. Note the extent of the spinal cord compression

44.3  Imaging Features

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Fig. 44.2  Case 1. Intraoperative view of the lymphoma (arrows) before (a) and after the surgical resection (b, c)

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44  Intraspinal Funicular Sciatica

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b

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d

Fig. 44.3  Case 1. Photomicrograph image showing histological and immunohistochemical features of extra-nodal marginal zone B cell lymphoma (MALT lymphoma). The tumor is composed of sheets of neoplastic small lymphocytes with irregular nuclear contours and inconspicuous nucleoli (centrocyte-like) (a) (Hematoxylin and eosin

stain HE x 200). Immunohistochemistry findings (×200): positivity for CD20 (b), positivity for Bcl2 (c), and positivity for ki-67 (Proliferation Index) estimated at 25% (d). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi.)

44.3  Imaging Features Fig. 44.4  Case 1. Postoperative MRI following radiotherapy and chemotherapy. Note the good spinal cord decompression as seen on sagittal T1- (a) and T2-weighted (b) MRI

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44  Intraspinal Funicular Sciatica

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Fig. 44.5  Case 2. Axial thoracic MRI (a–c) of a 32-year-old woman suffering from right lumbosciatica for two months. The first lumbosacral MRI was inconclusive. It was about multiple sclerosis (arrows). (Courtesy of Dr. Oussama Cherkaoui Rhazouani.)

44.3  Imaging Features

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Fig. 44.6  Case 3. This 48-year-old man had mild left-sided sciatica for some weeks without any neurologic or sphincter disturbances. Spinal MRI (a–c) with additional CT scan (d) showing a double calcified disc herniation on T9-T11 vertebral levels on the left side (arrows)

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44  Intraspinal Funicular Sciatica

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Fig. 44.7  Case 4. A 54-year-old woman with bilateral sciatic pain (predominantly on the right side). Spinal MRI (a, b) with a supplementary CT scan (c, d) showing a large ossified disc herniation (arrows) on T10-T11 vertebral level

44.4  Treatment Options and Prognosis

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Fig. 44.8  Case 4. Immediate postoperative CT scan (a–d) showing complete resection of the ossified disc lesion (a, c) (arrows). An additional short fusion surgery with rigid pedicle screw fixation was used via a posterior spinal approach (b, d)

44.4 Treatment Options and Prognosis Subsequent management is pathology-dependent. In all reported cases with sciatica caused by spinal cord compression, the leg pain resolved following spinal cord decompression.

Outcomes and prognosis are related to the causative lesions, coexisting symptoms, and potential underlying diseases. No case of recurrence has been described in the literature.

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Further Reading Alhardallo M, El Ansari W, Baco AM.  Second ever reported case of central cause of unilateral foot drop due to cervical disc herniation: case report and review of literature. Int J Surg Case Rep. 2021;83:105928. https://doi.org/10.1016/j.ijscr.2021.105928. Artner J, Leucht F, Schulz C, Cakir B. Sciatica and incomplete paraplegia after spontaneous haematoma of the spinal cord due to a cumarine—induced coagulopathy: case report. Open Orthop J. 2012;6:189–93. https://doi.org/10.2174/1874325001206010189. Chan CK, Lee HY, Choi WC, Cho JY, Lee SH. Cervical cord compression presenting with sciatica-like leg pain. Eur Spine J. 2011;20(Suppl 2):S217–21. https://doi.org/10.1007/s00586-­010-­1585-­5. Cho HL, Lee SH, Kim JS.  Thoracic disk herniation manifesting as sciatica-like pain--two case reports. Neurol Med Chir (Tokyo) 2011;51:67-71. doi: https://doi.org/10.2176/nmc.51.67. Collier J.  The false localizing signs of intracranial tumor. Brain. 1904;27:490–508. https://doi.org/10.1093/brain/27.4.490. Fujii K, Orisaka M, Yamamoto M, Nishijima K, Yoshida Y.  Primary intramedullary spinal cord tumour in pregnancy: a case report. Spinal Cord Ser Cases. 2018;4:25. https://doi.org/10.1038/ s41394-­018-­0059-­6. Giroud M, Guard O, Audry D, Soichot P, Dumas R. A unusual manifestation of multiple sclerosis: sciatica. Ann Med Interne (Paris). 1985;136:566–71. Golbakhsh M, Mottaghi A, Zarei M.  Lower thoracic disc herniation mimicking lower lumbar disk disease: a case report. Med J Islam Repub Iran. 2017;31:87. https://doi.org/10.14196/mjiri.31.87. Ito T, Homma T, Uchiyama S. Sciatica caused by cervical and thoracic spinal cord compression. Spine (Phila Pa 1976). 1999;24:1265–7. https://doi.org/10.1097/00007632-­199906150-­00017.

44  Intraspinal Funicular Sciatica Kato K, Yabuki S, Otani K, Nikaido T, Otoshi KI, Watanabe K, Kikuchi SI, Konno SI. Ossification of the ligamentum flavum in the thoracic spine mimicking sciatica in a young baseball pitcher:a case report. Fukushima J Med Sci. 2021;67:33–7. https://doi.org/10.5387/ fms.2020-­26. Kozaki T, Minamide A, Iwasaki H, Yuakawa Y, Ando M, Yamada H. Funicular pain: a case report of intermittent claudication induced by cervical cord compression. BMC Musculoskelet Disord. 2020;21:302. https://doi.org/10.1186/s12891-­020-­03299-­x. Langfitt TW, Elliott FA. Pain in the back and legs caused by cervical spinal cord compression. JAMA. 1967;200:382–5. Larner AJ.  False localising signs. J Neurol Neurosurg Psychiatry. 2003;74:415–8. https://doi.org/10.1136/jnnp.74.4.415. Park JM, Kim JH. False localizing sign caused by schwannoma in cervical spinal canal at C1-2 level: A case report. Medicine (Baltimore). 2018;97:e12215. https://doi.org/10.1097/MD.0000000000012215. Pinel B, Deshayes P, Sciatique cordonale. A propos de trois nouvelles observations [Funicular sciatica. Apropos of 3 new cases]. LARC Med. 1984;4:251. Scott M. Lower extremity pain simulating sciatica; tumors of the high thoracic and cervical cord as causes. J Am Med Assoc. 1956;160:528– 34. https://doi.org/10.1001/jama.1956.02960420008002. Seçer M, Ulutaş M. Tract pain because of cervical spondylotic myelopathy: a case series. J Clin Neurosci. 2021;92:75–7. https://doi. org/10.1016/j.jocn.2021.07.048. Westhout FD, Paré LS, Linskey ME. Central causes of foot drop: rare and underappreciated differential diagnoses. J Spinal Cord Med. 2007;30:62–6. https://doi.org/10.1080/10790268.2007.11753915.

Axial Spondyloarthritis (Spinal Ankylosing Spondylitis)

45.1 Generalities and Relevance Axial spondyloarthritis is a chronic auto-inflammatory rheumatic disease predominantly affecting the axial skeleton (mainly sacroiliac joints and spine) with a variable clinical presentation. The most common subtype of the axial spondyloarthritis disease group is ankylosing spondylitis (AKSP), also known as Marie-Strümpell disease or Bechterew disease. Other subtypes of spondyloarthritis include psoriasis arthritis, reactive arthritis (former Reiter syndrome), enteropathic arthritis, and  undifferentiated spondyloarthritis. In this chapter, we will focus only on AKSP, the most common subtype associated with lumbosacral radicular pain. The spine and the sacroiliac joints are the principal skeletal location involved in AKSP. The disease often begins in the lumbar spine and progresses rostrally. The spinal ligaments are replaced by bone, vertebral bodies become osteoporotic, and intervertebral discs become calcified; the whole giving an appearance of the so-called “bamboo spine”. Extraskeletal structures may also be involved in the disease including bowel, eye, cutaneous, cardiovascular, and pulmonary complications among others. In the late nineteenth century, the Russian neurophysiologist Vladimir Bekhterev  (1893), the German neurologic  Adolph Strümpell  (1897), and the French neurologist Pierre Marie (1898) were the first to provide sufficient descriptions of AKSP prior to severe spinal deformity. The underlying mechanism of AKSP is believed to be autoimmune or auto-inflammatory. The cause of this disease remains largely idiopathic, but HLA-B27 is the gene with the strongest association with AKSP. Overall, about 5% of people positive for HLA-B27 will develop AKSP. Unlike rheumatoid arthritis, antinuclear antibodies and serum rheumatoid factor are negative in AKSP. Sciatica related to AKSP may result from different mechanisms including: • Direct neural compression due to intraspinal expansion of the calcified and ossified ligaments

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• Osteoarthritis of posterior facet joints • Processes occurring independently of the disease such as discal displacement, lumbar spinal stenosis, and spondylolysis/spondylolisthesis • Further complications such as subluxation, vertebral compression fractures, postural anomalies (e.g., kyphosis and scoliosis), or spinal instability • Spinal epidural hematoma The disease develops progressively and patients often remain functionally active for a long time. The inflammatory process induces inflammation, then fibrosis, and finally ossification at sites of enthesitis (sites where tendons and ligaments attach to bones). In the vertebral column, spine stiffness and fragility predispose to frequent falls and vertebral fragility fractures with or without subluxations. AKSP has an incidence rate of 1 to 3 cases per 100.000 persons. The majority of patients are adult men between 30 and 40 years of age. Women are more expected than men to present inflammation rather than fusion.

45.2 Clinical Presentations Patients with AKSP may present with variable clinical presentation, including spinal, extraspinal, and extra-articular manifestations. A detailed medical history should be conducted to rule in/out any associated conditions. The majority of patients present with non-radiating chronic back pain inflammatory in nature. Typically, patients complain of morning stiffness mostly of the lower back with improvement on exercise, but not by inactivity. There is also night back pain with an improvement upon arising. Lumboradicular pain such as sciatica is unusual but may be confused with other leg pain related to sacroiliac joint involvement as well as knee or hip arthritis delaying the final diagnosis. The majority of patients with sciatic pain, ­paresthesia, and numbness develop insidious symptoms over many months before the diagnosis is made. However, patho-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_45

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logic fracture or subluxation cases tend to have more rapid gradual symptoms. The physical exam may show localized pain and tenderness, spinal stiffness and postural changes, spinal deformity or angulation, and decreased range of motion (or even immobility), with or without neurologic deficits. Bilateral lumbosacral radicular pain with or without neurogenic claudication is correlated to large involvement with bilateral extension. Cauda equina syndrome (CES) is rare and is often related to spinal stenosis or compressive lesion. Other neurological symptoms and clinical signs may be linked to occipito-­ cervical rotatory subluxation, basilar impression, compressive cervical/thoracic myelopathy, or acute spinal cord injury. Arthritis and enthesitis are the most common peripheral manifestations predominantly found in the lower limbs, especially buttock pain, hip pain, and calcaneal pain, habitually in an asymmetrical manner. The joints are generally swollen and painful. Furthermore, inflammatory bowel disease (e.g., ulcerative colitis, Crohn's disease), acute anterior uveitis, and psoriasis are the most frequent extraskeletal organs’ manifestation. More seriously, AKSP may be associated with pulmonary and cardiovascular complications.

45.3 Paraclinic Features Imaging of the spine is not usually required for early diagnosis of patients with AKSP because structural damage usually arises in the sacroiliac joints first (Fig. 45.1). On radiographic assessment, the earliest finding is sacroiliac joint involvement followed by osteoporosis and then sclerosis. Calcified and ossified spinal ligaments and intervertebral discs give the classic form of “bamboo spine” in

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45  Axial Spondyloarthritis (Spinal Ankylosing Spondylitis)

the late stage of the disease (Figs. 45.2 and 45.3). Because of potential multiple noncontiguous or asymptomatic spinal fractures, evaluation of the entire spine is recommended. In the absence of post-myelographic computed tomography (CT) scan, which is an invasive imaging technic, a combination of CT scan and magnetic resonance imaging (MRI) is a complementary tool for the diagnosis of spinal AKSP with neurologic manifestations as well as for planning surgical intervention. On CT scan, both anterior and posterior vertebral structures may be affected. Reconstruction CT scan on bone windows is important for determining the thickness, the form of the ossification, its extension, the degree of spinal canal stenosis as well as pathological fractures and subluxations (Figs. 45.4 and 45.5). Sometimes, in 10% of cases, there is an inflammatory involvement of the intervertebral disc corresponding to a noninfectious spondylodiscitis (AKA Anderson lesion). In the later stage of the disease, syndesmophyte formation and ankylosis develop (Fig. 45.3). Bamboo spine fracture is also known as “chalk stick”  or “carrot stick fractures” Electrophysiological studies help identify radicular lesions of the cauda equina, but are rarely used. On MRI, enhancement of the interspinous ligaments is indicative of enthesitis. Increased T2 signal correlates with edema or vascularized fibrous tissue. However, MRI remains the main method to assess neurological compromise. It reveals the intraspinal extension of the lesions and any potential compression of the nervous structures (Fig. 45.6). Bone scintigraphy may be helpful in selected patients for the evaluation of sacroiliac joint lesions (areas of increased uptake). In addition, inflammatory disorders (sacroiliitis) are better assessed on STIR sequence (short tau inversion recovery sequence) (Figs. 45.7 and 45.8).

b

Fig. 45.1  Bilateral Sacroiliitis in a 27-year-old man with ankylosing spondylosis as seen on axial (a) and coronal reconstruction (b) CT scan (arrows)

45.3  Paraclinic Features

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On neuroimaging, the diagnosis of AKSP is sometimes challenging and the disease may be confused with other possible lesions in the lumbosacral region such as: –– Rheumatoid arthritis –– Diffuse idiopathic skeletal hyperostosis (AKA Forestier’s disease) –– Posterior apophysis ring separation (Figs. 45.9 and 45.10) –– Primary or metastatic tumors –– Psoriatic spondylitis –– Large and extensive osteophytosis (advanced degenerative condition) –– Some congenital vertebral anomalies Biological markers in AKSP are generally nonspecific, but may help assist with diagnosis. About 50% to 75% of patients with the active disease have elevated erythrocyte sedimentation rate and elevated C-reactive protein. Fig. 45.2  Case 1. Anteroposterior pelvic plain radiography showing end-stage of sacroiliac joint ankylosis in a patient with ankylosing spondylosis. Note that both sacroiliac joints are not visible (arrows). (Courtesy of Pr. Redouane Niamane.) Fig. 45.3  The same case as in Fig. 45.2. Lateral (a) and anteropsterior (b) lumbosacral plain radiographs showing the classic form of “bamboo spine” in the late stage of the ankylosing spondylitis. Note the calcified and ossified spinal ligaments (AKA syndesmophyte formations) (arrows). (Courtesy of Pr. Redouane Niamane.)

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45  Axial Spondyloarthritis (Spinal Ankylosing Spondylitis)

b

c

d

Fig. 45.4  Ankylosing spondylitis with diffuse anterior (braces) and posterior (arrows) spinal ligamentous calcifications/ossifications as seen on sagittal (a, b) and axial (c, d) CT scan. Note the sclerosis and proliferation on the iliac side of the sacroiliac joints (stars) (d)

a

b

c

d

Fig. 45.5  Intervertebral disc calcifications in a 54-year-old man with ankylosing spondylosis (arrows). Sagittal lumbosacral CT scan on parenchymal (a) and bone windows (b) as well as on axial views (c, d)

45.3  Paraclinic Features

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c

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e

Fig. 45.6  The same case as in Fig. 45.4. Sagittal T1- (a) and T2-weighted MRI (b) as well as axial T2-weighted MRI (c–e) showing lumbar ankylosing spondylitis, epidural lipomatosis (arrows), spinal stenosis, and facet joint effusion

a

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Fig. 45.7  Sacroiliac joint disorders in a patient with lumbar ankylosing spondylitis as seen on axial (a) and coronal reconstruction (b) CT scan (arrows)

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45  Axial Spondyloarthritis (Spinal Ankylosing Spondylitis)

a

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Fig. 45.8  The same case as in Fig. 45.7. MRI disorders of the sacroiliac joints (arrows). Coronal (a) and axial MRI (b) on STIR sequences

a

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d

Fig. 45.9  Ring apophysis separation involving the posterior caudal endplate of the L4 vertebral body mimicking ankylosing spondylitis as seen on axial (a–d) and sagittal reconstruction CT scan (e). Note

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impingement of the bone fragment in the spinal canal (arrows) causing lumbar spinal stenosis

45.4  Treatment Options and Prognosis

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Fig. 45.10  The same case as in Fig. 45.9. Ring apophysis separation of the L4 vertebral body mimicking ankylosing spondylitis and causing lumbar spinal stenosis. Sagittal T1-(a) and T2-weighted MRI (b) as well as axial T2-weighted MRI (c, d) (arrows)

45.4 Treatment Options and Prognosis There is no cure for AKSP. However, some treatments and medications are used for symptomatic patients and for those with active signs. The goal of treatment is to relieve pain and stiffness, maintain axial spine motion and functional ability, prevent the progression of the disease, and avoid spinal complications. Nondrug procedures comprise regular exercise, postural training, and physical therapy program. Pain-relieving drugs are represented by daily nonsteroidal anti-inflammatory drugs (NSAIDs). Systemic glucocorticoids are not recommended, but local corticosteroid injections are sometimes considered. Medications used to treat the progression of the disease include: • Disease-modifying antirheumatic drugs (e.g., sulfasalazine and methotrexate)  • Tumor necrosis factor inhibitors (e.g., etanercept, infliximab, golimumab, adalimumab)  

• Anti-interleukin-6 inhibitors (e.g., tocilizumab and rituximab)  • Interleukin-17 inhibitors (e.g., secukinumab and ixekizumab)  • Janus kinase inhibitor (e.g., tofacitinib) All of these drugs have potentially serious side effects. Surgical indications for spinal involvement in AKSP comprise: • Neurologic deficit related to root(s) compression. • Spinal instability. • Undefined diagnosis. Surgical procedures are challenging due to both the rigidity of the spine and the concomitant osteoporosis. Different treatment strategies have been offered, including anterior, posterior, or combined anterior-posterior fixation, accompanying or not with various devices of external immobilization.

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Anesthesiologist and surgeons should be aware about some disorders that increase the risk of anesthesia complications in patients with AKSP including: –– –– –– ––

Difficult intubation due to cervical spine fragility Mitral or aortic valve problems Myocardial conduction disorders Reduced pulmonary compliance (restrictive pulmonary pattern) –– Difficult positioning for surgery If needed, a bilateral decompressive laminectomy may be needed in patients with CES, large extensive or bilateral lesion, and those with compressive fracture and subluxation. Care should be taken to minimize posterior facet joint damage and the possibility of CSF leak. Sometimes, an additional spinal fusion may be required if there is a potential preoperative instability and/or an iatrogenic instability because of the surgical procedure. The severe kyphotic deformity may be treated by spinal osteotomy, although this surgical procedure is considered dangerous. Rheumatologists may assist in a formal diagnosis, management, and monitoring, while dermatologists, ophthalmologists, gastroenterologists, and internal medicine specialists may support associated extraskeletal disorders of AKSP. Open spinal surgery in AKSP has some neurological improvement in about 80% of patients and post-surgery stabilization in 12% of the cases. However, in most patients with chronic and severe neurologic deficits, there is unchanged neurologic status. The prognosis for patients who are diagnosed and treated in the early phases of the disease is good. The majority of patients remain fully functional and able to work for a long time. Severe physical disability is uncommon. However, patients with severe and long-standing AKSP have poor outcomes and a great mortality rate, principally due to cardiovascular complications. Patient education in relation to spine fragility is important to avoid even minor trauma and to prevent spinal fractures.

Further Reading Akhaddar A, Moussa A.  Chalk-stick fracture. N Engl J Med. 2022;386:2507. https://doi.org/10.1056/NEJMicm2117454. Ahn NU, Ahn UM, Nallamshetty L, Springer BD, Buchowski JM, Funches L, et al. Cauda equina syndrome in ankylosing spondylitis (the CES-AS syndrome): meta-analysis of outcomes after medical and surgical treatments. J Spinal Disord. 2001;14:427–33. https:// doi.org/10.1097/00002517-­200110000-­00009.

45  Axial Spondyloarthritis (Spinal Ankylosing Spondylitis) Avrahami E, Wigler I, Stern D, Caspi D, Yaron M.  Computed tomographic demonstration of calcification of the ligamenta flava of the lumbosacral spine in ankylosing spondylitis. Ann Rheum Dis. 1988;47:62–4. https://doi.org/10.1136/ard.47.1.62. Caetano AP, Mascarenhas VV, Machado PM. Axial spondyloarthritis: mimics and pitfalls of imaging assessment. Front Med (Lausanne). 2021;8:658538. https://doi.org/10.3389/fmed.2021.658538. Deminger A, Klingberg E, Geijer M, Göthlin J, Hedberg M, Rehnberg E, et al. A five-year prospective study of spinal radiographic progression and its predictors in men and women with ankylosing spondylitis. Arthritis Res Ther. 2018;20:162. https://doi.org/10.1186/ s13075-­018-­1665-­1. Guo ZQ, Dang GD, Chen ZQ, Qi Q.  Treatment of spinal fractures complicating ankylosing spondylitis. Zhonghua Wai Ke Za Zhi. 2004;42:334–9. Ha SW, Son BC. Cauda equina syndrome associated with dural ectasia in chronic anlylosing spondylitis. J Korean Neurosurg Soc. 2014;56:517–20. https://doi.org/10.3340/jkns.2014.56.6.517. Hee HT, Thambiah J, Nather A, Wong HK.  A case report of neurologically unstable fracture of the lumbosacral spine in a patient with ankylosing spondylitis. Ann Acad Med Singap. 2002;31:115–8. Hudgins WR.  Ankylosing spondylitis and sciatica. J Neurosurg. 1978;48:668–9. https://doi.org/10.3171/jns.1978.48.4.0668a. Luken MG 3rd, Patel DV, Ellman MH.  Symptomatic spinal stenosis associated with ankylosing spondylitis. Neurosurgery. 1982;11:703– 5. https://doi.org/10.1227/00006123-­198211000-­00017. Markel DC, Graziano GP. Fracture of the S1 vertebral body in a patient with ankylosing spondylitis. J Spinal Disord. 1992;5:222–6. Mrabet D, Alaya Z, Mizouni H, Sahli H, Elleuch M, Chéour E, Mnif E, Meddeb N, Sellami S. Spine fracture in patient with ankylosing spondylitis: a case report. Ann Phys Rehabil Med. 2010;53:643–9. https://doi.org/10.1016/j.rehab.2010.09.008. Sapkas G, Kateros K, Papadakis SA, Galanakos S, Brilakis E, Machairas G, et  al. Surgical outcome after spinal fractures in patients with ankylosing spondylitis. BMC Musculoskelet Disord. 2009;10:96. https://doi.org/10.1186/1471-­2474-­10-­96. Secundini R, Scheines EJ, Gusis SE, Riopedre AM, Citera G, Maldonado Cocco JA.  Clinico-radiological correlation of enthesitis in seronegative spondyloarthropathies (SNSA). Clin Rheumatol. 1997;16:129–32. https://doi.org/10.1007/BF02247840. Sieper J, Poddubnyy D. Axial spondyloarthritis. Lancet. 2017;390:73– 84. https://doi.org/10.1016/S0140-­6736(16)31591-­4. Simkin PA, Downey DJ, Kilcoyne RF. Apophyseal arthritis limits lumbar motion in patients with ankylosing spondylitis. Arthritis Rheum. 1988;31:798–802. https://doi.org/10.1002/art.1780310617. Sudhakar PV, Kandwal P, Mch KA, Ifthekar S, Mittal S, Sarkar B. Management of Andersson lesions of spine: a systematic review of the existing literature. J Clin Orthop Trauma. 2022;29:101878. https://doi.org/10.1016/j.jcot.2022.101878. Tang C, Moser FG, Reveille J, Bruckel J, Weisman MH. Cauda equina syndrome in ankylosing spondylitis: challenges in diagnosis, management, and pathogenesis. J Rheumatol. 2019;46:1582–8. https:// doi.org/10.3899/jrheum.181259. Tüzün C, Peker O, Küçüktaş F, Gülbahar S, Kovanlikaya I, Füzün S. An atypical psoriatic spondylitis case, successfully treated with methotrexate. Clin Rheumatol. 1996;15:403–9. https://doi.org/10.1007/ BF02230367. Wang YF, Teng MM, Chang CY, Wu HT, Wang ST. Imaging manifestations of spinal fractures in ankylosing spondylitis. AJNR Am J Neuroradiol. 2005;26:2067–76.

Spinal Pigmented Villonodular Synovitis

46.1 Generalities and Relevance Pigmented villonodular synovitis (PVNS) is a rare proliferative disorder characterized by villous and nodular overgrowths of the synovial joints of either a tendon sheath or a joint. Most cases are monoarticular which interest peripheral joints of the lower extremities. It is a well-recognized entity that has the potential for focal destruction. The etiology of PVNS remains controversial, but degenerative change, trauma, inflammation, metabolic derangement, and even neoplasms have been suspected. The first description of the condition was by Chassaignac in 1852 who had described a nodular lesion of the synovial membrane of the flexor tendons of the fingers. Furthermore, the term “pigmented villonodular synovitis” was first proposed by Jaffe and his colleagues in 1949. PVNS affects only rarely the axial skeleton, where it develops particularly in the vertebral articular facet joint. In 1980, Kleinman reported the first case of spinal PVNS. Within the spine, lumbar localizations are the less affected (about 30% of cases). Fewer than 30 cases of patients with PVNS have been reported in the lumbar spine. The histological findings of spinal PVNS are similar to those seen in lesions of the appendicular skeleton consistent with reactive hyperplasia and neoplastic overgrowth of the synovium. The estimated incidence of PVNS is about 1.8 cases per million with the vast majority affecting the knee and hip. On the spine, PVNS occurs equally in both sexes, most commonly in adults of varying ages.

46.2 Clinical Presentations When the lumbosacral spine is involved in PVNS, the majority of clinical features are nonspecific. Most patients present posterior chronic localized pain related to the facet joint invasion.

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Lumbosacral radiculopathies are present in about half of the cases because of the mass effect of the lesion. The majority of patients develop insidious symptoms over many weeks or months before the diagnosis is made. Sciatic pain can be associated or not with neurologic deficits. These symptoms are often unilateral and related to compression or even an invasion of the intracanalar nervous elements. Bilateral lumbosacral radicular pain with or without neurogenic claudication is correlated to the large lesion with bilateral extension; however, complete cauda equina syndrome and spinal deformity are rare. In the majority of cases, the general condition remains preserved without other concomitant symptoms related to supplementary peripheral joint involvement.

46.3 Paraclinic Features Pigmented villonodular synovitis can be identified on plain radiography, but the diagnosis is often missed because of the small size of the radiotransparent lesions as well as bone density and joint space are preserved until the late stages of the disease. There is no calcification. Computed tomography scan usually shows hyperdense enhancing soft-tissue mass eroding the posterior facet joint and sometimes the posterior vertebral body. Nodular irregularities can be seen with mass extension into the spinal canal inducing radicular compression. Concomitant joint effusion is common. Most patients have only one vertebral level involved. The key imaging investigation for the diagnosis of spinal PVNS is magnetic resonance imaging (MRI). It characteristically shows a mixed signal of the mass lesion on T2-weighted images, related to bleeding and hemosiderin deposition. MRI is also helpful to reveal the extent of the lesion and any potential compression of the nervous structures. Continuity between the mass lesion and the posterior facet joint can help with the correct diagnosis (Figs. 46.1 and 46.2).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_46

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Fig. 46.1  Sagittal MRI showed the compression of the dural tube due to an extradural mass at the L4 level. Left: The mass lesion showed mixed high and isointensity on T1-weighted imaging. Right: The mass lesion showed mixed high and low intensity on T2-weighted imaging.

(Reproduced from Oe K, Sasai K, Yoshida Y, Ohnari H, Iida H, Sakaida N, Uemura Y.  Pigmented villonodular synovitis originating from the lumbar facet joint: a case report. Eur Spine J. 2007;16 Suppl 3:301–5. doi: 10.1007/s00586-007-0403-1.; with permission)

On neuroimaging, the diagnosis is challenging, and pigmented villonodular synovitis may be confused with other possible lesions in the lumbosacral region such as:

–– –– –– ––

–– –– –– –– –– –– ––

Aneurysmal bone cyst Osteoblastoma Giant cell tumor Hemangiopericytoma Synovial cyst Schwannoma Metastatic carcinoma

Lymphomas Fibrohistiocytic tumor Hypertrophic synovitis Chordoma

Most often, the definitive diagnosis of PVNS is only made with a histopathological study. The lesion is characterized by the massive proliferation of synovial cells. There is a tissue infiltration of lymphocytes and lipid or hemosiderin-laden histiocytes. In addition, giant cells are seen interposed with areas of bleeding.

Further Reading

Fig. 46.2  The mass compressed the dural tube and was continuous with the left L4–5 facet joint. Left: The mass displayed rim enhancement with Gd on T1-weighted imaging. Right: The mass lesion invaded the lamina. (Reproduced from Oe K, Sasai K, Yoshida Y, Ohnari H, Iida

46.4 Treatment Options and Prognosis Sciatic pain secondary to lumbar spinal PVNS can be managed conservatively including pharmacologic treatment, physiotherapy, and other physical modalities resulting in more or less control of the patient’s pain. However, the aim of the treatment is the total surgical removal of the mass lesion and the synovium with functional spinal and neurologic preservation. Rheumatological expertise could be requested during the management of these patients. If needed, an extensive bilateral laminectomy may be needed in patients with a large extensive, or bilateral lesion. Care should be taken to minimize posterior facet joint damage and the possibility of CSF leak. Most often, diagnosis is made postoperatively after anatomopathological study. An additional spinal fusion may sometimes be required if there is a potential preoperative instability and/or an iatrogenic instability because of the surgical procedure.

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H, Sakaida N, Uemura Y. Pigmented villonodular synovitis originating from the lumbar facet joint: a case report. Eur Spine J. 2007;16 Suppl 3:301–5. doi: 10.1007/s00586-007-0403-1.; with permission)

A total removal should be achieved during the first operation to prevent the recurrence. However, total extirpation of these tumors is often difficult with local recurrence rates reaching up to 50% for all spinal sites when surgical resection is incomplete. Repeat (additional) surgical excision for recurrent spinal lesions appears to be curative. The role of radiotherapy remains unclear. Almost all cases presented with lumbar radicular pain were operated on because of the compressive lesion. However, the majority of patients had postoperative satisfactory results.

Further Reading Aboulafia AJ, Kaplan L, Jelinek J, Benevenia J, Monson DK.  Neuropathy secondary to pigmented villonodular synovitis of the hip. Clin Orthop Relat Res. 1996;325:174–80. https://doi. org/10.1097/00003086-­199604000-­00020.

630 Campbell AJ, Wells IP. Pigmented villonodular synovitis of a lumbar vertebral facet joint. J Bone Jt Surg Am. 1982;64:145–6. Dimeco F, Rizzo P, Li KW, Ciceri E, Casali C, Pollo B, Lasio G. Pigment villonodular synovitis of the spine. Case report and review of the literature. J Neurosurg Sci. 2001;45:216–9. Gader G, Belaïd A, Zehani A, Daghfous A, Zammel I, Badri M. Villonodular synovitis of the lumbar spine: case report of a rare pathology. Clin Case Rep. 2020;8:2346–9. https://doi.org/10.1002/ ccr3.3107. Giannini C, Scheithauer BW, Wenger DE, Unni KK. Pigmented villonodular synovitis of the spine: a clinical, radiological, and morphological study of 12 cases. J Neurosurg. 1996;84:592–7. https://doi. org/10.3171/jns.1996.84.4.0592. Khoury GM, Shimkin PM, Kleinman GM, Mastroianni PP, Nijensohn DE.  Computed tomography and magnetic resonance imaging findings of pigmented villonodular synovitis of the spine. Spine (Phila Pa 1976). 1991;16:1236–7. https://doi. org/10.1097/00007632-­199110000-­00018. Kleinman GM, Dagi TF, Poletti CE. Villonodular synovitis in the spinal canal: case report. J Neurosurg. 1980;52:846–8. https://doi. org/10.3171/jns.1980.52.6.0846. Motamedi K, Murphey MD, Fetsch JF, Furlong MA, Vinh TN, Laskin WB, et al. Villonodular synovitis (PVNS) of the spine. Skelet Radiol. 2005;34:185–95. https://doi.org/10.1007/s00256-­004-­0880-­9. Müslüman AM, Cavuşoğlu H, Yilmaz A, Dalkiliç T, Tanik C, Aydin Y.  Pigmented villonodular synovitis of a lumbar intervertebral facet joint. Spine J. 2009;9:e6–9. https://doi.org/10.1016/j. spinee.2008.12.010. Oda Y, Takahira T, Yokoyama R, Tsuneyoshi M.  Diffuse-type giant cell tumor/pigmented villonodular synovitis arising in the sacrum: malignant form. Pathol Int. 2007;57:627–31. https://doi. org/10.1111/j.1440-­1827.2007.02150.x. Oe K, Sasai K, Yoshida Y, Ohnari H, Iida H, Sakaida N, et al. Pigmented villonodular synovitis originating from the lumbar facet joint: a case report. Eur Spine J. 2007;16(Suppl 3):301–5. https://doi. org/10.1007/s00586-­007-­0403-­1.

46  Spinal Pigmented Villonodular Synovitis Oh SW, Lee MH, Eoh W. Pigmented villonodular synovitis on lumbar spine: a case report and literature review. J Korean Neurosurg Soc. 2014;56:272–7. https://doi.org/10.3340/jkns.2014.56.3.272. Orhan Z, Oktas B, Yildirim U.  An unusual presentation of peroneal neuropathy secondary to pigmented villonodular synovitis: a case report. Knee Surg Sports Traumatol Arthrosc. 2009;17:518–20. https://doi.org/10.1007/s00167-­009-­0720-­5. Pulitzer DR, Reed RJ. Localized pigmented villonodular synovitis of the vertebral column. Arch Pathol Lab Med. 1984;108:228–30. Retrum ER, Schmidlin TM, Taylor WK, Pepe RG.  CT myelography of extradural pigmented villonodular synovitis. AJNR Am J Neuroradiol. 1987;8:727–9. Rovner J, Yaghoobian A, Gott M, Tindel N.  Pigmented villonodular synovitis of the zygoapophyseal joint: a case report. Spine (Phila Pa 1976). 2008;33:E656–8. https://doi.org/10.1097/ BRS.0b013e31817eb85a. Sampathkumar K, Rajasekhar C, Robson MJ.  Pigmented villonodular synovitis of lumbar facet joint: a rare cause of nerve root entrapment. Spine (Phila Pa 1976). 2001;26:E213–5. https://doi. org/10.1097/00007632-­200105150-­00022. Savitz MH, Katz SS, Goldstein H, Worcester D. Hypertrophic synovitis of the lumbar facet joint in two cases of herniated intervertebral disc. Mt Sinai J Med. 1982;49:434–7. Titelbaum DS, Rhodes CH, Brooks JS, Goldberg HI. Pigmented villonodular synovitis of a lumbar facet joint. AJNR Am J Neuroradiol. 1992;13:164–6. Weidner N, Challa VR, Bonsib SM, Davis CH Jr, Carrol TJ Jr. Giant cell tumors of synovium (pigmented villonodular synovitis) involving the vertebral column. Cancer. 1986;57:2030–6. https://doi. org/10.1002/1097-­0142(19860515)57:103.0.co;2-­c. Yener U, Konya D, Bozkurt S, Ozgen S.  Pigmented villonodular synovitis of the spine: report of a lumbar case. Turk Neurosurg. 2010;20:251–6. https://doi.org/10.5137/1019-­5149.JTN.1590-­08.3.

Spinal Paget’s Disease and Sciatica

47.1 Generalities and Relevance Paget’s disease of the bone (AKA osteitis deformans) is a chronic skeletal growth disorder characterized by excessive abnormal bone remodeling. The etiology is not entirely known, but it is a disease of osteoclasts. Both genetic and acquired factors (mainly viral agents) have been suggested to be involved. The affected bone (one or multiple) is less compact, mechanically weaker, highly vascularized, and more susceptible to fracture and adjacent arthritis. The disease can affect nearly every bone in the skeleton, but has an affinity for the pelvis (70%), spine (50%), skull, tibia, and femur. Malignant transformation (mainly sarcomas) is rare (1% of cases) but life-threatening due to the possibility of systemic metastases. The disease was first described by the English surgeon James Paget in 1877. Paget told of five patients with “a rare disease of bones” which presented with slowly progressive bone deformities called “osteitis deformans”. More than 70% of patients with Paget’s disease are asymptomatic and discovered incidentally. In the lumbar spine, the usual site of spinal affectation, the majority of symptomatic patients present with low back pain, vertebral fractures, compressive syndromes, or lumbosacral radicular pain. Sciatica related to Paget’s disease may result from different mechanisms including: • Direct neural compression due to intraspinal expansion of woven bone and osteoid tissue • Pagetic extension into epidural fat and ligamentum flavum • Osteoarthritis of posterior facet joints • Processes occurring independently of the disease such as discal displacement, lumbar spinal stenosis, and spondylolysis/spondylolisthesis • Further complications such as vertebral compression fractures, malignant sarcomatous transformation, postural anomalies (e.g., scoliosis), or spinal instability

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• Neurovascular involvement by compression of intraspinal blood vessels or pagetic vascular steal • Spinal epidural hematoma • Spinal epidural lipomatosis • Peripheral neuropathy due to sciatic nerve entrapment (very rare) Besides sciatic radiculopathy, other neurological manifestations can occur in Paget’s disease such as cervical or thoracic spinal cord compression, skull involvement with compression of cranial nerves (mainly vestibule-cochlear nerve), or vascular ischemic myelopathy secondary to spinal artery steal syndrome. Paget’s disease affects about 3% of the population; this condition is more common in people of United Kingdom origin and is less common in Asia and Africa. The majority of patients are adult men older than 55 years. A family history of the disease is possible and found in about 20% of cases. The histological findings of Paget’s disease involve the osseous architecture and include 3 phases of the disease: osteolytic, mixed, and osteosclerotic. At the advanced stage of the disease, there is excessive bone formation which is fibrous and coarse. The marrow space is filled with vascularized fibrous tissue. However, the new bone does not have centralized blood vessels or classic Haversian systems.

47.2 Clinical Presentations When the lumbosacral spine is involved in Paget’s disease, the majority of clinical features are nonspecific. Most patients present mechanical low back pain with or without lumbosacral radicular pain. The majority of patients with sciatic pain, paresthesia, and numbness develop insidious symptoms over many months before the diagnosis is made. However, cases with pathologic fractures (even mild injuries) or those with malignant degeneration tend to have more rapid gradual symptoms.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_47

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The physical exam may show localized pain and tenderness, spinal deformity or angulation, and decreased range of motion, with or without neurologic deficits. Bilateral lumbosacral radicular pain with or without neurogenic claudication is correlated to a large lesion with bilateral extension; however, complete cauda equina syndrome is rare. Paget’s disease-related sciatica should be distinguished from other leg pain related to tibial or femoral involvement as well as knee or hip arthritis, so diagnosis may be delayed. Advanced Paget’s disease may lead to other concomitant neurologic and extraspinal medical conditions including symptoms related to compressive or vascular myelopathy, headaches, cranial nerve neuropathies (e.g., hearing loss), proximal long bones deformities, kidney stones, heart failure, and chronic dental problems.

47.3 Paraclinic Features Imaging appearance depends upon the phase of the disease. However, on plain X-rays spine frequently manifests with cortical thickening, bone expansion, and sclerosis encasing the vertebral margins (AKA “picture frame sign”). More diffuse sclerosis of the vertebral body gives the appearance of an “ivory vertebra”. Involvement of the spine may affect one or multiple vertebral levels or even all lumbar vertebral segments. The posterior neural arch may also be affected. About 10% of patients with lumbar spinal involvement have intradiscal invasion from the adjacent vertebral body. This last condition is called “pagetic vertebral ankylosis” and may be associated with spinal ligamentous ossification. Furthermore, on lateral radiographs, flattening of the normal concavity of the anterior margin of the vertebral body also adds to the rectangular appearance. Computed tomography (CT) scan features are more helpful in identifying vertebral lesions such as pathological fractures, facet joint arthropathies, spondylolysis/ spondylolisthesis, intervertebral disc involvement, lumbar spinal stenosis, ligament ossifications, coarse trabeculations, and sarcomatous degeneration (Fig. 47.1).

47  Spinal Paget’s Disease and Sciatica

Bone scintigraphy is highly sensitive but not specific to the disease. It is useful to define the overall extent and distribution of bony lesions. On magnetic resonance imaging (MRI), the overall signal characteristics are variable, likely reflecting the natural course of the disease process in different phases. However, fatty marrow signal is typically preserved in all sequences unless there is a complication. MRI remains the main method to assess neurological compromise. It reveals the intraspinal extension of the lesions and any potential compression of the nervous structures (Fig. 47.1). On neuroimaging, the diagnosis is sometimes challenging and Paget’s disease may be confused with other possible lesions in the lumbosacral region such as: –– Vertebral hemangioma –– Large and extensive osteophytosis (advanced degenerative condition) –– Primary or metastatic tumors –– Osteopetrosis (marble bone) –– Osteomalacia –– Renal osteodystrophy –– Hyperparathyroidism –– Focal fatty marrow –– Spondylodiscitis Sometimes, the definitive diagnosis of Paget’s disease is only made with a histopathological study. Many cases will remain asymptomatic and the disease will be found only incidentally on imaging during medical evaluation for another problem. Biological markers often found: –– Elevation of serum alkaline phosphatase –– Normal serum calcium and phosphate –– Elevation of urine hydroxyproline –– Hyperuricemia –– Secondary hyperparathyroidism (in about 10% of patients)

47.3  Paraclinic Features

Fig. 47.1  CT scan images (1-sagittal; 2-transverse): biconcave deformity of the vertebral endplates; enlargement of the vertebral body with multiple sclerotic foci of compact bone; MRI (T2; 3-sagittal; 4-­transverse): spinal canal stenosis with subtotal stenosis at L3/L4 and L4/L5 affecting both nerve roots of L3 and L4. (Reproduced from

633

Hofmann A, Opitz S, Heyde CE, von der Höh NH. Paget’s disease of the lumbar spine: decompressive surgery following 17 years of bisphosphonate treatment. Eur Spine J. 2018;27:3066–70. doi: 10.1007/ s00586-018-5751-5.; with permission)

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47.4 Treatment Options and Prognosis There is no cure for Paget’s disease. However, some medications are used for symptomatic patients and for those with active signs. The goal of treatment is to relieve bone pain and prevent the progression of the disease and some complications. Additionally, medical therapy helps to avoid excessive bleeding prior to surgery. Some of the more used medications include: • Bisphosphonates for bone remodeling (e.g. risedronic acid, alendronic acid, pamidronic acid, and etidronic acid). • Calcitonin derivatives for bone absorption (e.g., salcatonin, miacalcin). • Calcium and vitamin D supplementation provides some symptomatic benefit. • Classic analgesics and nonsteroid anti-inflammatory drugs for pain management. In addition, adequate sunshine exposure and physical exercise are important in maintaining skeletal health, avoiding weight gain and stress, and preserving joint mobility. For some authors, medications can improve some neurologic deficits in up to 50% of cases, but need over 6 months of treatment before any improvement. Conservative treatment of fractures requires a long duration due to delayed consolidation. The majority of neurologic symptoms, even those that are moderately severe, can be treated with medication and do not need spinal surgery as a first-line method. Surgical indications for spinal involvement in Paget’s disease comprise: • Rapid progression of the lesions • Possible malignant change • Spinal instability • Undefined diagnosis • No improvement following medication and conservative measures Different treatment strategies have been offered, including anterior, posterior, or combined anterior–posterior fixation, accompanying or not with various devices of external immobilization. Some surgical considerations should be underlined such as profuse bleeding, postoperative medications to prevent recurrences, and the possibility of occurrence of osteogenic sarcoma. If needed, a bilateral decompressive laminectomy may be needed in patients with cauda equina syndrome, large extensive or bilateral lesions, and those with compressive frac-

47  Spinal Paget’s Disease and Sciatica

tures. Care should be taken to minimize posterior facet joint damage and the possibility of CSF leak. An additional spinal fusion may sometimes be required if there is a potential preoperative instability and/or an iatrogenic instability because of the surgical procedure. In some cases, vertebroplasty via percutaneous bilateral transpedicular approach was performed with clinical improvement. Open spinal surgery for Paget’s disease has some improvement in up to 85% of patients. However, in more than 25% of cases, there is a persistence of neurologic deficits. About 10% of operated patients may need reoperation. The overall postoperative mortality rate is about 11%. Postoperative pain may require further medical therapy. The prognosis for patients who are treated is good, especially if the disease is in its early phases. Some complications are rather related to the patient’s fragile condition. Patients with sarcomatous degeneration have a very high mortality rate.

Further Reading Caetano AP, Mascarenhas VV, Machado PM. Axial spondyloarthritis: mimics and pitfalls of imaging assessment. Front Med (Lausanne). 2021;8:658538. https://doi.org/10.3389/fmed.2021.658538. Carvalho AD, Ibiapina JO, Santos LG, Carvalho TC, Ribeiro MB.  Monostotic Paget’s disease in lumbar vertebrae: an atypical location. Rev Bras Ortop. 2015;45:200–2. https://doi.org/10.1016/ S2255-­4971(15)30294-­9. Chen JR, Rhee RS, Wallach S, Avramides A, Flores A.  Neurologic disturbances in Paget disease of bone: response to calcitonin. Neurology. 1979;29:448–57. https://doi.org/10.1212/wnl.29.4.448. Chrisman OD, Snook GA, Walker HR. Paget’s disease as differential diagnosis in sciatica. Clin Orthop Relat Res. 1964;37:154–9. Davis DP, Bruffey JD, Rosen P.  Coccygeal fracture and Paget’s disease presenting as acute cauda equina syndrome. J Emerg Med. 1999;17:251–4. https://doi.org/10.1016/s0736-­4679(98)00163-­2. Dell'Atti C, Cassar-Pullicino VN, Lalam RK, Tins BJ, Tyrrell PN. The spine in Paget’s disease. Skelet Radiol. 2007;36:609–26. https://doi. org/10.1007/s00256-­006-­0270-­6. Dinneen SF, Buckley TF.  Spinal nerve root compression due to monostotic Paget’s disease of a lumbar vertebra. Spine (Phila Pa 1976). 1987;12:948–50. https://doi. org/10.1097/00007632-­198711000-­00021. Hadgaonkar S, Patwardhan S, Bhilare P, Sancheti P, Shyam A. A polyostotic Paget’s disease involving lumbar spine presenting with cauda equina syndrome: an unusual entity. J Orthop Case Rep. 2021;11:1–5. https://doi.org/10.13107/jocr.2021.v11.i10.2440. Hadjipavlou A, Shaffer N, Lander P, Srolovitz H.  Pagetic spinal stenosis with extradural pagetoid ossification. A case report. Spine (Phila Pa 1976). 1988;13:128–30. https://doi. org/10.1097/00007632-­198801000-­00034. Hadjipavlou AG, Gaitanis LN, Katonis PG, Lander P. Paget’s disease of the spine and its management. Eur Spine J. 2001;10:370–84. https:// doi.org/10.1007/s005860100329. Hofmann A, Opitz S, Heyde CE, von der Höh NH. Paget’s disease of the lumbar spine: decompressive surgery following 17 years of bisphosphonate treatment. Eur Spine J. 2018;27:3066–70. https:// doi.org/10.1007/s00586-­018-­5751-­5.

Further Reading Jorge-Mora A, Amhaz-Escanlar S, Lois-Iglesias A, Leborans-Eiris S, Pino-Minguez J.  Surgical treatment in spine Paget’s disease: a systematic review. Eur J Orthop Surg Traumatol. 2016;26:27–30. https://doi.org/10.1007/s00590-­015-­1659-­5. Karaoğlan A, Akdemir O, Erdoğan H, Colak A.  A rare emergency condition in neurosurgery: foot drop due to Paget’s disease. Turk Neurosurg. 2009;19:208–10. Kremer MA, Fruin A, Larson TC 3rd, Roll J, Weil RJ. Vertebroplasty in focal Paget disease of the spine. Case report. J Neurosurg. 2003;99:110–3. https://doi.org/10.3171/spi.2003.99.1.0110. Llorente MJ, Corts JR, Olmedo FJ, Laguia M.  Spinal nerve root compression as onset of monostotic Paget’s disease. Computed tomography and magnetic resonance image findings. Br J Rheumatol. 1994;33:1194–5. https://doi.org/10.1093/ rheumatology/33.12.1194. Misaki M, Hasegawa O, Takeuchi T. Paget’s disease of bone presenting with peripheral neuropathy. Intern Med. 2018;57:1177–8. https:// doi.org/10.2169/internalmedicine.9757-­17. Mischis-Troussard C, Maillefert JF, Baulot E, Ramon JF, Tavernier C.  Osteosarcoma of the sacrum complicating Paget’s disease of bone. Rev Rhum Engl Ed. 1998;65:361–2. Morales H.  MR imaging findings of Paget’s disease of the spine. Clin Neuroradiol. 2015;25:225–32. https://doi.org/10.1007/ s00062-­015-­0376-­0. Paget J.  On a form of chronic inflammation of bones (osteitis deformans). Med Chir Trans. 1877;60:37–64.9. https://doi. org/10.1177/095952877706000105. Poncelet A.  The neurologic complications of Paget’s disease. J Bone Miner Res. 1999;14(Suppl 2):88–91. https://doi.org/10.1002/ jbmr.5650140218.

635 Rolvien T, Butscheidt S, Zustin J, Amling M.  Skeletal dissemination in Paget’s disease of the spine. Eur Spine J. 2018;27:453–7. https:// doi.org/10.1007/s00586-­018-­5477-­4. Rosen MA, Matasar KW, Irwin RB, Rosenberg BF, Herkowitz HN. Osteolytic monostotic Paget’s disease of the fifth lumbar vertebra. A case report. Clin Orthop Relat Res. 1991;262:119–23. Rubin DJ, Levin RM.  Neurologic complications of Paget disease of bone. Endocr Pract. 2009;15:158–66. https://doi.org/10.4158/ EP.15.2.158. Sadar ES, Walton RJ, Gossman HH.  Neurological dysfunction in Paget’s disease of the vertebral column. J Neurosurg. 1972;37:661– 5. https://doi.org/10.3171/jns.1972.37.6.0661. Saifuddin A, Hassan A.  Paget’s disease of the spine: unusual features and complications. Clin Radiol. 2003;58:102–11. https://doi. org/10.1053/crad.2002.1152. Scottish Bone Tumor Registry, Sharma H, Mehdi SA, MacDuff E, Reece AT, Jane MJ, Reid R.  Paget sarcoma of the spine: Scottish Bone Tumor Registry experience. Spine (Phila Pa 1976). 2006;31:1344– 50. https://doi.org/10.1097/01.brs.0000218506.72608.49. Senthil V, Balaji S. Monostotic Paget disease of the lumbar vertebrae: a pathological mimicker. Neurospine. 2018;15:182–6. https://doi. org/10.14245/ns.1834922.461. Steinbach LS, Johnston JO. Case report 777. Osteolytic Paget’s disease of the fifth lumbar vertebra. Skelet Radiol. 1993;22:203–5. https:// doi.org/10.1007/BF00206156. Weisz GM.  Lumbar spinal canal stenosis in Paget’s disease. Spine (Phila Pa 1976). 1983;8:192–8. https://doi. org/10.1097/00007632-­198303000-­00011. Wu LC, Tseng CH, Chiang YF, Tsuang YH.  Monostotic vertebral Paget’s disease of the lumbar spine. J Chin Med Assoc. 2009;72:52– 5. https://doi.org/10.1016/S1726-­4901(09)70022-­X.

Spinal Rheumatoid Arthritis

48.1 Generalities and Relevance Rheumatoid arthritis (RA) is a long-term autoimmune inflammatory disorder that primarily affects peripheral joints such as those in the hands, knees, hips, and feet. This disease mainly leads to erosion and joint damage. Spinal involvement is uncommon in RA and had a predilection for the cervical level. Some patients may present low back pain and sciatic radicular pain when the lumbosacral column is affected. Unlike cervical spine lesions (involving 40–80% of patients with RA), lumbar spine abnormalities have been often overlooked in patients with RA, although the early description of distinctive radiological characteristics of lumbar spine lesions in patients with RA was first reported by Lawrence et al. (1964). In the lower lumbar spine, rheumatoid arthritis mainly affects the facet joints and vertebral endplates. Less frequently, other spinal structures may be involved such as vertebral bodies, neural arch ligaments, neural foramen, and even the epidural space (extradural rheumatoid nodules). There is also a higher incidence of osteoporosis and osteopenia in RA patients compared with non-RA patients. Erosive features are more pronounced in RA while proliferative features are less frequent. When the spine is involved in RA, spinal synovitis probably starts in facet joints with the erosion of cartilage and subchondral bone (in the same manner as seen in classic peripheral joints) causing intervertebral instability. Sciatica related to RA may result from various mechanisms including: • The underlying disease such as inflammation/erosion of the posterior facet joints and vertebral endplates, synovial cysts, extradural rheumatoid nodules, and peripheral neuropathies • Therapeutic adverse events: steroid-induced vertebral compression fractures, ischemic necrosis of the vertebral

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bodies, or peripheral neuropathy associated with antitumor necrosis factor agents • Processes occurring independently of rheumatoid arthritis such as discal displacement and lumbar spinal stenosis • Further complications such as vertebral compression fractures, spondylolisthesis, postural anomalies (e.g., scoliosis), and spinal instability (e.g., olisthesis) In about 30% of patients with RA, the disease affects other possible “extra-articular” organ systems causing systemic symptoms. Besides sciatic radiculopathy, other neurological manifestations can occur in RA such as peripheral neuropathy, cervical myelopathy (due to upper cervical spine involvement), entrapment neuropathy, and cerebral vasculitis. Spinal RA can be encountered in some patients with a history of peripheral joint arthritis (late stage of RA), but sciatica can also be one of the first symptoms of this chronic arthritic disease (early stage of RA). Unfortunately, sometimes lumbar spinal involvement is not diagnosed until after surgery. A rheumatological evaluation could be requested for better characterizing and treating these patients. The worldwide prevalence of RA is about 1% with a female predominance (two to threefold more frequent than in men). This disease can be encountered at any age, but it is most common between 40 and 60 years old. Lumbar spinal involvement seems more common in women and older patients with RA. The prevalence of lumbar lesions on spinal imaging varies greatly from 5 to 50% in cases with RA.

48.2 Clinical Presentations When the lumbosacral spine is involved in RA, the majority of clinical features are nonspecific. Most patients present low back pain, but are rarely associated with typical lumbosacral radicular symptoms. Patients with sciatic pain presented variably, with acute, subacute, or chronic symptoms. However, most cases pres-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_48

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638

ent insidious symptoms developing over many weeks or months before the diagnosis is made. Uni or bilateral sciatica may be isolated or concomitant with paresthesia, numbness, or even neurogenic claudication related to lumbar spinal stenosis. Neurological deficits are less frequent and include sensory and/or motor radicular deficits with or without reflex abnormalities. Cauda equina compression syndrome is very rare. Clinicians should be checked for possible lumbar facet joint syndrome and spinal deformity. In the majority of cases, the general condition remains preserved. However, many other concomitant symptoms related to the systemic “extra-articular” involvement should be considered in clinical presentations such as skin, pulmonary, pericarditis, ophthalmologic, and vascular manifestations. In some cases, separating lumbosacral radiculopathy from other peripheral neuropathy on a clinical basis can be difficult. Therefore, in such cases electrophysiological studies are decisive. Subclinical peripheral neuropathy can be observed in up to 30% of patients with RA. RA-related sciatica should be distinguished from other leg pain related to peripheral neuropathy, foot, knee, or hip pain induced by RA.

48.3 Paraclinic Features Plain radiography is a simple and useful technique for diagnosing spinal bony lesions and for evaluating spinal alignment and instability. Unlike computed tomography (CT) scan, plain radiography is not suitable for soft-tissue lesions such as intervertebral disk and spinal ligament disease. CT scan should include parenchymatous and bony windows as well as 3D reconstructions. As mentioned previously, the most frequent radiographic and CT findings in patients with lumbar spine RA are: • • • • • • •

Disc space narrowing Endplate erosion Facet joint (apophyseal) erosion Osteophyte formation Spondylolisthesis/retrolisthesis Scoliosis Vertebral fractures (mainly in patients treated with corticosteroids)

Magnetic resonance imaging (MRI) offers the most complete assessment of RA in the lumbar spine. It is typically performed to evaluate for the presence of foraminal and central stenosis and neural element compression associated with the deformity. In addition, MRI can detect early inflammatory changes in bone (bone marrow edema) and joints.

48  Spinal Rheumatoid Arthritis

Interestingly, endplate lesions appear as a wave-like image with low signal intensity on both T1- and T2-weighted MRI images. This may indicate invasion of the pannus or rheumatoid nodule invasion around the vertebral endplate. Concomitant cervical spine lesions may be seen in 50–80% of patients with RA-related lumbar spinal abnormalities. The two most common types of cervical spine involvement are anterior atlantoaxial subluxation and basilar impression. On spinal imaging, the diagnosis may be challenging, and lumbar spinal lesions related to RA may be confused with other possible diseases such as: –– Discitis or spondylodiscitis –– Vertebral osteomyelitis –– Benign or malignant neoplasms –– Synovial cysts –– Gout and pseudogout –– Other spondyloarthropathies

48.4 Treatment Options and Prognosis Lumbar spinal RA-inducing sciatica can be managed conservatively or surgically. Conservative therapy includes pharmacologic treatment physiotherapy, and other physical modalities resulting in more or less control of the patient’s radicular pain. If sciatica does not improve following conservative measures or patients present with neurological deficits, surgery may be the next step in order to decompress lumbosacral radicular structures. If needed, an extensive bilateral laminectomy may be required in patients with the associated stenotic lumbar spinal canal. Care should be taken to minimize joint damage and the possibility of a CSF leak. An additional spinal fusion may sometimes be required if there is a potential preoperative instability or spinal deformity. In patients with poor health conditions, some authors recommend decompression surgery without fixation and a postoperative orthosis device. Peripheral neuropathy associated with therapeutic agents will be reversed upon discontinuation of implicated drugs. Possible delayed postoperative complications can occur such as wound infection, instrumentation failure, pathological fracture, and respiratory deterioration. These complications are likely related to immunodeficiency and osteopenia caused by RA itself or therapeutic drugs such as steroids and methotrexate. Postoperative results depend on the duration of the symptomatology, type, and severity of spinal damage and neurologic disorders, the patient’s general health condition, and

Further Reading

the surgical procedure used. However, most patients with RA-related sciatica had postoperative satisfactory outcomes unless there is a severe neurologic deficit.

Further Reading Akasbi N, Abourazzak FE, Harzy T.  A rare cause of non discal sciatica: rheumatoid arthritis. Pan Afr Med J. 2014;19:76. https://doi. org/10.11604/pamj.2014.19.76.3621. Aneja R, Singh MB, Shankar S, Dhir V, Grover R, Gupta R, et  al. Prevalence of peripheral neuropathy in patients with newly diagnosed rheumatoid arthritis. Indian J Rheumatol. 2007;2:47–50. https://doi.org/10.1016/S0973-­3698(10)60037-­4. Buratti L.  Rheumatoid arthritis and sciatalgia. Reumatismo. 1971;23:29–36. Chen CH, Hsu CW, Lu MC.  Risk of spine surgery in patients with rheumatoid arthritis: a secondary cohort analysis of a nationwide, population-based health claim database. Medicina (Kaunas). 2022;58:777. https://doi.org/10.3390/medicina58060777. Harzy T, Allali F, Bennani-Othmani M, Hajjaj-Hassouni N. Radiological characteristics of the lumbar spine in patients with rheumatoid arthritis. Presse Med. 2007;36:1385–9. https://doi.org/10.1016/j. lpm.2007.04.014. Hirohashi N, Sakai T, Sairyo K, Oba K, Higashino K, Katoh S, et al. Lumbar radiculopathy caused by extradural rheumatoid nodules. Case report. J Neurosurg Spine. 2007;7:352–6. https://doi. org/10.3171/SPI-­07/09/352. Ibrahim M, Suzuki A, Yamada K, Takahashi S, Yasuda H, Dohzono S, et  al. The relationship between cervical and lumbar spine lesions in rheumatoid arthritis with a focus on endplate erosion. J Spinal Disord Tech. 2015;28:E154–60. https://doi.org/10.1097/ BSD.0000000000000197. Inaoka M, Tada K, Yonenobu K.  Problems of posterior lumbar interbody fusion (PLIF) for the rheumatoid spondylitis of the lumbar spine. Arch Orthop Trauma Surg. 2002;122:73–9. https://doi. org/10.1007/s004020100321. Jacob JR, Weisman MH, Mink JH, Metzger AL, Feldman GR, Dorfman HD, et al. Reversible cause of back pain and sciatica in rheumatoid arthritis: an apophyseal joint cyst. Arthritis Rheum. 1986;29:431–5. https://doi.org/10.1002/art.1780290320. Joo P, Ge L, Mesfin A.  Surgical management of the lumbar spine in rheumatoid arthritis. Glob Spine J. 2020;10:767–74. https://doi. org/10.1177/2192568219886267. Kang CN, Kim CW, Moon JK. The outcomes of instrumented posterolateral lumbar fusion in patients with rheumatoid arthritis. Bone Jt J. 2016;98-B:102–8. https://doi.org/10.1302/0301-­620X.98B1.36247.

639 Kawaguchi Y, Matsuno H, Kanamori M, Ishihara H, Ohmori K, Kimura T.  Radiologic findings of the lumbar spine in patients with rheumatoid arthritis, and a review of pathologic mechanisms. J Spinal Disord Tech. 2003;16:38–43. https://doi. org/10.1097/00024720-­200302000-­00007. Lawrence JS, Sharp J, Ball J, Bier F. Rheumatoid arthritis of the lumbar spine. Ann Rheum Dis. 1964;23:205–17. https://doi.org/10.1136/ ard.23.3.205. Mitsuyama T, Kubota M, Yuzurihara M, Mizuno M, Hashimoto R, Ando R, et al. The pitfalls in surgical management of lumbar canal stenosis associated with rheumatoid arthritis. Neurol Med Chir (Tokyo). 2013;53:853–60. https://doi.org/10.2176/nmc.oa2012-­0299. Nakase T, Fujiwara K, Kohno J, Owaki H, Tomita T, Yonenobu K, et al. Pathological fracture of a lumbar vertebra caused by rheumatoid arthritis—a case report. Int Orthop. 1998;22:397–9. https://doi. org/10.1007/s002640050286. Park JS, Park SJ, Park J, Shin G, Hong JY. The influence of rheumatoid arthritis on higher reoperation rates over time following lumbar spinal fusion—a nationwide cohort study. J Clin Med. 2022;11:2788. https://doi.org/10.3390/jcm11102788. Sakai T, Sairyo K, Hamada D, Higashino K, Katoh S, Takata Y, et al. Radiological features of lumbar spinal lesions in patients with rheumatoid arthritis with special reference to the changes around intervertebral discs. Spine J. 2008;8:605–11. https://doi.org/10.1016/j. spinee.2007.03.008. Schellinger D, Wener L, Ragsdale BD, Patronas NJ.  Facet joint disorders and their role in the production of back pain and sciatica. Radiographics. 1987;7:923–44. https://doi.org/10.1148/ radiographics.7.5.2969603. Sims-Williams H, Jayson MI, Baddeley H.  Rheumatoid involvement of the lumbar spine. Ann Rheum Dis. 1977;36:524–31. https://doi. org/10.1136/ard.36.6.524. Tektonidou MG, Serelis J, Skopouli FN.  Peripheral neuropathy in two patients with rheumatoid arthritis receiving infliximab treatment. Clin Rheumatol. 2007;26:258–60. https://doi.org/10.1007/ s10067-­006-­0317-­z. Tung KK, Wu YC, Chen KH, Pan CC, Lu WX, Chin NC, et  al. The radiological outcome in lumbar interbody fusion among rheumatoid arthritis patients: a 20-year retrospective study. BMC Musculoskelet Disord. 2021;22:658. https://doi.org/10.1186/s12891-­021-­04531-­y. Wang N, Guo Y, Yang L, Fu W, Xu Y, Hou L, et  al. Effect of tumor necrosis factor inhibitors on rheumatoid arthritis-induced peripheral neuropathy: a cohort study. Neural Regen Res. 2012;7:862–6. https://doi.org/10.3969/j.issn.1673-­5374.2012.11.011. Yamada K, Suzuki A, Takahashi S, Yasuda H, Tada M, Sugioka Y, et al. MRI evaluation of lumbar endplate and facet erosion in rheumatoid arthritis. J Spinal Disord Tech. 2014;27:E128–35. https://doi. org/10.1097/BSD.0b013e3182a22a34.

Spinal Diffuse Idiopathic Skeletal Hyperostosis (Forestier’s Disease)

49.1 Generalities and Relevance Diffuse idiopathic skeletal hyperostosis (DISH) (AKA Forestier’s disease) is a noninflammatory entity characterized by bony proliferation (hyperostosis) at sites of tendinous and ligamentous insertion surrounding the spinal joints. This phenomenon occurs in the absence of degenerative, traumatic, or infectious abnormalities. The majority of lesions are found along the anterior longitudinal ligament and less frequently along the posterior longitudinal ligament, the whole responsibility for a partial or complete spinal fusion. DISH is most frequent in the thoracic spine, followed by the lumbar and then the cervical spine. About 70% of cases have all three spinal columns involved. Other enthesopathies may occur especially at the iliac crest, ischial tuberosities, and greater trochanters, but not the sacroiliac joints (unlike ankylosing spondylitis). In the lumbar spine, DISH can lead to spinal canal stenosis; however, this condition rarely produces clinical symptoms. Sometimes, patients present with stiffness, low back pain, and neurogenic claudication with or without lumbosacral radiculopathies confusing with other degenerative spinal diseases. In 1950, the French internist, Jacques Forestier (1890– 1978), who was a pioneer in the field of rheumatology, was the first to provide a complete clinical and radiological description of DISH in nine patients who presented spinal rigidity and had exuberant osteophytes on plain radiography. He also had joint necropsy findings in two specimens. With his collaborator, they termed this entity “senile vertebral ankylosing hyperostosis”. However, it was only in 1975 that the term “diffuse idiopathic skeletal hyperostosis” was originally coined by the American radiologist Donald Resnick (1940-). DISH affects habitually Caucasian males in their sixties (about one-third of patients are females). The estimated fre-

49

quency in the elderly is about 10–20%. While the etiology is unknown, various risk factors have been recognized in the literature such as metabolic disorders. Many authors have reported a significant association between Forestier’s disease and diabetes mellitus, hyperinsulinemia, obesity, dyslipidemia, and hyperuricemia.

49.2 Clinical Presentations The majority of individuals with DISH are asymptomatic, and the disease is often incidentally discovered in spinal imaging studies done for some other reasons (Fig. 49.1). Patients may complain of early morning back pain and stiffness and mild limitations of physical activities. Neurologic symptoms are unusual, but when they happen, it is above all progressive neurogenic claudication related to lumbar spinal stenosis. Lumboradicular pain such as sciatica is unusual and insidious but may be confused with other leg pain related to peripheral enthesiopathies except for the sacroiliac joints. Lower limb weakness and cauda equina syndrome rarely occur. Cases with pathologic fracture or subluxation tend to have more rapid gradual symptoms. Some patients may present with dysphagia, or even dyspnea related to large anterior cervical spine osteophytes that compress the esophagus or the larynx. The physical exam may show localized pain and tenderness, spinal stiffness, and rarely postural changes or spinal deformity. There is also decreased range of motion (or even immobility). Neurologic deficits are rare. Other neurological symptoms and clinical signs may be linked to compressive cervical or thoracic myelopathy. Clinicians should check for possible concomitant peripheral joint involvement including the shoulder,  iliac crest, ischial tuberosity, greater trochanter, tibial tuberosities,  patellar ligaments, calcaneum, and olecranon.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_49

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642

a

49  Spinal Diffuse Idiopathic Skeletal Hyperostosis (Forestier’s Disease)

b

c

Fig. 49.1  Cervical Forestier’s disease in a 48-year-old woman who developed minimal cervical pain following a fall without neurologic symptoms. Note the extensive C4–C7 anterior vertebral hyperostosis

(arrows). Lateral plain radiograph (a), sagittal CT scan (b), and sagittal T2-weighted MRI (c)

49.3 Paraclinic Features

Magnetic resonance imaging remains the main method to assess neurological compromise. It reveals the intraspinal extension of the lesions and any potential compression of the nervous structures. In the case of dysphagia, barium swallow pharyngo-­ esophagography and esophagoscopy are essential to help localize the precise compression area and rule out an intrinsic esophageal lesion. On spinal imaging, the diagnosis of DISH is sometimes challenging and the disease may be confused with other possible lesions in the lumbosacral region such as:

Plain radiographic evaluation will show ossification of the spinal longitudinal ligaments, especially the anterior longitudinal one, producing an anterior tortuous paravertebral mass along the vertebral bodies. This appearance is classically known as “candle wax dripping” or “flowing candle wax,” which is too different from the vertical “bamboo spine” that forms intra-articular disc space ossification in ankylosing spondylitis. Classically, the zygapophyseal and sacroiliac joints as well as disc space are not involved in DISH. Reconstruction CT scan on bone windows is more accurate for determining the thickness, the form of the o­ ssification, its extension, the degree of spinal canal stenosis as well as pathological fractures and subluxations (Fig. 49.2). On the thoracic spine, hyperostosis is most common on the right side of the spine given the left-sided position of the aorta. Because of potential multiple noncontiguous or asymptomatic spinal lesions, evaluation of the entire spine is recommended. Some cases may have ossification of peripheral joints in other parts of the skeleton.

–– –– –– –– –– –– –– ––

Ankylosing spondylitis (above all) Degenerative spine (large and extensive osteophytosis) Fluorosis Psoriatic spondylitis Charcot’s spine Acromegaly Hyperparathyroidism Gout

Biological markers in DISH are generally nonspecific (HLA B27 is often negative). Some cases may have hyperglycemia, hyperinsulinemia, dyslipidemia, and hyperuricemia.

49.4  Treatment Options and Prognosis

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a

c

b

d

e

Fig. 49.2  Sagittal CT-scan reconstructions on parenchymal (a) and bone (b) windows as well as on axial views (c–e). There is an anterior tortuous paravertebral ossified mass (arrows) along the L3–L4–L5 ver-

tebral bodies with concomitant spinal canal stenosis (double arrows and red triangles)

49.4 Treatment Options and Prognosis

Surgical decompression and stabilization may be required for some unusual specific forms: • Failure to respond to conservative treatment • Severe neurogenic claudication • Neurologic deficits • Fracture and/or subluxation • Painful deformity

There is no cure for DISH. However, some treatments and medications are used for symptomatic patients. The goal of treatment is to relieve pain and stiffness, maintain axial spine motion and functional ability, prevent the progression of the disease, and avoid spinal complications. Nondrug procedures comprise regular exercise, postural training, bracing, and physical therapy program. Pain-relieving drugs are repThe most frequently performed surgical procedure is a resented by daily analgesics and nonsteroidal anti-­ wide laminectomy of affected segments with or without inflammatory drugs (NSAIDs). foraminotomies. Limited resection techniques have also Rheumatologists may assist in a formal diagnosis, man- been advocated such as hemilaminectomies or laminotoagement, and monitoring of the patients. mies. Surgeons should minimize posterior facet joint dam-

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49  Spinal Diffuse Idiopathic Skeletal Hyperostosis (Forestier’s Disease)

age and the possibility of CSF leak when performing laminectomy. An additional spinal fusion may sometimes be required if there is a potential preoperative instability and/or an iatrogenic instability because of the surgical procedure. According to some authors, short-segment fusion surgery is not recommended as standard surgery for DISH-related lumbar spinal stenosis. Potential metabolic disorders should be managed appropriately. The prognosis for symptomatic patients who are diagnosed and treated in the early periods of the disease is good. Most patients remain fully functional. Severe physical ­disability is uncommon. However, patients about 10% of operated patients may need further revision surgery. Specific complications related to DISH include unstable spinal fractures, dysphagia, postsurgical heterotopic ossification, difficult intubation, difficult esophagoscopy, pneumonia, and myelopathy. Patient education in relation to spine fragility is important to avoid even minor trauma and prevent spinal fractures.

Further Reading Akhaddar A, Moussa A.  Chalk-stick fracture. N Engl J Med. 2022;386:2507. https://doi.org/10.1056/NEJMicm2117454. Ashraf O, Channapatna Suresh S, Raju B, Jumah F, Sun H, Gupta G, et al. Jacques Forestier: forgotten contributions of a rheumatologist to spine surgery. World Neurosurg. 2021;148:136–40. https://doi. org/10.1016/j.wneu.2020.12.170. Belanger TA, Rowe DE. Diffuse idiopathic skeletal hyperostosis: musculoskeletal manifestations. J Am Acad Orthop Surg. 2001;9:258– 67. https://doi.org/10.5435/00124635-­200107000-­00006. Cammisa M, De Serio A, Guglielmi G.  Diffuse idiopathic skeletal hyperostosis. Eur J Radiol. 1998;27(Suppl 1):S7–11. https://doi. org/10.1016/s0720-­048x(98)00036-­9. Forestier J, Rotes-Qerol J.  Senile ankylosing hyperostosis of the spine. Ann Rheum Dis. 1950;9:321–30. https://doi.org/10.1136/ ard.9.4.321. Kato S, Terada N, Niwa O, Yamada M.  Risk factors affecting cage retropulsion into the spinal canal following posterior lumbar interbody fusion: association with diffuse idiopathic skeletal hyperostosis. Asian Spine J. 2021;15:840–8. https://doi.org/10.31616/ asj.2020.0434.

Misaki H, Morino T, Hino M, Murakami Y, Imai H, Miura H. Can diffuse idiopathic skeletal hyperostosis be diagnosed by plain lumbar spine X-ray findings alone? Glob Spine J. 2022;12:198–203. https:// doi.org/10.1177/2192568220948038. Nakajima H, Honjoh K, Watanabe S, Kubota A, Matsumine A. Negative impact of short-level posterior lumbar interbody fusion in patients with diffuse idiopathic skeletal hyperostosis extending to the lumbar segment. J Neurosurg Spine. 2021a;36:392. https://doi.org/10.3171 /2021.5.SPINE21412. Nakajima H, Watanabe S, Honjoh K, Kubota A, Matsumine A. Pathomechanism and prevention of further surgery after posterior decompression for lumbar spinal canal stenosis in patients with diffuse idiopathic skeletal hyperostosis. Spine J. 2021b;21:955–62. https://doi.org/10.1016/j.spinee.2021.01.009. Nakajima H, Honjoh K, Watanabe S, Matsumine A. Prognostic factors and optimal surgical management for lumbar spinal canal stenosis in patients with diffuse idiopathic skeletal hyperostosis. J Clin Med. 2022;11:4133. https://doi.org/10.3390/jcm11144133. Okada E, Yagi M, Fujita N, Suzuki S, Tsuji O, Nagoshi N, et al. Lumbar spinal canal stenosis in patients with diffuse idiopathic skeletal hyperostosis: surgical outcomes after posterior decompression surgery without spinal instrumentation. J Orthop Sci. 2019;24:999– 1004. https://doi.org/10.1016/j.jos.2019.08.010. Otsuki B, Fujibayashi S, Takemoto M, Kimura H, Shimizu T, Matsuda S. Diffuse idiopathic skeletal hyperostosis (DISH) is a risk factor for further surgery in short-segment lumbar interbody fusion. Eur Spine J. 2015;24:2514–9. https://doi.org/10.1007/s00586-­014-­3603-­5. Resnick D, Shaul SR, Robins JM.  Diffuse idiopathic skeletal hyperostosis (DISH): Forestier’s disease with extraspinal manifestations. Radiology. 1975;115:513–24. https://doi.org/10.1148/15.3.513. Resnick D, Shapiro RF, Wiesner KB, Niwayama G, Utsinger PD, Shaul SR.  Diffuse idiopathic skeletal hyperostosis (DISH) [ankylosing hyperostosis of Forestier and Rotes-Querol]. Semin Arthritis Rheum. 1978;7:153–87. https://doi.org/10.1016/0049-­0172(78)90036-­7. Yamada K, Satoh S, Abe Y, Yanagibashi Y, Hyakumachi T, Masuda T. Diffuse idiopathic skeletal hyperostosis extended to the lumbar segment is a risk factor of reoperation in patients treated surgically for lumbar stenosis. Spine (Phila Pa 1976). 2018;43:1446–53. https://doi.org/10.1097/BRS.0000000000002618. Yamada K, Satoh S, Hashizume H, Yoshimura N, Kagotani R, Ishimoto Y, et al. Diffuse idiopathic skeletal hyperostosis is associated with lumbar spinal stenosis requiring surgery. J Bone Miner Metab. 2019;37:118–24. https://doi.org/10.1007/s00774-­017-­0901-­0. Yamada K, Abe Y, Yanagibashi Y, Hyakumachi T, Nakamura H. Risk factors for reoperation at same level after decompression surgery for lumbar spinal stenosis in patients with diffuse idiopathic skeletal hyperostosis extended to the lumbar segments. Spine Surg Relat Res. 2021;5:381–9. https://doi.org/10.22603/ssrr.2020-­0227.

Lumbar Spinal Gout and Pseudogout

50.1 Generalities and Relevance Gout and pseudogout (AKA chondrocalcinosis) are the two main forms of microcrystalline arthropathy that typically affect peripheral joints including the knee, ankle, wrist, hand, and metatarsophalangeal joints. Gouty arthritis results from the deposition of monosodium urate crystals within and around the joints and soft tissues, whereas pseudogouty is caused by the deposition of calcium pyrophosphate dihydrate crystals within the articular cartilage. Pseudogout is also known as calcium pyrophosphate dihydrate crystal deposition disease or CPPD. Both entities lead to erosion and joint damage. Additionally, in gout chronic form, there are solid urate crystal collections (tophi or tophaceous gout) in periarticular soft tissue. The term “pseudogout” (or false gout) is used because the disease can lead to clinical symptoms similar to gouty arthritis. On polarized light microscopy, gouty arthritis is characterized by negatively birefringent crystals, while pseudogout shows positively birefringent crystals. Spinal crystal deposition disease is rare and the majority of clinical features are nonspecific. Since the first case reported in the literature by George Kersley et al. (1950), less than 200 cases have been described. Among them, about 70 cases were located in the lumbar spine: gouty (60%) being slightly more common than pseudogouty (40%) lumbar arthritis. In 6 cases, pseudogout was associated with a lumbar spinal synovial cyst. Most patients were between 40 and 70 years of age. Lumbar spinal gout more commonly affects men while pseudogout was more common in women. The etiology of spinal involvement is supposed to be related to local tissue modification including a previous injury, microtrauma, tissue necrosis, or degenerative disease. In the lower lumbar spine, gout and pseudogout diseases mainly affect the facet joints, followed by vertebral endplates, pedicles, laminas, yellow ligaments, neural foramen, and the epidural space. Intradural localization is possible but very rare. Some authors suggested that tophaceous accumulation began from the posterior facet joints and then spread to

50

the yellow ligament and epidural space. Due to the direct nerve root and epidural compression as well as the involvement of inflammatory and vascular phenomena, crystal arthritis may be a rare source of unilateral or bilateral sciatic pain and even cauda equina syndrome. Spinal crystal arthritis can be encountered in some patients with a history of peripheral gout or pseudogout, but sciatica can also be one of the first symptoms of arthritic disease. Unfortunately, involvement is often not diagnosed until after surgery.

50.2 Clinical Presentations Half of the patients with lumbar spinal microcrystalline arthropathy had a known history of peripheral gouty or pseudogouty arthropathy. Such information should alert the treating clinician to the possibility of the diagnosis. However, low back with or without sciatic pain can also be the first manifestation of gouty/pseudogouty symptoms. Patients with this condition presented variably with acute, subacute, or chronic symptoms. Clinical presentations in both gout and pseudogout of the lumbar spine were similar. In acute forms, fever and important low back pain develop within a short time mimicking an infectious disease. Local and systemic inflammatory signs are possible as well as a lumbar facet joint syndrome. In subacute and chronic forms, symptoms are more insidious and may develop over many months or years. Patients can present with uni or bilateral sciatic pain, numbness, and symptoms of lumbar spinal stenosis. Neurological deficits are less frequent and include sensory and/or motor radicular deficits with or without reflex abnormalities, and even cauda equina compression syndrome. In the majority of cases, the general condition remains preserved. However, many other concomitant symptoms related to the systemic disease should be considered in clinical presentations such as renal, skin, peripheral joints, and acromioclavicular involvement.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_50

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50.3 Paraclinic Features Crystal deposits can be identified on plain radiography, but the diagnosis is often missed because the deposits are radiotransparent. In advanced forms of spinal gout, there are signs of nonspecific degenerative spondylosis, vertebral endplate erosions, osseous destruction causing joint subluxation, spinal deformity, spontaneous fusion, and even pathologic fractures. In pseudogout, X-rays may be normal or may show radio-opaque shadows at the posterior border of the spinal canal. Most patients have only one spinal region involved, but sometimes there are multiple spinal regions affected. Classical computed tomography (CT) scan findings of gout may show lobular juxta-articular mass with clear-cut erosive changes and sclerotic borders. On magnetic ­resonance imaging (MRI), uric acid crystals are hypointense in T1- and heterointense in T2-weighted images. The tophi are enhanced after gadolinium administration, but vary from homogeneous to heterogeneous peripheral enhancement. The intervertebral

50  Lumbar Spinal Gout and Pseudogout

disc spaces, facet joints, adjacent posterior bony elements, and epidural space may all be involved (Figs. 50.1 and 50.2). Dual-energy CT is a newer imaging technic that is both sensitive and specific for monosodium urate deposits. It can distinguish between urate mineralization and calcification. In pseudogout, CT scan demonstrates nodular or ovoid calcified lesions continuous with the posterior spinal structures that may compromise the spinal canal. Similarly, MRI may show round or oval hypointense masses, similar to gouty tophi in both T1- and T2-weighted images. On neuroimaging, the diagnosis is challenging, and spinal gout/pseudogout may be confused with other possible lesions in the lumbosacral region such as: –– –– –– –– ––

Epidural abscess Osteomyelitis Discitis Benign or malignant neoplasms Hematoma

a

Fig. 50.1 (a, b) T2-weighted axial and sagittal images show extradural lesions with severe dural sac and right root compression by the gout tophaceous deposits. (Reproduced from Hasturk AE, Basmaci M,

b

Canbay S, Vural C, Erten F. Spinal gout tophus: a very rare cause of radiculopathy. Eur Spine J. 2012;21 Suppl 4:S400–3. doi: 10.1007/ s00586-011-1847-x.; with permission)

Further Reading

Fig. 50.2  Axial CT shows bone erosions with calcifications over the right L4–5 facet joint and surrounding soft tissue masses. (Reproduced from Hasturk AE, Basmaci M, Canbay S, Vural C, Erten F. Spinal gout tophus: a very rare cause of radiculopathy. Eur Spine J. 2012;21 Suppl 4:S400–3. doi: 10.1007/s00586-011-1847-x.; with permission)

–– Synovial cysts –– Calcified ligamentum flavum –– Disc fragment

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and even prednisolone as a pain control modality. Targeted treatment of interleukin 1β can be useful in acute gouty inflammation that fails to respond to standard therapies. In chronic forms, anti-inflammatory prophylaxis is complemented by urate-lowering therapy (allopurinol or febuxostat with or without probenecid, or pegloticase). Rheumatological expertise could be requested for better characterizing and managing these patients. If symptoms do not improve or patients present with neurological deficits, surgery may be the next step in order to decompress radicular structures and remove the gouty/pseudogouty mass. If needed, an extensive bilateral laminectomy may be needed in patients with associated stenotic spinal canal. Care should be taken to minimize joint damage and the possibility of CSF leak. Most often, diagnosis is made during the surgical procedure; a pasty chalk-white mass is frequently encountered in gout. Sometimes, an additional spinal fusion may be required if there is a potential preoperative instability and/or an iatrogenic instability because of the surgical procedure. Many authors suggested a less invasive approach via a percutaneous biopsy or even a percutaneous transforaminal endoscopic decompression than a classic open surgical exploration using laminectomy. Almost all cases presented with sciatic pain were operated on because the diagnosis was not suspected preoperatively or lesions were confused with an epidural infection or neoplasm. However, the majority of patients had postoperative satisfactory results without recurrence.

Some inflammatory biomarkers such as erythrocyte sedimentation rate, C-reactive protein level, and white blood cell count are usually elevated but are not specific. The most frequent laboratory finding indicative of gout is elevated uric acid levels (hyperuricemia). Renal insufficiency may also be found in some patients. Although neuroimaging modalities can be suggestive, histopathological, cytological, and crystal examinations are the key to the diagnosis. Indeed, despite the risks of image-­ guided needle biopsy and the low yield of samples, only a Further Reading tissue sample could provide a correct diagnosis. In gout, the tissues display characteristic granulomatous infiltrates of Amouzougan A, Vassal F, Peoc'h M, Marotte H, Thomas T.  Calcium pyrophosphate deposition disease arthropathy-related sciatica. multinucleated giant cells, histiocytes, fibroblasts, and Arthritis Rheumatol. 2019;71:2099. https://doi.org/10.1002/ needle-­ shaped, negatively birefringent crystals. However, art.41099. identification of rod/rectangular-shaped crystals with posi- Barrett K, Miller ML, Wilson JT.  Tophaceous gout of the spine mimicking epidural infection: case report and review of tively birefringent crystals confirms the diagnosis of the literature. Neurosurgery. 2001;48:1170–2. https://doi. pseudogout. org/10.1097/00006123-­200105000-­00046.

50.4 Treatment Options and Prognosis Lumbar spinal gout and pseudogout can be managed conservatively or surgically. Conservative therapy includes pharmacologic treatment physiotherapy and other physical modalities resulting in more or less control of the patient’s pain. Treatment for nonurgent cases should initially be conservative and is similar to the treatment of other traditional forms of gouty arthritis. In acute episodes, medications include colchicine, nonsteroidal anti-inflammatory drugs,

Ben Tekaya A, Nacef L, Bellil M, Saidane O, Rouached L, Bouden S, et  al. Lumbar spinal involvement in calcium pyrophosphate dihydrate disease: a systematic literature review. Int J Gen Med. 2022;15:7639–56. https://doi.org/10.2147/IJGM.S360714. Brown TR, Quinn SF, D'Agostino AN.  Deposition of calcium pyrophosphate dihydrate crystals in the ligamentum flavum: evaluation with MR imaging and CT. Radiology. 1991;178:871–3. https://doi. org/10.1148/radiology.178.3.1994435. Buenzli D, So A.  Inflammatory sciatica due to spinal tophaceous gout. BMJ Case Rep. 2009;2009:0492. https://doi.org/10.1136/ bcr.07.2008.0492. Cardoso FN, Omoumi P, Wieers G, Maldague B, Malghem J, Lecouvet FE, et  al. Spinal and sacroiliac gouty arthritis: report of a case and review of the literature. Acta Radiol Short Rep. 2014;3:2047981614549269. https://doi. org/10.1177/2047981614549269.

648 Chen X, Xu G, Hu Q, Zhao T, Bi Q, Huang Y, Shao H, Zhang J.  Percutaneous transforaminal endoscopic decompression for the treatment of intraspinal tophaceous gout: a case report. Medicine (Baltimore). 2020;99:e20125. https://doi.org/10.1097/ MD.0000000000020125. Elgafy H, Liu X, Herron J.  Spinal gout: a review with case illustration. World J Orthop. 2016;7:766–75. https://doi.org/10.5312/wjo. v7.i11.766. Fujishiro T, Nabeshima Y, Yasui S, Fujita I, Yoshiya S, Fujii H.  Pseudogout attack of the lumbar facet joint: a case report. Spine (Phila Pa 1976). 2002;27:E396–8. https://doi. org/10.1097/00007632-­200209010-­00028. Gadgil AA, Eisenstein SM, Darby A, Cassar PV. Bilateral symptomatic synovial cysts of the lumbar spine caused by calcium pyrophosphate deposition disease: a case report. Spine (Phila Pa 1976). 2002;27:E428– 31. https://doi.org/10.1097/00007632-­200210010-­00024. Hall MC, Selin G.  Spinal involvement in gout. J Bone Jt Surg Am. 1960;42:341–3. https://doi. org/10.2106/00004623-­196042020-­00014. Hasturk AE, Basmaci M, Canbay S, Vural C, Erten F.  Spinal gout tophus: a very rare cause of radiculopathy. Eur Spine J. 2012;21(Suppl 4):S400–3. https://doi.org/10.1007/ s00586-­011-­1847-­x. Kersley GD, Mandel L, Jeffrey MR. Gout; an unusual case with softening and subluxation of the first cervical vertebra and splenomegaly. Ann Rheum Dis. 1950;9:282–304. https://doi.org/10.1136/ ard.9.4.282. Kim T, Kim BJ, Kim SH, Lee SH.  Tophaceous gout in the lumbar spinal canal mimicking epidural spinal tumor. Korean J Spine. 2017;14:50–2. https://doi.org/10.14245/kjs.2017.14.2.50. Lam HY, Cheung KY, Law SW, Fung KY. Crystal arthropathy of the lumbar spine: a report of 4 cases. J Orthop Surg (Hong Kong). 2007;15:94–101. https://doi.org/10.1177/230949900701500122. Lo PC, Yue CT, Kung WM.  Lumbar extradural pseudogout mass manifesting as radiculopathy: a case report. J Multidiscip Healthc. 2021;14:1593–8. https://doi.org/10.2147/JMDH.S316738. Lu H, Sheng J, Dai J, Hu X. Tophaceous gout causing lumbar stenosis: a case report. Medicine (Baltimore). 2017;96:e7670. https://doi. org/10.1097/MD.0000000000007670.

50  Lumbar Spinal Gout and Pseudogout Ma S, Zhao J, Jiang R, An Q, Gu R. Diagnostic challenges of spinal gout: a case series. Medicine (Baltimore). 2019;98:e15265. https:// doi.org/10.1097/MD.0000000000015265. Mahmud T, Basu D, Dyson PH. Crystal arthropathy of the lumbar spine: a series of six cases and a review of the literature. J Bone Jt Surg Br. 2005;87:513–7. https://doi.org/10.1302/0301-­620X.87B4.15555. Miller LJ, Pruett SW, Losada R, Fruauff A, Sagerman P.  Clinical image. tophaceous gout of the lumbar spine: MR findings. J Comput Assist Tomogr. 1996;20:1004–5. https://doi. org/10.1097/00004728-­199611000-­00028. Ng W, Sin CH, Wong CH, Chiu WF, Chung OM. Unusual presentation of spinal gout: 2 cases report and literature review. J Orthop Case Rep. 2017;7:50–4. https://doi.org/10.13107/jocr.2250-­0685.946. Ribeiro da Cunha P, Peliz AJ, Barbosa M. Tophaceous gout of the lumbar spine mimicking a spinal meningioma. Eur Spine J. 2018;27:815–9. https://doi.org/10.1007/s00586-­016-­4831-­7. Sun JM, Hsieh CT.  Spinal tophus mimicking, a migration disc with acute sciatica. Neurol India. 2022;70:1714–6. https://doi. org/10.4103/0028-­3886.355145. Toprover M, Krasnokutsky S, Pillinger MH. Gout in the spine: imaging, diagnosis, and outcomes. Curr Rheumatol Rep. 2015;17:70. https:// doi.org/10.1007/s11926-­015-­0547-­7. Ujihara T, Yamamoto K, Kitaura T, Katanami Y, Kutsuna S, Takeshita N, et  al. Calcium pyrophosphate deposition disease involving a lumbar facet joint following urinary tract infection. Intern Med. 2019;58:1787–9. https://doi.org/10.2169/internalmedicine.2099-­18. Wan SA, Teh CL, Jobli AT, Cheong YK, Chin WV, Tan BB. A rare cause of back pain and radiculopathy—spinal tophi: a case report. J Med Case Rep. 2019;13:8. https://doi.org/10.1186/s13256-­018-­1940-­4. Wu Z, Liu C, Dai K, Zheng C.  Intraspinal extradural gout tophus in the lumbar vertebral canal: case reports. Medicine (Baltimore). 2022;101:e28418. https://doi.org/10.1097/MD.0000000000028418. Yang Y, Guo Y, Yu S, Zou B. CT image findings of spinal gout. Spinal Cord. 2022;60:722. https://doi.org/10.1038/s41393-­022-­00773-­2. Yip CM, Lee HP. Spinal gouty tophus presenting as an epidural mass lesion—a case report. Int J Surg Case Rep. 2021;84:106063. https:// doi.org/10.1016/j.ijscr.2021.106063. Zou Y, Li Y, Liu J, Zhang B, Gu R. Gouty spondylodiscitis with lumbar vertebral body retrolisthesis: a case report. Medicine (Baltimore). 2019;98:e14415. https://doi.org/10.1097/MD.0000000000014415.

Spinal Langerhans Cell Histiocytosis (Eosinophilic Granuloma)

51.1 Generalities and Relevance Langerhans cell histiocytosis (LCH), previously known as histiocytosis X, is a rare benign nonneoplastic (tumor-like) disease of the reticuloendothelial system associated with a proliferation of Langerhans cells and comprises three different forms: (a) Letterer–Siwe disease (b) Hand–Schüller–Christian disease (c) Eosinophilic granuloma Eosinophilic granuloma (EOG) is by far the most benign and frequent form of LCH (up to 80%). The disease is more common in the pediatric population under the age of 10 years with a male predominance by a 2:1 ratio. Adult presentations have also been reported but are rare. The skeletal system is the most common site involved in LCH, especially the skull, pelvis, and long bones. Spinal localization is seen in between 6 and 25% of cases. Lesions generally affect the vertebral bodies of the thoracic and cervical spine. Lumbar and sacral involvement is unusual but may cause local pain, lumboradicular symptoms, and a kyphotic attitude. More extensive lesions can cause neurological deficits and spinal instability. The spinal lesion may be solitary or multiple, synchronous or asynchronous. Systemic involvement is more severe when associated with Hand–Schüller–Christian disease or Letterer–Siwe disease. The “Langerhans cell” was discovered by the German pathologist Paul Langerhans (1847–1888) in 1865 when he was still a medical student. Paul Langerhans is also recognized for the discovery of the islets of Langerhans that represent pancreatic cells secreting insulin. The term eosinophilic granuloma was coined by Lichtenstein and Jaffe in 1940. Lichtenstein in 1953 included EG, Hand–Schüller–Christian

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disease, and Letterer–Siwe disease under the entity histiocytosis X referring to the proliferation of histiocytes (Langerhans cells) due to an indefinite etiology. Classically, histopathologic examination reveals abundant histiocytic cells, with a combination of neutrophils, eosinophils, and lymphocytes. The Langerhans cells are positive for S-100 protein, CD1a, and CD207 immunostains. On electron microscopy, the cells contain “Birbeck granules” representing intracytoplasmic “tennis-racket” organelles with a central linear density and striated form.

51.2 Clinical Presentations The majority of patients with LCH complain of local pain, especially for lumbar spine localization. There is often a history of traumatic injury, but most presentations are considered subacute or chronic because the duration of symptoms usually ranges from a few weeks to months prior to the diagnosis. Patients can present with uni- or bilateral sciatic pain and numbness in the more evolved forms. Acute presentations and those with rapidly progressive courses are more often encountered with one of the systemic forms. The spinal examination will find a restricted lumbar range of motion, swelling, and tenderness around the lesion and deformity such as kyphosis and/or scoliosis. Neurological deficits are less frequent and include sensory and/or motor radicular deficits with or without reflex abnormalities and even cauda equina compression syndrome in case of extensive spine involvement. In the majority of cases, the general condition remains conserved. Sometimes, there is overall discomfort, and more rarely, fever with leukocytosis. Many other concomitant symptoms and signs related to the systemic disease should be considered in clinical presentations including skin, lung,

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liver, spleen, salivary, pituitary, and ophthalmologic manifestations. Clinicians should consider the two following forms: • The classic triad of exophthalmos, diabetes insipidus, and osteolytic skull lesions in Hand–Schuller–Christian Disease. • Lymphadenopathy, skin rash, hepatosplenomegaly, and pancytopenia in Letterer–Siwe Disease.

51.3 Paraclinic Features In children, LCH of the spine typically appears as a symmetric “pancake” appearance classically known as “vertebra plana”, resulting in an extreme collapse of the vertebral body with normal to a little enlarged adjacent intervertebral disc spaces. In adults, there is no vertebral collapse but a relatively small asymmetric osteolytic area of the anterior part of the vertebrae. Plain radiography and computed tomography (CT) scan show the osteolytic vertebral lesion with or without soft tissue extension (Fig.  51.1). Some forms may be more ­aggressive and the lesions look like a malignancy with irregular lytic lesions that involve posterior vertebral elements. CT scan is helpful for biopsy or surgical planning. Sometimes, bone scintigraphy can be recommended when there are multiple bony lesions. A skeletal survey is then important to recognize other asymptomatic localizations. Magnetic resonance imaging helps confirm the diagnosis and particularly analyzes paravertebral and intracanalar

a

51  Spinal Langerhans Cell Histiocytosis (Eosinophilic Granuloma)

extension with or without radicular compression. The lesions are typically hypo- to isointense on T1-weighted images and hyperintense on T2-weighted images and short tau inversion recovery (STIR) sequences. The mass shows diffuse enhancement after gadolinium injection. On spinal imaging, the diagnosis of LCH is challenging and the lesions (even a “vertebra plana” presentation) may be confused with other possible diseases in the lumbosacral region including: –– Benign tumors (e.g., aneurysmal bone cyst, hemangioma) –– Primary malignant tumors (e.g., neuroblastoma, rhabdomyosarcoma, Ewing’s sarcoma, myeloma) –– Metastasis –– Germ cell tumors (mainly teratoma) –– Gaucher’s disease –– Osteogenesis imperfecta –– Lymphoma and leukemia (acute lymphoblastic) –– Tuberculosis –– Osteomyelitis (chronic recurrent multifocal) Sometimes, definitive confirmation of this lesion is obtained only by biopsy, especially if there is a soft-tissue mass or disc involvement. Further paraclinic and biological investigations may be indicated for specific cases in the search for other systemic lesions as part of Hand–Schüller–Christian or Letterer–Siwe disease. Lastly, many cases remain pauci- or asymptomatic and the lesion will be discovered only incidentally on spinal imaging.

b

Fig. 51.1  Axial lumbar CT scan (a, b) showing small asymmetric osteolytic areas of the anterior part of the L5 vertebrae (arrows) with sclerotic margins

Further Reading

51.4 Treatment Options and Prognosis Lumbar spinal LCH can be managed conservatively or surgically. Various treatments have been proposed, including prolonged bed rest, immobilization with orthoses and bracing, physiotherapy, analgesics/anti-inflammatory drugs, intralesional steroid injection, hormonal therapy, chemotherapy, radiation therapy, and surgery. Nevertheless, the most suitable treatment for the patients is unclear. The majority of cases without neurological deficit or spinal instability may be managed conservatively because spinal LCH often improves spontaneously by fibrosis within 12–24  months, especially in children. However, patients need to be followed up regularly. Conservative therapy results in more or less control of the patient’s pain. Moreover, orthoses are useful for preventing kyphosis and/or kyphoscoliosis. However, intractable pain may require hormonal or low-dose radiation therapy. For some authors, radiotherapy may be also given in patients with moderate neurological deficits. Chemotherapy may be used if LCH is associated with systemic and/or multifocal disease. For many authors, any collapse or neurologic deficit from compression requires spinal reduction and radicular decompression with or without fusion. Regarding different forms of LCH, the prognosis is variable with EOG having the best and Letterer–Siwe disease having the worst prognosis. Most patients with single vertebral lesions and without neurological deficits were managed conservatively with good results. When indicated, surgery had satisfactory results. Patients with multiple lesions have a high rate of recurrence. Some cases associated with malignant features such as Langerhans cell sarcoma have a negative impact on survival.

Further Reading Akhaddar A, Boucetta M. Eosinophilic granuloma of the cervical spine manifesting as torticollis in a child. Pan Afr Med J. 2014;19:36. https://doi.org/10.11604/pamj.2014.19.36.3970. Angelini A, Mavrogenis AF, Rimondi E, Rossi G, Ruggieri P. Current concepts for the diagnosis and management of eosinophilic granu-

651 loma of bone. J Orthop Traumatol. 2017;18:83–90. https://doi. org/10.1007/s10195-­016-­0434-­7. Baillet A, Grange L, Lafaix PA, Gaudin P, Juvin R. Radiculopathy as a manifestation of Langerhans’ cell histiocytosis. Jt Bone Spine. 2007;74:190–3. https://doi.org/10.1016/j.jbspin.2006.05.013. Baky F, Milbrandt TA, Arndt C, Houdek MT, Larson AN.  Vertebra plana in children may result from etiologies other than eosinophilic granuloma. Clin Orthop Relat Res. 2020;478:2367–74. https://doi. org/10.1097/CORR.0000000000001409. Bavbek M, Atalay B, Altinörs N, Caner H.  Spontaneous resolution of lumbar vertebral eosinophilic granuloma. Acta Neurochir. 2004;146:165–7. https://doi.org/10.1007/s00701-­003-­0182-­3. Bilge T, Barut S, Yaymaci Y, Alatli C.  Solitary eosinophilic granuloma of the lumbar spine in an adult. Case report. Paraplegia. 1995;33:485–7. https://doi.org/10.1038/sc.1995.107. Chen L, Chen Z, Wang Y. Langerhans cell histiocytosis at L5 vertebra treated with en bloc vertebral resection: a case report. World J Surg Oncol. 2018;16:96. https://doi.org/10.1186/s12957-­018-­1399-­1. Dhillon CS, Tantry R, Ega SR, Pophale C, Medagam NR, Chhasatia N. Langerhans cell histiocytosis in the adult lumbar spine—a case report and literature review. J Orthop Case Rep. 2020;10:28–32. https://doi.org/10.13107/jocr.2020.v10.i09.1892. El Asri AC, Akhaddar A, Naama O, Sinaa M, Oukabli M, Al Bouzidi A, et  al. Multiple lytic lesions of the spine: a rare diagnosis of eosinophilic granuloma in an adult: a case report. Acta Neurochir. 2010;152:703–6. https://doi.org/10.1007/s00701-­009-­0434-­y. Garg S, Mehta S, Dormans JP. Langerhans cell histiocytosis of the spine in children. Long-term follow-up. J Bone Jt Surg Am. 2004;86:1740– 50. https://doi.org/10.2106/00004623-­200408000-­00019. Hassan BW, Moon BJ, Kim YJ, Kim SD, Choi KY, Lee JK. Langerhans cell histiocytosis in the adult lumbar spine: case report. Springerplus. 2016;5:1398. https://doi.org/10.1186/s40064-­016-­3006-­7. Huang WD, Yang XH, Wu ZP, Huang Q, Xiao JR, Yang MS, et  al. Langerhans cell histiocytosis of spine: a comparative study of clinical, imaging features, and diagnosis in children, adolescents, and adults. Spine J. 2013;13:1108–17. https://doi.org/10.1016/j. spinee.2013.03.013. Montalti M, Amendola L. Solitary eosinophilic granuloma of the adult lumbar spine. Eur Spine J. 2012;21(Suppl 4):S441–4. https://doi. org/10.1007/s00586-­011-­2052-­7. Peng XS, Pan T, Chen LY, Huang G, Wang J.  Langerhans’ cell histiocytosis of the spine in children with soft tissue extension and chemotherapy. Int Orthop. 2009;33:731–6. https://doi.org/10.1007/ s00264-­008-­0529-­8. Sapkas G, Papadakis M. Vertebral Langerhans cell histiocytosis in an adult patient: case report and review of the literature. Acta Orthop Belg. 2011;77:260–4. Thakur NA, Daniels AH, Schiller J, Valdes MA, Czerwein JK, Schiller A, et  al. Benign tumors of the spine. J Am Acad Orthop Surg. 2012;20:715–24. https://doi.org/10.5435/JAAOS-­20-­11-­715. Yeom JS, Lee CK, Shin HY, Lee CS, Han CS, Chang H.  Langerhans’ cell histiocytosis of the spine. Analysis of 23 cases. Spine (Phila Pa 1976). 1999;24:1740–9. https://doi. org/10.1097/00007632-­199908150-­00016.

Vertebral Osteomyelitis and Spondylodiscitis

52

52.1 Generalities and Relevance Spinal infections may interest the vertebral column (osteomyelitis), the intervertebral disc space (discitis), the spinal canal (epidural, subdural, and spinal cord abscesses), and the adjacent soft tissues (especially pyomyositis). The most common type of spinal infection involves the intervertebral disc space and the adjacent vertebral bodies, known as “spondylodiscitis” (Fig. 52.1). Spondylodiscitis is a serious entity that can lead to spinal deformities, segmental instabilities, neurologic deficits, and even life-threatening sepsis. Infection may be bacterial, mycobacterial (Pott’s disease), fungal (mycotic), or parasitic. Development of spondylodiscitis may occur through three main contamination ways: • Hematogenous spread (arterial or venous) from a remote infectious source • Direct inoculation from an open spinal trauma • Contiguous extension of infection from adjacent surrounding areas However, some cases remain “cryptogenic”. The most common site of spondylodiscitis was the lumbar (about 60%) and thoracic (about 30%) spines. Concomitant epidural abscess and/or surrounded paraspinal soft tissue infections and multiple contiguous or noncontiguous vertebral involvement are not rare. Isolated discitis is a rare condition, typically seen in the pediatric population. Many underlying diseases and some predisposing factors can be identified in the patients such as diabetes mellitus, intravenous drug abuse, immunocompromised states, alcoholism, chronic renal failure, hepatic cirrhosis, and some extraspinal infections (urinary tract, pelvic, skin, heart, dental, and pulmonary). Sciatica related to vertebral osteomyelitis and/or spondylodiscitis may result from lumbosacral nerve root compres-

Fig. 52.1  Illustration of the most common types of spinal infection: intervertebral disc space involvement (discitis), verttypesbral bodies involvement (spinal osteomyelitis), or both known as “spondylodiscitis”

sion and/or inflammation secondary to various lesions and mechanisms including: –– –– –– –– –– –– ––

Epidural suppurative collections or granulomatous lesions Inflammatory lumbosacral roots Foraminal and/or central spinal stenosis Sequestered bony or disc fragments Intervertebral instability Secondary spondylolisthesis Concomitant spinal epidural abscess(s)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_52

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52  Vertebral Osteomyelitis and Spondylodiscitis

Rarely, some thoracolumbar discitis and/or osteomyelitis may induce lumbosacral radicular pain secondary to discovertebral epidural infection (c.f. Chap. 43 about Conus Medullaris Lesions). In addition, some patients with paravertebral and especially psoas-iliac suppurations may induce lumbosacral plexopathies (c.f. Chap. 86 about Lumbosacral Plexopathies). Spondylodiscitis can occur in any age group but has two modes of distribution: childhood and aging population (over 65 years of age) with a marked male predominance.

52.2 Clinical Presentations Frequently, clinical signs and symptoms of spinal infections are nonspecific. Initially, clinical findings may be unclear and confusing due to other predisposing medical problems. The clinical presentation can be fulminant, acute, subacute, or chronic. However, the course of this infectious disease is often long and more indolent in granulomatous

a

(mycobacteria, brucellosis, or mycosis) and parasitic spondylodiscitis than in pyogenic ones. Fever is unusual in granulomatous infections and normally absent in parasitic spondylodiscitis. Signs and symptoms vary depending on the type of spinal infection and the region involved, but generally, pain is localized initially at the site of the infection. In the lumbosacral spine, patients with acute pyogenic forms present with lumbar backache (site-specific pain) and varying degrees of radicular pain with or without sciatica. Other clinical data include fever, paraspinal tenderness and rigidity, spinal deformity, and partial or complete cauda equina syndrome (CES) secondary to nerve root compression. Systemic findings may also include chills, night sweats, weight loss, anorexia, and general malaise. More rarely, chronic forms may present with a suppurating cutaneous sinus tract (Fig. 52.2). Possible underlying diseases and some predisposing factors should constantly be taken into consideration, especially recent history of sepsis, invasive diagnosis technique, or surgical procedure.

b

Fig. 52.2  Case 1. Suppurating cutaneous sinus tract (a, b) in a young patient with chronic sacral osteomyelitis manifesting as unilateral sciatic pain with sacralgia

52.3  Imaging Features

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52.3 Imaging Features Imaging studies are the mainstay to identify the site and extension of the infectious lesions which is important for planning surgery (Figs.  52.3, 52.4, 52.5, 52.6, 52.7, 52.8, 52.9, 52.10, 52.11, 52.12, 52.13, 52.14, 52.15, 52.16, 52.17, 52.18, 52.19, 52.20 and 52.21). Simple radiographs may be useful as a primary screening study; however, narrowing of the intervertebral disc space and erosion of contiguous endplates can only be seen after several weeks of disease progression. Nuclear medicine imaging explorations (Fig. 52.19), particularly single photon emission computed tomography (SPECT) combined with computed tomography (CT) scan and fluorodeoxyglucose-positron emission tomography (FDG-PET), are more sensitive in the early recognition of suspected spondylodiscitis. CT scan provides valuable information on the degree of osseous destruction, which is important for surgical planning and performing image-guided percutaneous biopsies or paraspinal abscess drainage if required (Figs.  52.3, 52.7, 52.8, 52.9, 52.10, 52.11, 52.12, 52.15, 52.18, and 52.21). Overall, magnetic resonance imaging (MRI) with gadolinium administration is considered the imaging modality of choice for the

a

b

diagnosis of spondylodiscitis (Figs.  52.4, 52.3, 52.4, 52.5, 52.6, 52.9, 52.10, 52.11, 52.12, 52.14, 52.16, 52.17, and 52.20). On T1-weighted images, the vertebral body and the narrowed intervertebral disc space have low signal intensity. The inflammatory lesions will enhance following gadolinium administration, especially the vertebral endplates and associated abscess collections. On T2-weighted images, the bony and discal lesions are hyperintense due to increased edema. Collections that are fluid-filled and thus easily drained tend to be hyperintense on T2-weighted images and will enhance peripherally around a central core of hypointensity on T1-weighted images. Fat suppression sequences (e.g., short inversion time inversion recovery [STIR]) are particularly important in making the diagnosis by removing the increased signals of epidural fat tissue and bone marrow. MRI is also valuable in demonstrating intraspinal canal lesions, especially combined epidural abscesses and cauda equina compression. The diffusion weighted-image (DWI) sequence can help to differentiate between the acute and chronic stages of the infection: high intensity in the acute stage and low intensity in the chronic stage.

c

Fig. 52.3  Case 2. Acute L4–L5 spondylodiscitis (arrows) with concomitant anterior epidural abscess (star) as seen on lumbosacral sagittal reconstructions (a, b) and axial CT scan (c)

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a

52  Vertebral Osteomyelitis and Spondylodiscitis

b

Fig. 52.4  Case 2. Acute L4–L5 spondylodiscitis (arrows) with concomitant anterior epidural abscess (stars) as seen on sagittal post-gadolinium T1- (a) and T2-weighted (b) MRI

a

b

Fig. 52.5  Case 2. Acute L4–L5 spondylodiscitis with concomitant anterior epidural abscess (stars) as seen on axial post-gadolinium T1- (a) and T2-weighted (b) MRI

52.3  Imaging Features

a

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b

c

d

Fig. 52.6  Case 3. Acute L4–L5–S1 spondylodiscitis (arrows) due to E. coli with concomitant bilateral psoas abscesses (stars). Lumbosacral sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c, d)

a

b

c

d

Fig. 52.7  Case 4. Chronic sacral osteomyelitis (arrows) due to S. aureus as seen on axial (a, b) and coronal reconstructions (c, d) CT-scan

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52  Vertebral Osteomyelitis and Spondylodiscitis

a

b

c

Fig. 52.8  Case 5. Subacute L5–S1 tuberculous spondylodiscitis (Pott’s disease) (arrows) as seen on axial (a) and sagittal reconstructions (b, c) CT-scan

a

b

c

Fig. 52.9  Case 6. Chronic L5–S1 Pott’s disease (yellow arrows) with intracanalar epidural extension (black arrows) and presacral abscess (stars). Sagittal reconstructions (a, b) CT scan and T2-weighted MRI (c)

52.3  Imaging Features

a

659

b

c

Fig. 52.10  Case 6. Chronic L5–S1 Pott’s disease with intracanalar epidural extension (arrows) as seen on axial CT scan (a), post-gadolinium T1- (b), and T2-weighted MRI (c)

a

b

c

Fig. 52.11  Case 7. L4–L5 tuberculous spondylodiscitis (arrows) with epidural involvement and concomitant bilateral abscesses (stars). Pelvic axial (a) and lumbosacral sagittal reconstruction (b) post-contrast CT scan as well as on sagittal T2-weighted MRI (c)

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52  Vertebral Osteomyelitis and Spondylodiscitis

a

b

c

Fig. 52.12  Case 7. L4–L5 tuberculous spondylodiscitis with epidural involvement (arrows) as seen on lumbosacral axial CT scan (a, b) and T2-weighted MRI (c)

Fig. 52.13  Case 7. Percutaneous punction (arrow) of the paraspinal tuberculous abscess on the left side (a, b)

a

b

52.3  Imaging Features

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a

c

b

Fig. 52.14  Case 8. L4–S1 brucellar spondylodiscitis with anterior epidural extension. Note the anterior vertebral body involvement (arrowheads). Lumbosacral axial (a, b) and sagittal (c) T2-weighted MRI

Fig. 52.15  Case 9. Chronic sacral hydatid cyst in a young girl presenting with isolated right-sided sciatica. Note the epidural extension (arrows). Pelvic axial CT scan on both parenchymal (a) and bone (b) windows

a

b

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a

52  Vertebral Osteomyelitis and Spondylodiscitis

b

c

Fig. 52.16  Case 1. Chronic cutaneous fistula (arrows) due to S1 sacral osteomyelitis (stars) secondary to Streptococcus species infection. Note the presacral abscess (arrowheads). Lumbosacral sagittal T1 without (a) and with gadolinium injection (b), as well as on T2-weighted MRI (c)

52.3  Imaging Features

a

663

b

c

Fig. 52.17  Case 1. Chronic cutaneous fistula with paraspinal abscesses (arrows) due to S1 sacral osteomyelitis (dotted circle) secondary to Streptococcus species infection. Lumbosacral axial post-gadolinium T1-(a, b) and T2-weighted MRI (c)

a

b

Fig. 52.18  Case 1. Chronic S1 sacral osteomyelitis (arrows) as seen on axial CT scan on both parenchymal (a) and bone windows (b)

664 Fig. 52.19  Case 1. Chronic sacral osteomyelitis detected on anterior (a) and posterior (b) whole body bone scintigraphy using Tc-99m MDP bone scan. Note the increased radiotracer localization in the sacral area (dotted frame)

52  Vertebral Osteomyelitis and Spondylodiscitis

a

b

52.3  Imaging Features

a

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b

c

Fig. 52.20  Case 10. Postoperative L5–S1 spondylodiscitis (arrows) following herniectomy and discectomy at an outside institution for a lumbar disc herniation. Lumbosacral sagittal T1- (a) and T2-weighted MRI (b). Axial post-gadolinium T1-weighted MRI (c)

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d

Fig. 52.21  Case 10. Postoperative L5–S1 spondylodiscitis (arrows). Lumbosacral sagittal reconstruction (a, b) and axial (c, d) CT scan

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52  Vertebral Osteomyelitis and Spondylodiscitis

52.4 Laboratory Findings Leukocyte count, erythrocyte sedimentation rate, and C-reactive protein are frequently found elevated but they are not very sensitive nor specific indicators in establishing the diagnosis. However, elevated procalcitonin levels can be a strong indication for determining the presence of pyogenic bacterial infections. Also, blood culture may be positive. Screen for other potential causes of infection is important for identifying the causative pathogens. Spondylodiscitis may be bacterial, mycobacterial, fungal/ mycotic, or parasitic. The most common pathogen involved is Staphylococcus aureus (about 60% of cases) followed by gram-negative rods (particularly Escherichia coli and Proteus species), Streptococcus species, and Enterococcus species. Other pathogens are rare. Mycobacterium tuberculosis is more common in many developing countries (especially from Asia and Africa); on the other side, brucellosis is seen in countries around the Mediterranean Sea and is related to animal contact or the consumption of raw milk or its derivatives. Fungal Spondylodiscitis is rare (e.g., aspergillosis, blastomycosis, candidiasis, coccidioidomycosis, and histoplasmosis), but is more expected to be encountered in immunocompromised patients. Although rare, hydatidosis is the most common parasite involving the vertebral column. Polymicrobial infections are infrequent and are usually the consequence of a contiguous spread. Percutaneous CT-guided biopsy can be very useful for the diagnosis (Fig. 52.13). Purulent material should be tested for aerobic and anaerobic microorganisms, antimicrobial susceptibility, and additional Mycobacteria. Anatomopathologic studies are an important tool for diagnosing acute, subacute, and chronic forms as well as specific infections such as mycobacteria, fungi, and parasites (Figs.  52.22, 52.23 and

Fig. 52.23 Chronic tuberculous spondylodiscitis on microscopic image. There are epithelioid cell granulomas with Langerhans giant cells (arrow) and caseation necrosis (star) suggesting a Pott’s disease (hematoxylin–eosin stain, original magnification × 60). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi)

Fig. 52.24  Chronic tuberculous spondylodiscitis. Microscopic image showing epithelioid cell granuloma with Langerhans giant cells (arrows) and caseation necrosis (star), suggesting a Pott’s disease (tuberculous spondylitis) (hematoxylin–eosin stain, original magnification × 200). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi)

52.24). Serologic or antigen testing for specific bacteria, mycotic, or parasitic infections may be helpful in some patients from countries where these diseases are endemic.

52.5 Treatment Options and Prognosis Fig. 52.22  Subacute spondylodiscitis on microscopic image. There are bone trabeculae (arrows) with sites of subacute inflammatory cell infiltration, associated with granulation tissue (hematoxylin–eosin stain, original magnification × 60). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi)

Spondylodiscitis treatment aims to eradicate the infection definiteness of the nervous structures and preserve spinal stability and neurologic function.

Further Reading

Most patients require a long-term intravenous antibiotic, antifungal, or antiparasitic drug with extended hospitalization time. External immobilization may be recommended when there is significant pain or the potential for spine instability. For traditional bacterial infections, appropriate intravenous antibiotic agents are used for 4–6 weeks (empiric antibiotics include third-generation cephalosporin, vancomycin, and metronidazole), followed by additional 2–3  months of oral antibiotics. Antibiotic therapy should always be personalized according to culture results, antibiotic susceptibility testing, patient’s clinical conditions, and severity of the infection. Spinal tuberculosis needs a first-line regimen of a combination of isoniazid, rifampicin, pyrazinamide, and ethambutol or streptomycin for 2 months followed by two drugs (isoniazid and rifampicin) for 6–9  months. Brucellosis is habitually treated with an association of doxycycline and rifampicin for 6 months. Fungal/mycotic infections must be treated with the appropriate anti-infectious agents (amphotericin B or azole drugs). Oral antihelminthic drugs such as albendazole/mebendazole are encouraging for spinal hydatidosis. Surgical procedures are indicated to get diagnostic cultures, decompress cauda equina nerve roots, maintain/restore spinal instability, treat significant deformity, drain associated suppurative collections, and debride infected and necrotic tissue when infection continues or deteriorates regardless of appropriate anti-infectious agents. It is important to preserve the dura mater. Various spinal approaches are used: anterior, posterior, posterolateral, or combined. Fusion with or without implants can be achieved despite infection. Less invasive surgical procedures may be used such as limited hemilaminectomy, interlaminar fenestration, endoscopy, or CT-guided aspiration. Conservative management with antimicrobial therapy and external spinal immobilization can be proposed in some patients in the early stage of infection, those with poor clinical conditions, or those without the neurologic disorder. The outcome depends mainly on the preoperative neurologic conditions of the patient, the delay in diagnosis and initiation of treatment, the potential underlying diseases, the associated lesions, the virulence of the causative pathogen(s), and the response to treatment. Although some cases have serious clinical and neurologic development, spondylodiscitis can be successfully treated in many patients. Mortality is rare nowadays. However, a significant number of patients require long-term rehabilitation to regain neurologic function. During the recovery, decubitus complications are also a common finding. Associated sequels include chronic pain, persistent weakness, lower extremity

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spasticity, sphincter dysfunction, pseudarthrosis, and chronic infection. The recurrence rate is about 10% and is even more important in cases with spinal hydatidosis.

Further Reading Akhaddar A. Vertebral body and discal infections. In: Akhaddar A, editor. Atlas of infections in neurosurgery and spinal surgery. Cham: Springer International Publishing; 2017. p.  159–70. https://doi. org/10.1007/978-­3-­319-­60086-­4_17. Akhaddar A, Gourinda H, el Alami Z, el Madhi T, Miri A. Hydatid cyst of the sacrum. Report of a case. Rev Rhum Engl Ed. 1999;66:289–91. Akhaddar A, Hall W, Ramraoui M, Nabil M, Elkhader A.  Primary tuberculous psoas abscess as a postpartum complication: case report and literature review. Surg Neurol Int. 2018;9:239. https:// doi.org/10.4103/sni.sni_329_18. Celik SE. Pott disease mimics postsurgical pyogenic spondylodiscitis. J Neurosurg Sci. 2009;53:161–4. Chen Z, Cao P, Zhou Z, Yuan Y, Jiao Y, Zheng Y.  Overview: the role of Propionibacterium acnes in nonpyogenic intervertebral discs. Int Orthop. 2016;40:1291–8. https://doi.org/10.1007/ s00264-­016-­3115-­5. de Leeuw CN, Fann PR, Tanenbaum JE, Buchholz AL, Freedman BA, Steinmetz MP, Mroz TE.  Lumbar epidural abscesses: a systematic review. Glob Spine J. 2018;8:85S–95S. https://doi. org/10.1177/2192568218763323. Del Pozo FJ, Alonso JV, Ruiz MÁ, Vythilingam S, Ruiz DL. Community acquired spondylodiscitis caused by Escherichia coli; case report and literature review. Bull Emerg Trauma. 2016;4:174–9. Erraoui M, Amine B, Tahiri L, El Binoune I, Bahha J, Hajjaj-Hassouni N. Noncontiguous multi-tiered spinal tuberculosis associated with sternal localization: a case report. J Med Case Rep. 2017;11:181. https://doi.org/10.1186/s13256-­017-­1323-­2. Ferri I, Ristori G, Lisi C, Galli L, Chiappini E. Characteristics, management and outcomes of spondylodiscitis in children: a systematic review. Antibiotics (Basel). 2020;10:30. https://doi.org/10.3390/ antibiotics10010030. Franco-Jiménez S, Romero-Aguilar JF, Bervel-Clemente S, Martínez-­ Váquez M, Alvarez-Benito N, Grande-Gutiérrez P, et  al. Garre’s chronic sclerosing osteomyelitis with sacral involvement in a child. Rev Esp Cir Ortop Traumatol. 2013;57:145–9. https://doi. org/10.1016/j.recot.2012.11.003. Fu TS, Chen LH, Chen WJ. Minimally invasive percutaneous endoscopic discectomy and drainage for infectious spondylodiscitis. Biom J. 2013;36:168–74. https://doi.org/10.4103/2319-­4170.112742. Guglielmino A, Sorbello M, Murabito P, Naimo J, Palumbo A, Lo Giudice E, et al. A case of lumbar sciatica in a patient with spondylolysis and spondylolysthesis and underlying misdiagnosed brucellar discitis. Minerva Anestesiol. 2007;73:307–12. Hammami F, Koubaa M, Feki W, Chakroun A, Rekik K, Smaoui F, et al. Tuberculous and brucellar spondylodiscitis: comparative analysis of clinical, laboratory, and radiological features. Asian Spine J. 2021;15:739–46. https://doi.org/10.31616/asj.2020.0262. Jahng J, Kim YH, Lee KS.  Tuberculosis of the lower lumbar spine with an atypical radiological presentation—a case mimicking a malignancy. Asian Spine J. 2007;1:102–5. https://doi.org/10.4184/ asj.2007.1.2.102. Kotilainen E, Sonninen P, Kotilainen P.  Spinal epidural abscess: an unusual cause of sciatica. Eur Spine J. 1996;5:201–3. https://doi. org/10.1007/BF00395515. Mastoraki A, Mastoraki S, Papanikolaou IS, Tsikala-Vafea M, Tsigou V, Lazaris A, et al. Spondylodiscitis associated with major abdomi-

668 nal surgical intervention: challenging diagnostic and therapeutic modalities. Indian J Surg Oncol. 2017;8:274–8. https://doi. org/10.1007/s13193-­017-­0641-­6. Nomura S, Toyama Y, Akatsuka J, Endo Y, Kimata R, Suzuki Y, et al. Prostatic abscess with infected aneurysms and spondylodiscitis after transrectal ultrasound-guided prostate biopsy: a case report and literature review. BMC Urol. 2021;21:11. https://doi.org/10.1186/ s12894-­021-­00780-­0. Perna A, Ricciardi L, Sturiale CL, Fantoni M, Tamburrelli FC, Bonfiglio N, et al. Skipped vertebral spontaneous spondylodiscitis caused by Granulicatella adiacens: case report and a systematic literature review. J Clin Orthop Trauma. 2020;11:937–41. https://doi. org/10.1016/j.jcot.2019.07.002. Pola E, Logroscino CA, Gentiempo M, Colangelo D, Mazzotta V, Di Meco E, et al. Medical and surgical treatment of pyogenic spondylodiscitis. Eur Rev Med Pharmacol Sci. 2012;16(Suppl 2):35–49. Postacchini F, Montanaro A. Tuberculous epidural granuloma simulating a herniated lumbar disk: a report of a case. Clin Orthop Relat Res. 1980;148:182–5. Potsios C, Xaplanteri P, Zoitopoulos V, Patrinos P, Giannakopoulou II, Tzivaki I, et al. Pyogenic spondylodiscitis due to Streptococcus constellatus in an immunocompromised male patient: a case report and review of the literature. Case Rep Infect Dis. 2019;2019:9364951. https://doi.org/10.1155/2019/9364951. Qu DC, Chen HB, Yang MM, Zhou HG.  Management of lumbar spondylodiscitis developing after laparoscopic sacrohysteropexy with a mesh: a case report and review of the literature. Medicine (Baltimore). 2019;98:e18252. https://doi.org/10.1097/ MD.0000000000018252. Rozis M, Vlamis J, Pneumaticos SG.  Chronic undiagnosed brucellosis presenting as sciatica. Cureus. 2021;13:e13114. https://doi. org/10.7759/cureus.13114. Shields DW, Robinson PG.  Iliopsoas abscess masquerading as ‘sciatica’. BMJ Case Rep. 2012;2012:bcr2012007419. https://doi. org/10.1136/bcr-­2012-­007419.

52  Vertebral Osteomyelitis and Spondylodiscitis Stabile G, Romano F, Topouzova GA, Mangino FP, Di Lorenzo G, Laganà AS, et  al. Spondylodiscitis after surgery for pelvic organ prolapse: description of a rare complication and systematic review of the literature. Front Surg. 2021;8:741311. https://doi.org/10.3389/ fsurg.2021.741311. Stangenberg M, Mende KC, Mohme M, Krätzig T, Viezens L, Both A, Rohde H, Dreimann M. Influence of microbiological diagnosis on the clinical course of spondylodiscitis. Infection. 2021;49:1017–27. https://doi.org/10.1007/s15010-­021-­01642-­5. Torres-Martos E, Pérez-Cortés S, Sánchez-Calvo JM, López-Prieto MD.  Spondylodiscitis due to Aerococcus urinae infection in an elderly immunocompetent patient. Enferm Infecc Microbiol Clin. 2017;35:682–4. https://doi.org/10.1016/j.eimc.2017.02.005. Turgut M, Akhaddar A, Turgut AT, Garg RK, (editors). Tuberculosis of the central nervous system: pathogenesis, imaging, and management. Cham: Springer International Publishing; 2017. https://doi. org/10.1007/978-­3-­319-­50712-­5. Unuvar GK, Kilic AU, Doganay M.  Current therapeutic strategy in osteoarticular brucellosis. North Clin Istanb. 2019;6:415–20. https://doi.org/10.14744/nci.2019.05658. Waheed G, Soliman MAR, Ali AM, Aly MH.  Spontaneous spondylodiscitis: review, incidence, management, and clinical outcome in 44 patients. Neurosurg Focus. 2019;46:E10. https://doi. org/10.3171/2018.10.FOCUS18463. Wang X, Tao H, Zhu Y, Lu X, Hu X.  Management of postoperative spondylodiscitis with and without internal fixation. Turk Neurosurg. 2015;25:513–8. https://doi.org/10.5137/1019-­5149.JTN.9008-­13.1. Wilhelm N, Sire S, Le Coustumier A, Loubinoux J, Beljerd M, Bouvet A. First case of multiple discitis and sacroiliitis due to Abiotrophia defectiva. Eur J Clin Microbiol Infect Dis. 2005;24:76–8. https:// doi.org/10.1007/s10096-­004-­1265-­7. Yuksel KZ, Senoglu M, Yuksel M, Gul M. Brucellar spondylo-discitis with rapidly progressive spinal epidural abscess presenting with sciatica. Spinal Cord. 2006;44:805–8. https://doi.org/10.1038/ sj.sc.3101938.

Spinal Epidural Abscesses

53.1 Generalities and Relevance Most intraspinal suppurative collections are contained in the epidural or extradural space between the spinal dura mater and the osseous-ligamentous structures of the spine (Fig. 53.1). Intraspinal infections are less often encountered within the spinal cord parenchyma or the subdural space. “Abscess” is characterized by a capsule that separates the suppurative material from normal adjacent structures; while “empyema” is attributed to a purulent material within a preexisting anatomic cavity. However, “abscess” and “empyema” are often used interchangeably in the literature. In the spinal epidural space, the most common site of this infection was the lumbar and thoracic. Generally, 3–5 vertebral levels are involved anterior or posterior to the dura. Epidural abscesses are less extensive than subdural ones

53

because the extradural space has no smooth anatomic borders like those found in the subdural space. Spinal epidural abscess is an unusual disease within the spinal canal; however, its incidence has been increasing in recent years (about 1.2 per 10,000 patients). About 600 cases of lumbar spinal epidural abscesses were previously reported in the literature between 2000 and 2017. As with other intraspinal canal infections, epidural abscesses represent a serious pathologic entity that can lead to life-threatening sepsis if not diagnosed promptly and treated appropriately. In the lumbosacral spinal canal, epidural purulent collections have the potential to cause secondary neurologic damage by compressing the cauda equina nerve roots. Concomitant vertebral and/or discal infections (spondylodiscitis) are not rare. Development of spinal extradural abscess may occur through: • Hematogenous spread from a distant source of infection. • Contiguous extension from a contiguous infection. • Direct iatrogenic inoculation (diagnosis or surgical procedures). • A significant number of cases remain “cryptogenic”.

Fig. 53.1  Illustration of a lumbar epidural abscess compressing the thecal sac contents as seen in axial and sagittal sections. The dura is shown in green and the arachnoid in blue

Many underlying diseases and some predisposing factors can be identified in the patients such as diabetes mellitus, intravenous drug abuse, human immunodeficiency virus infection, alcoholism, chronic renal failure, hepatic cirrhosis, concomitant malignant tumor, morbid obesity, and tuberculosis. Furthermore, any immunosuppressive treatment can predispose to support spinal canal infections. Spinal epidural abscesses are encountered in all age groups, but they are more common in the aging population with multiple comorbidities and are relatively unusual among children with male predominance.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_53

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53  Spinal Epidural Abscesses

53.2 Clinical Presentations Usually, clinical signs and symptoms of intraspinal canal infections are nonspecific. Initially, clinical findings may be unclear and confusing due to other predisposing medical problems. Generally, neurologic symptoms develop through 4 stages: (a) Spinal pain. (b) Radicular pain such as sciatica. (c) Muscular weakness. (d) Complete paralysis. In the lumbosacral spine, patients with acute forms present with lumbar backache (site-specific pain) and varying degrees of radicular pain with or without sciatica. Then, rapidly progressive neurologic deficits developed below the level of the abscess including muscle weakness in one or both legs, sphincter dysfunction, and erectile dysfunction. Indeed, many patients will present with partial or complete cauda equina syndrome due to nerve root compression. Unlike subdural abscesses, there is a spinal focal percussion tenderness in patients with spinal epidural abscesses. However, systemic signs of infection are common but inconstant (fever, malaise, irritability, night sweats, and headache). Meningism is a rare symptom. Chronic presentations tend to have less specific symptomatology simulating epidural tumors with a progressive neurological deficit and low back pain without fever. Nevertheless, signs and symptoms depend on the exact location of the suppuration, the volume and number of collections/abscesses and their chronicity, and the associated lesions. Progression of neurologic symptoms tends to be faster in patients with a spinal subdural abscess than in those with an epidural abscess.

a

b

Potential underlying diseases and some predisposing factors should constantly be taken into consideration, especially recent history of sepsis, invasive diagnosis technique, or surgical procedure.

53.3 Imaging Features Computed tomography (CT) scan is normal unless there is a combination of spinal osteomyelitis and/or discitis. Sometimes, intraspinal gas (air bubbles) or calcifications may be seen in the epidural space (Fig. 53.2a). Magnetic resonance imaging (MRI) is the imaging procedure of choice to confirm the presence of an epidural suppurative collection and to determine its exact location in the spinal canal (anterior, lateral, posterior, or circumferential) which is important for planning surgery (Figs. 53.2, 53.3, 53.4 and 53.5). Usually, an abscess appears as a well-delimited collection with a hypo or isointense signal on T1-weighted images and a hyperintense signal on T2-weighted images. There is a rim enhancement following gadolinium injection (Figs.  53.2b and 53.3b). Collections that are fluid-filled and thus easily drained tend to be hyperintense on T2-weighted images and will enhance peripherally around a central core of hypointensity on T1-weighted images. Unlike subdural abscess, the extradural fat tissue is pushed back and/or poorly identified in epidural abscess and there is also an interior displacement of the dura. Fat suppression sequences are particularly important in making the diagnosis by removing the increased signals of extradural fat and bone marrow. Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) usually demonstrate restricted diffusion of the collection; this can be useful in differentiating abscesses from some tumors especially lymphoma and epidural metastasis.

c

Fig. 53.2  Calcified tuberculous epidural abscess on L4 vertebral level (arrows) as seen on axial CT scan (a), post-gadolinium T1- (b), and T2-weighted (c) MR imaging

53.3  Imaging Features

671

b

a

c

Fig. 53.3  Case 1. L4–S1 spondylodiscitis with concomitant epidural abscesses (arrows). Sagittal T1-weighted MRI before (a) and after gadolinium injection (b), as well as on T2-weighted MR imaging (c)

a

b

c

Fig. 53.4  Case 1. Antero-lateral epidural abscess on S1 vertebral level (arrows) as seen on axial T2-weighted MRI (a–c)

Screening for the paraspinal, vertebral body, and/or discal involvement can help determine the diagnosis (Figs.  53.3 and 53.5). MRI is also useful in detecting changes in epidural abscesses from progression to remission/regression in patients under antibiotic therapy. On spinal imaging, some spinal epidural abscesses may be confused with a wide spectrum of other epidural lumbosacral pathologies such as: • Degenerative lesions (free/sequestered disc fragment, synovial cyst, ligamentum flavum lesions)

• Epidural hematomas • Tarlov cysts • Vascular lesions (cavernous angioma, vascular malformations, varices) • Benign or malignant vertebro-epidural tumors • Congenital lesions (arachnoid cyst, meningocele, lipoma, dermoid, epidermoid cysts) • Spinal epidural lipomatosis • Granulomatous lesions (tuberculoma, sarcoidosis) • Subdural abscesses • Some rheumatologic diseases (gouty tophus, pigmented villonodular synovitis, rheumatoid nodules)

672 Fig. 53.5  Case 2. Extensive epidural abscess from L4 to S1 vertebral level (arrows) as seen on sagittal (a) and axial T2-weighted MRI (b, c). Note the concomitant L4–L5 discitis (arrowheads)

53  Spinal Epidural Abscesses

a

b

c

53.4 Laboratory Findings

53.5 Treatment Options and Prognosis

Leukocyte count, erythrocyte sedimentation rate, and C reactive protein are frequently found elevated, but they are not very sensitive nor have specific indicators. However, elevated procalcitonin levels can be a strong indication for determining the presence of bacterial infections. Also, blood culture may be useful. Lumbar puncture for CSF analysis is not necessary and has potential morbidity. Screening for other potential causes of infection is important. Purulent material should be tested for aerobic and anaerobic microorganisms, antimicrobial susceptibility, and additional Mycobacteria species. Most spinal subdural abscesses were attributed to Staphylococcus aureus infection. However, other various pathogens can also be involved such as gram-negative bacilli and Streptococcus species. Other bacteria, Mycobacteria, and fungi are rare.

Usually, the spinal epidural abscess is treated by prompt surgical drainage of the purulent material and appropriate antibiotics administration. Surgical procedures typically comprise decompressive laminectomy at the appropriate levels, surgical drainage of the purulent collection with or without debridement of granulation tissue, and antiseptic irrigation. However, the dura mater must be kept intact. Less invasive surgical procedures may be used such as limited hemilaminectomy, interlaminar fenestration, or CT-guided aspiration. Surgery can also be used to obtain diagnostic cultures. Potential spinal instability can require spinal reconstruction and surgical implants. Appropriate intravenous antibiotic agents are used for 4–6  weeks (empiric antibiotics include third-generation

Further Reading

cephalosporin and vancomycin), followed by additional 2–3  months of oral antibiotics. Antibiotic therapy should always be personalized according to culture results and antibiotic susceptibility testing. Tubercular and fungal abscesses should be treated with correct anti-infective drugs for a longer duration. Conservative management with antibiotic therapy and external spinal immobilization can be proposed in some patients in the early stage of infection, those with poor clinical conditions, or those without the neurologic disorder. Overall prognosis is considerably better for patients who undergo surgical therapy. Early surgery improves neurologic outcomes compared with surgical procedures delayed by provisional conservative management. The outcome depends mainly on the preoperative neurologic conditions of the patient, the delay in diagnosis and initiation of treatment, the potential underlying diseases, the associated lesions, and the response to treatment. Spinal epidural abscess is a serious pathologic entity with a mortality rate of up to 5%. Although some cases have fulminant clinical and neurologic development, the disease can be successfully treated in many patients. However, a significant number of patients require long-term rehabilitation to regain neurologic function. During the recovery, decubitus complications are also a common finding.

Further Reading Abdel-Magid RA, Kotb HI.  Epidural abscess after spinal anesthesia: a favorable outcome. Neurosurgery. 1990;27:310–1. https://doi. org/10.1097/00006123-­199008000-­00025. Akhaddar A.  Spinal epidural abscesses. In: Akhaddar A, editor. Atlas of infections in neurosurgery and spinal surgery. Cham: Springer International Publishing; 2017. p.  171–6. https://doi. org/10.1007/978-­3-­319-­60086-­4_18. Bakar B, Tekkok IH. Lumbar periradicular abscess mimicking a fragmented lumbar disc herniation: an unusual case. J Korean Neurosurg Soc. 2008;44:385–8. https://doi.org/10.3340/jkns.2008.44.6.385.

673 Darouiche RO, Hamill RJ, Greenberg SB, Weathers SW, Musher DM. Bacterial spinal epidural abscess. Review of 43 cases and literature survey. Medicine (Baltimore). 1992;71:369–85. de Leeuw CN, Fann PR, Tanenbaum JE, Buchholz AL, Freedman BA, Steinmetz MP, et  al. Lumbar epidural abscesses: a systematic review. Glob Spine J. 2018;8:85S–95S. https://doi. org/10.1177/2192568218763323. Houston R, Gagliardo C, Vassallo S, Wynne PJ, Mazzola CA. Spinal epidural abscess in children: case report and review of the literature. World Neurosurg. 2019;126:453–60. https://doi.org/10.1016/j. wneu.2019.01.294. Khalifé M, Lebeaux D, Mainardi JL, Guigui P, Bouyer B. Neurological deficit secondary to a pre-sacral abscess with epidural extension up to L3: a case report and literature review. Orthop Traumatol Surg Res. 2017;103:133–5. https://doi.org/10.1016/j.otsr.2016.10.002. Kotilainen E, Sonninen P, Kotilainen P.  Spinal epidural abscess: an unusual cause of sciatica. Eur Spine J. 1996;5:201–3. https://doi. org/10.1007/BF00395515. Marshman LA, Bhatia CK, Krishna M, Friesem T. Primary erector spinae pyomyositis causing an epidural abscess: case report and literature review. Spine J. 2008;8:548–51. https://doi.org/10.1016/j. spinee.2006.12.011. Nyc MA, Francis L, Woloski JR. Spontaneous multiloculated lumbar abscess in a middle-aged male with unexplained progressive back pain and muscle weakness. Cureus. 2022;14:e27346. https://doi. org/10.7759/cureus.27346. Patel AR, Alton TB, Bransford RJ, Lee MJ, Bellabarba CB, Chapman JR.  Spinal epidural abscesses: risk factors, medical versus surgical management, a retrospective review of 128 cases. Spine J. 2014;14:326–30. https://doi.org/10.1016/j.spinee.2013.10.046. Pitaro NL, Tang JE, Arvind V, Cho BH, Geng EA, Amakiri UO, et al. Readmission and associated factors in surgical versus non-surgical management of spinal epidural abscess: a nationwide readmissions database analysis. Glob Spine J. 2021;13:1533–40. https://doi. org/10.1177/21925682211039185. Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a meta-­ analysis of 915 patients. Neurosurg Rev. 2000;23:175–204. https:// doi.org/10.1007/pl00011954. Schwab JH, Shah AA. Spinal epidural abscess: diagnosis, management, and outcomes. J Am Acad Orthop Surg. 2020;28:e929–38. https:// doi.org/10.5435/JAAOS-­D-­19-­00685. Yuksel KZ, Senoglu M, Yuksel M, Gul M. Brucellar spondylo-discitis with rapidly progressive spinal epidural abscess presenting with sciatica. Spinal Cord. 2006;44:805–8. https://doi.org/10.1038/ sj.sc.3101938.

Spinal Subdural Abscesses

54.1 Generalities and Relevance Most intraspinal suppurative collections are contained in the epidural space, rarely within the spinal cord parenchyma. Suppurative material can also develop between the dura mater and the arachnoid layer of the meninges (also known as subdural space or intradural-extramedullary space) and is called spinal subdural abscess or spinal subdural empyema (Fig. 54.1). “Abscess” is characterized by a capsule that separates the suppurative material from normal adjacent structures; while “empyema” is attributed to a purulent material within a preexisting anatomic cavity. However, “abscess” and “empyema” are often used interchangeably in the literature. Until 2009, some 65 cases of spinal subdural abscesses have been previously reported in the literature. As with other intraspinal canal infections, subdural abscesses represent a serious pathologic entity that can lead

54

to life-threatening sepsis if not diagnosed promptly and treated appropriately. In the lumbosacral spinal canal, subdural suppurations have the potential to cause secondary neurologic damage by compressing the cauda equina nerve roots. In the spinal subdural space, the most common site of this infection was the lumbar and thoracic; but involvement of multiple spinal segments is not rare because the suppurative material can spread easily through the subdural space. Development of this spinal infectious disease may occur through: –– Hematogenous spread from a distant source of infection. –– Contiguous extension from a contiguous infection. –– Direct inoculation (iatrogenic procedures). –– A significant number of cases remain “cryptogenic”. Many underlying diseases and some predisposing factors can be identified in the patients such as intravenous drug abuse, human immunodeficiency virus infection, diabetes mellitus, alcoholism, chronic renal failure, hepatic cirrhosis, concomitant malignant tumor, morbid obesity, rheumatic heart valve disease, and tuberculosis. Furthermore, any immunosuppressive treatment can predispose to support spinal canal infections. Spinal subdural abscesses are encountered in all age groups from children (especially those with spinal congenital midline defects) to aging adults (particularly those with one or more comorbidities).

54.2 Clinical Presentations

Fig. 54.1  Illustration of a lumbar subdural abscess compressing the thecal sac contents as seen in axial and sagittal sections. The dura is shown in green and the arachnoid in blue

Usually, clinical signs and symptoms of intraspinal canal infections are nonspecific. Initially, clinical findings may be unclear and confusing due to other predisposing medical problems.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_54

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In 1973, Fraser et  al. defined the classical symptomatic triad spinal subdural abscesses containing: • Fever. • Neck or back pain. • Spinal cord or cauda equina compression. In the lumbosacral spine, patients with acute forms present with lumbar backache and varying degrees of radicular pain with or without sciatica. Then, rapidly progressive neurologic deficits developed below the level of the abscess including muscle weakness in one or both legs, sphincter dysfunction, and erectile dysfunction. Indeed, many patients will present with partial or complete cauda equina syndrome (CES) due to nerve root compression. Unlike epidural forms, there is no to mild spinal tenderness on spinal percussion in patients with spinal subdural abscess. However, meningism is a common symptom. Overall, systemic signs of infection (fever, malaise, irritability, night sweats, and headache) are common but inconstant. Chronic presentations tend to have less specific symptomatology simulating intradural tumors with a progressive neurological deficit and low back pain without fever. ­ Nevertheless, signs and symptoms depend on the exact location of the suppuration, the volume and number of collections/abscesses and their chronicity, and the associated lesions. Progression of neurologic symptoms tends to be faster in patients with a spinal subdural abscess than in those with an epidural abscess. Potential underlying diseases and some predisposing factors should constantly be taken into consideration, especially the recent history of sepsis or an invasive procedure or a congenital spinal malformation.

54.3 Imaging Features Computed tomography (CT) scan is normal unless there is a combination of spinal osteomyelitis or discitis. Sometimes, intraspinal gas (air bubbles) may be seen in the subdural space. MRI is the imaging procedure of choice to confirm the presence of a subdural suppurative collection and to determine its exact location in the spinal canal which is important for planning surgery. Typical abscess appears as a poorly delimited collection with hypo or isointense signal on T1-weighted images and hyperintense signal on T2-weighted images. There is a rim enhancement following gadolinium injection. Collections that are fluid-filled and thus easily drained tend to be hyper-

Table 54.1  The main intradural lumbosacral lesions mimicking spinal subdural abscesses Vascular

Cavernoma, vascular malformations (AVM, AVF) Hematoma Spontaneous (anticoagulation), post-traumatic Arachnoid cysts Leptomeningeal cysts Granulomatous Tuberculoma, sarcoidosis Tumors Schwannoma, meningioma, neurofribroma, or metastases Inflammation Arachnoiditis, Guillain–Barré syndrome Dysembryogenetic Lipoma, epidermoid cyst, dermoid cyst, teratoma, neurenteric cyst Degenerative Intradural lumbar disc herniation Iatrogenic Foreign bodies

intense on T2-weighted images and will enhance peripherally around a central core of hypointensity on T1-weighted images. Unlike epidural abscess, the extradural fat tissue is conserved in subdural abscess and there is no interior displacement of the dura. Fat suppression sequences are particularly important in making the diagnosis by removing the increased signals of extradural fat and bone marrow. Also, diffusion-weighted imaging (DWI) can be a useful tool in differentiating abscesses from tumors. Generally, the purulent fluid demonstrates a high signal intensity on DWI and low ADC values, reflecting decreased diffusion properties unlike those for other purely cystic collections such as arachnoid cysts. Screening for a congenital spine anomaly can help determine the diagnosis, especially in children. MRI is also useful in detecting changes of subdural abscesses from progression to remission/regression in patients under antimicrobial therapy. Topographically, the spinal subdural abscess should be differentiated from other intradural lumbosacral lesions (Table  54.1) whether they are vascular, tumoral, traumatic, iatrogenic, inflammatory, granulomatous, or malformative.

54.4 Laboratory Findings Leukocyte count, erythrocyte sedimentation rate, and C-reactive protein are frequently found elevated, but they are not sensitive nor specific indicators. However, elevated procalcitonin levels can be a strong indication for determining the presence of bacterial infections. Furthermore, blood culture can be useful. Lumbar puncture for CSF analysis is not necessary and has potential morbidity. Screening for other potential causes of infection is important.

Further Reading

Purulent material should be tested for aerobic and anaerobic microorganisms, antimicrobial susceptibility, and additional Mycobacteria species. Most spinal subdural abscesses were attributed to Staphylococcus aureus infection. However, other various pathogens can also be involved such as Streptococcus species, Escherichia coli, Pseudomonas aeruginosa, S. pneumoniae, Peptococcus magnus, and Mycobacterium tuberculosis.

54.5 Treatment Options and Prognosis Generally, the spinal subdural abscess is treated by prompt surgical drainage of the purulent material and appropriate antibiotics administration. Surgical procedures typically comprise decompressive laminectomy at the appropriate levels, dura incision (durotomy), surgical drainage of the suppuration, and antiseptic irrigation. At best, the arachnoid layer must be conserved. Then the dura mater will be closed in a hermetic manner to avoid a possible postoperative CSF fistula. Surgery can also be used to establish the diagnosis. Appropriate intravenous antibiotic agents are used for 4–6 weeks, followed by additional 2–3 months of oral antibiotics. Tubercular and fungal abscesses should be treated with correct anti-infective drugs for many months. Conservative management with antibiotic therapy alone is not desirable, although some patients were treated conservatively with good results. Overall prognosis is considerably better for patients who undergo surgical treatment. The outcome depends mainly on the preoperative neurologic conditions of the patient, the delay in diagnosis and initiation of treatment, the potential underlying diseases, the associated lesions, and the response to treatment. Spinal subdural abscess is a serious pathologic entity with a mortality rate of up to 25% in 1992. Nowadays, death is a relatively rare event. Although clinical and neurologic development is frequently fulminant, the disease can be successfully treated in many patients with motor function improved more easily than sphincter one. A significant number of patients require long-term rehabilitation and nursing to regain neurologic function. During the recovery, decubitus complications are also a common problem.

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Further Reading Akhaddar A.  Spinal subdural abscesses. In: Akhaddar A, editor. Atlas of infections in neurosurgery and spinal surgery. Cham: Springer International Publishing; 2017. p.  177–81. https://doi. org/10.1007/978-­3-­319-­60086-­4_19. Bartels RH, de Jong TR, Grotenhuis JA. Spinal subdural abscess. Case report. J Neurosurg. 1992;76:307–11. https://doi.org/10.3171/ jns.1992.76.2.0307. Chen SZ, Shimer AL, Nacey NC.  Spinal subdural abscess following repeat lumbar microdiscectomy: a case report of imaging findings for a rare infection. Clin Imaging. 2017;44:74–8. https://doi. org/10.1016/j.clinimag.2017.04.010. Collis RE, Harries SE.  A subdural abscess and infected blood patch complicating regional analgesia for labour. Int J Obstet Anesth. 2005;14:246–51. https://doi.org/10.1016/j.ijoa.2005.03.002. Coumans JV, Walcott BP.  Rapidly progressive lumbar subdural empyema following acromial bursal injection. J Clin Neurosci. 2011;18:1562–3. https://doi.org/10.1016/j.jocn.2011.03.009. Gleeson JJ, Berg AJ, Loughenbury PR, Selvanathan SK, Leung A. Spontaneous posterior subdural pyogenic Escherichia coli abscess secondary to lumbar spondylodiscitis. Cureus. 2021;13:e13703. https://doi.org/10.7759/cureus.13703. Kraeutler MJ, Bozzay JD, Walker MP, John K.  Spinal subdural abscess following epidural steroid injection. J Neurosurg Spine. 2015;22:90–3. https://doi.org/10.3171/2014.9.SPINE14159. Miura I, Kubota M, Momosaki O, Takebayashi K, Kawamata T, Yuzurihara M.  Spinal subdural abscess following transforaminal lumbar interbody fusion. Case Rep Orthop. 2020;2020:7372821. https://doi.org/10.1155/2020/7372821. Park SW, Yoon SH, Cho KH, Shin YS, Ahn YH.  Infantile lumbosacral spinal subdural abscess with sacral dermal sinus tract. Spine (Phila Pa 1976). 2007;32:E52–5. https://doi.org/10.1097/01. brs.0000251012.37188.37. Ramos AD, Rolston JD, Gauger GE, Larson PS. Spinal subdural abscess following laminectomy for symptomatic stenosis: a report of 2 cases and review of the literature. Am J Case Rep. 2016;17:476–83. https://doi.org/10.12659/ajcr.897463. Sandler AL, Thompson D, Goodrich JT, van Aalst J, Kolatch E, El Khashab M, et  al. Infections of the spinal subdural space in children: a series of 11 contemporary cases and review of all published reports. A multinational collaborative effort. Childs Nerv Syst. 2013;29:105–17. https://doi.org/10.1007/s00381-­012-­1916-­4. Sorenson TJ, Lanzino G. Intradural Staphylococcus aureus abscess of the cauda equina in an otherwise healthy patient. Case Rep Surg. 2019;2019:4860420. https://doi.org/10.1155/2019/4860420. Velissaris D, Aretha D, Fligou F, Filos KS.  Spinal subdural Staphylococcus aureus abscess: case report and review of the literature. World J Emerg Surg. 2009;4:31. https://doi. org/10.1186/1749-­7922-­4-­31. Vural M, Arslantaş A, Adapinar B, Kiremitçi A, Usluer G, Cuong B, Atasoy MA. Spinal subdural Staphylococcus aureus abscess: case report and review of the literature. Acta Neurol Scand. 2005;112:343– 6. https://doi.org/10.1111/j.1600-­0404.2005.00496.x.

Lumbar Adhesive Arachnoiditis

55.1 Generalities and Relevance Lumbar adhesive arachnoiditis is a rare pathologic condition defined as an inflammation of the arachnoid layer and the arachnoid space leading to scar formation between the intrathecal rootlets and resulting in compression of the cauda equina nerve roots (Fig. 55.1). Adhesive arachnoiditis of lumbosacral nerve roots is an important clinical entity because it may induce various degrees of neurological symptoms from asymptomatic to painful lumbosacral radicular pain and even complete paraplegia. So, the true incidence of this rare disease is not known. However, adult women seem more usually affected than men with a mean age of around 50 years old. In histopathology study, there is a mixture of arachnoid and pia mater inflammatory changes, thickening, radicular edema, and fibrosis. Also, arachnoid hyalinization can be associated. For some authors, some chronic forms of adhesive arachnoiditis may induce an arachnoiditis ossificans [c.f. Chap. 56 about Arachnoiditis Ossificans]. Inflammatory biomarkers may be elevated but are not specific.

55

Many factors or associated diseases are typically seen in patients with lumbar adhesive arachnoiditis such as: • Trauma: postspinal surgery (postoperative healing process) or external trauma • Infection (mainly bacterial meningitis) • Other inflammatory conditions of the meninges • Spinal tumors • Spinal anesthesia • Spinal epidural steroid injections • Myelography contrast agents (the most common cause in the past) • Bleeding Sometimes, the exact cause is not known and the arachnoiditis is then considered “idiopathic”. For a long time, the most common cause of arachnoiditis was the injection of oil-based contrast media into the subarachnoid space during myelography. Nowadays, other iatrogenic damages (i.e., spinal surgery, dural violation, spinal tap, injectable subarachnoid drugs, or contrast agents) are among the most frequent factors for the development of lumbar adhesive arachnoiditis.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_55

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a

b

c

d

Fig. 55.1  The three main features of “Adhesive Arachnoiditis” compared to normal appearance (a). Central conglomerations of adherent nerve roots (b). “Empty thecal sac sign”: the thecal sac appears devoid

of its cauda equina roots (c). Subarachnoid space is filed with inflammatory soft tissue mass without CSF (d). The dura appears in blue, the arachnoid layer in green, and the nerve roots in brown

55.2 Clinical Presentations

Some cases can be “asymptomatic” and the lesions will be detected on neuroimaging studies performed for an unrelated reason sometimes several years ago (incidental imaging findings). There was no uniform clinical presentation in the patients. Nevertheless, most cases develop progressive spinal and neurologic radicular symptoms over several weeks or months. Acute forms are rare. Other symptoms may be correlated to other underlying etiologies of the disease. Neurophysiologic studies (e.g., electromyography) may be used to assess the lower limbs’ nerve damage.

Anamnestic data on preexisting disease, previous spinal surgery, spinal tap, or injectable subarachnoid drugs/contrast agents could be very helpful to identify the expected cause of symptoms. Clinical symptoms and signs of lumbar adhesive arachnoiditis are very variable, overall nonspecific, and similar to those associated with more common lumbosacral spinal conditions including low back pain, uni or bilateral lower limb radiculopathy paresthesia, lower limb weakness, bowel/ bladder dysfunction, and even partial or complete cauda equina syndrome. However, “neuropathic” manifestations are more common than those found with other degenerative lumbosacral diseases.

55.3  Imaging Features

681

55.3 Imaging Features Adhesive arachnoiditis is principally an imaging diagnosis. Magnetic resonance imaging (MRI) is the neuroimaging procedure of choice for the diagnosis. There are three main features: (Fig. 55.1). (a) Central conglomerations of adherent nerve roots into the dural sac. (b) “Empty thecal sac sign”: the thecal sac appears devoid of its cauda equina roots because nerve roots are adherent to the parietal arachnoid peripherally (Fig. 55.2). (c) Subarachnoid space is filed with inflammatory soft tissue mass without CSF signal (Fig. 55.3).

Fig. 55.2  “Empty thecal sac sign”: the thecal sac appears devoid of its cauda equina roots (arrows) because nerve roots are adherent to the parietal arachnoid peripherally as seen on lumbar sagittal (a) and axial T2-weighted MRI (b, c). This patient was previously operated on for an L4–L5 disc herniation

a

There is usually no or slight gadolinium contrast enhancement (Fig. 55.4). When used, myelography may show complete block or clumping cauda equina nerve roots. Rarely, adhesive arachnoiditis can be associated with intrathecal calcification/ossification recognized as “arachnoiditis ossificans”. This last form is better demonstrated on computed tomography scan [c.f. Chap. 56 about Arachnoiditis Ossificans]. The main differential of adhesive arachnoiditis is  leptomeningeal carcinomatosis and sometimes secondary arachnoid cysts.

b

c

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55  Lumbar Adhesive Arachnoiditis

Fig. 55.3 Adhesive arachnoiditis from L4 to S1 vertebral level (arrows) as seen on sagittal (a) and axial T2-weighted MRI (b). Subarachnoid space is filed with inflammatory soft tissue mass without CSF signal. The appearance of normal cauda equina nerve roots (c)

a

b

c

a

b

c

Fig. 55.4  Lumbar sagittal T2- (a) and post-gadolinium T1-weighted MRI (b, c) showing diffuse adhesive arachnoiditis (arrowheads) with slight gadolinium contrast enhancement (arrows)

Further Reading

55.4 Treatment Options and Prognosis The best management strategy for patients with adhesive arachnoiditis is not well known due to the complexity of this disease. Most therapeutic methods are conservative using pain control and physical therapies. Opioid and non-opioid painkillers, steroids, and spinal cord stimulation can be named among the most widely used systems. These may result in more or less control of the patient’s pain. Some other neuroinflammation suppressor agents have been suggested for refracted pains like naltrexone, ketorolac, and corticosteroid (methylprednisolone or dexamethasone), but the results are controversial. The efficacy of decompressive surgical procedures (arachnoid dissection with or without duraplasty) remains debated and rarely used. Indeed, it is important to know that there is an important adherence of the lesion to the cauda equina nerve roots. Therefore, some authors recommended a simple decompressive laminectomy without durotomy. Overall, the decisions are founded on individual cases. Clinicians should be aware of this rare but existing pathologic entity.

Further Reading Bourne IH.  Lumbo-sacral adhesive arachnoiditis: a review. J R Soc Med. 1990;83:262–5. Eisenberg E, Goldman R, Schlag-Eisenberg D, Grinfeld A.  Adhesive arachnoiditis following lumbar epidural steroid injections: a report of two cases and review of the literature. J Pain Res. 2019;12:513–8. https://doi.org/10.2147/JPR.S192706. Etchepare F, Roche B, Rozenberg S, Dion E, Bourgeois P, Fautrel B. Post-lumbar puncture arachnoiditis. The need for directed ques-

683 tioning. Jt Bone Spine. 2005;72:180–2. https://doi.org/10.1016/j. jbspin.2004.03.013. Grewal P, Hall JP, Jhaveri M, Dafer RM.  Cerebral vasculopathy and spinal arachnoiditis: two rare complications of ventriculitis post subarachnoid hemorrhage. Cureus. 2020;12:e12241. https://doi. org/10.7759/cureus.12241. Iampreechakul P, Jitpun E, Wangtanaphat K, Lertbutsayanukul P, Khunvutthidee S, Siriwimonmas S. Filum terminale arteriovenous fistula coexisting with a large L2–L3 disc sequestration and associated diffuse lumbar arachnoiditis. Asian J Neurosurg. 2021;16:412– 7. https://doi.org/10.4103/ajns.AJNS_489_20. Johnson CE, Sze G.  Benign lumbar arachnoiditis: MR imaging with gadopentetate dimeglumine. AJR Am J Roentgenol. 1990;155:873– 80. https://doi.org/10.2214/ajr.155.4.2119124. Jurga S, Szymańska-Adamcewicz O, Wierzchołowski W, Pilchowska-­ Ujma E, Urbaniak Ł. Spinal adhesive arachnoiditis: three case reports and review of literature. Acta Neurol Belg. 2021;121:47–53. https://doi.org/10.1007/s13760-­020-­01431-­1. Krätzig T, Dreimann M, Mende KC, Königs I, Westphal M, Eicker SO.  Extensive spinal adhesive arachnoiditis after extradural spinal infection-spinal dura mater is no barrier to inflammation. World Neurosurg. 2018a;116:e1194–203. https://doi.org/10.1016/j. wneu.2018.05.219. Krätzig T, Dreimann M, Mende KC, Königs I, Westphal M, Eicker SO. Extensive spinal adhesive arachnoiditis after extradural spinal infection-spinal dura mater is no barrier to inflammation. World Neurosurg. 2018b;116:e1194–203. https://doi.org/10.1016/j. wneu.2018.05.219. Parenti V, Huda F, Richardson PK, Brown D, Aulakh M, Taheri MR.  Lumbar arachnoiditis: does imaging associate with clinical features? Clin Neurol Neurosurg. 2020;192:105717. https://doi. org/10.1016/j.clineuro.2020.105717. Petty PG, Hudgson P, Hare WS.  Symptomatic lumbar spinal arachnoiditis: fact or fallacy? J Clin Neurosci. 2000;7:395–9. https://doi. org/10.1054/jocn.1999.0223. Quiles M, Marchisello PJ, Tsairis P.  Lumbar adhesive arachnoiditis. Etiologic and pathologic aspects. Spine (Phila Pa 1976). 1978;3:45– 50. https://doi.org/10.1097/00007632-­197803000-­00010. Ross JS, Masaryk TJ, Modic MT, Delamater R, Bohlman H, Wilbur G, Kaufman B.  MR imaging of lumbar arachnoiditis. AJR Am J Roentgenol. 1987;149:1025–32. https://doi.org/10.2214/ ajr.149.5.1025.

Arachnoiditis Ossificans

56

56.1 Generalities and Relevance

–– Type III: calcifications englobing the caudal nerve roots [in lumbar spine]

Arachnoiditis ossificans is a rare pathologic entity defined by calcification or ossification of the spinal arachnoid layer. The lesion is typically limited to the spinal thoracic regions (2/3 of cases) and less frequently in the lumbar spine (1/4 of cases).

Arachnoiditis ossificans is typically seen in patients with a history of prior surgery or dural violation. However, multiple factors or associated pathologies may exist such as:

Arachnoiditis ossificans should be distinguished from: • The asymptomatic benign meningeal calcifications are sometimes found in surgery in elderly or autopsy studies. • Adhesive arachnoiditis that is an inflammation of the arachnoid layer and the cauda equina nerve roots that adhere to the meninges. (c.f. Chap. 55 about Lumbar Adhesive Arachnoiditis). First described in 1971 by Kaufman and Dunsmore, spinal arachnoiditis ossificans is a rare disease with fewer than a hundred cases reported to date in the literature. Ossification of the leptomeninges is an important condition because it may induce various degrees of progressive neurological deterioration by compressing the spinal cord or nerve roots. The pathogenesis of arachnoiditis ossificans is thought to develop in the setting of chronic adhesive arachnoiditis. The phenomenon starts with arachnoid membrane inflammation that can lead to scarring or fibrosis, which finally calcify or ossify. Sometimes, the exact cause is not known and the arachnoiditis ossificans is then considered “idiopathic”. Three types of arachnoiditis ossificans have been previously described: –– Type I: semicircular calcification [regularly in thoracic spine] –– Type II: circular calcification [in thoracic or lumbar spine]

• Chemically induced injury (e.g., injectable subarachnoid drugs or contrast agents) • Mechanically induced injury (e.g., spinal surgery, trauma, or bleeding) • Infection (e.g., meningitis or myelomeningitis) Besides these local factors, other general causes have been suspected.

56.2 Clinical Presentations Anamnestic data on preexisting disease, previous surgery, or trauma as well as spinal tap could be very helpful to identify the expected cause of symptoms. Clinical symptoms are various and nonspecific and are similar to those associated with other more common spinal conditions including low back pain, lower limb radiculopathy with or without paresthesia, or even partial or complete cauda equina syndrome (mostly lower limb weakness with bowel/bladder dysfunction). However, some patients may be asymptomatic (incidental imaging findings). There was no uniform clinical presentation in the patients. However, most cases develop progressive spinal and neurologic radicular symptoms over several months or years. Acute forms are rare. Electromyogram (EMG) or nerve conduction velocity (NCV) tests may be used to study the lower limb nerve damage. Other symptoms may be related to other primary etiologies of the disease.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_56

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56.3 Imaging Features

a

b

Magnetic resonance imaging (MRI) may sometimes demonstrate the calcifications/ossifications, but the results are nonspecific and may be confusing. The appearance of the ossification is variable and depends on the stage of the calcification/ossification. Most ossifications present with a high signal on T1-weighted sequences and a low or high signal on T2-weighted sequences. However, MRI is particularly useful for visualizing effects on adjacent cauda equina nerve roots. A spinal computed tomography scan is the imaging procedure of choice for the diagnosis of arachnoiditis ossificans. It demonstrates the intrathecal calcification/ossification within the spinal canal and evaluates the complete extension of the lesions. Both parenchymatous and bone windows are necessary as well as multiplanar reconstructions (MPR) (Figs. 56.1 and 56.2). In the axial planes, the hyperdense lesions may be circular (type II) or englobing the cauda equina roots (type III). Sometimes imaging appearances are atypical and may be confused with other potential calcified or ossified intradural lesions in the lumbosacral region such as: –– Benign meningeal calcifications (asymptomatic, small, and without the involvement of neurologic structures).

a

b

Fig. 56.2  Some calcifications/ossifications can be seen on lumbosacral anteroposterior X-ray (arrow) (a); however, these lesions are undetected on MRI (b)

c

d

Fig. 56.1  Lumbar arachnoiditis ossificans in a patient who had undergone multiple myelographic studies using oil-based contrast agents. Sagittal CT scan on parenchymatous (a) and bone windows (b) as well

as on axial views (c, d). There are multiple intrathecal calcified/ossified lesions within the spinal canal (arrows)

Further Reading

–– –– –– ––

Calcified hematoma. Calcified tumors (e.g., schwannoma or meningioma). Calcified abscesses. Retained intrathecal contrast medium.

56.4 Treatment Options and Prognosis The best management strategy for patients with arachnoiditis ossificans is unknown due to the rarity of this entity. In the literature, patients with no or mild symptomatology can be treated conservatively using pain control and physical therapies. In patients with severe or deteriorating symptoms due to this leptomeningeal ossification, surgery is often performed via decompressive laminectomy with or without intradural plaque excision. However, it is important to know that there is an important adherence of the lesion to the cauda equina nerve roots. Overall, in the lumbar spine, type II cases are more likely to be treated surgically. On the opposite, type III forms will be managed medically due to the high operative risk of nerve root sequel and even re-ossification. Approximately only one-half of those treated surgically showed improvement. Therefore, many authors recommended a decompressive laminectomy without intradural resection of the lesions developed in the lumbar spine.

Further Reading Benyaich Z, Laghmari M, Ait BS.  Arachnoiditis ossificans of the lumbar spine: a rare cause of progressive cauda equina syndrome. World Neurosurg. 2021;148:116–7. https://doi.org/10.1016/j. wneu.2021.01.057. Brunner A, Leoni M, Eustacchio S, Kurschel-Lackner S. Spinal arachnoiditis ossificans: a case-based update. Surg J (N Y). 2021;7:e174– 8. https://doi.org/10.1055/s-­0041-­1731448.

687 Domenicucci M, Ramieri A, Passacantilli E, Russo N, Trasimeni G, Delfini R.  Spinal arachnoiditis ossificans: report of three cases. Neurosurgery. 2004;55:985. https://doi.org/10.1227/01. neu.0000137281.65551.54. Faure A, Khalfallah M, Perrouin-Verbe B, Caillon F, Deschamps C, Bord E, et  al. Arachnoiditis ossificans of the cauda equina. Case report and review of the literature. J Neurosurg. 2002;97:239–43. https://doi.org/10.3171/spi.2002.97.2.0239. Frizzell B, Kaplan P, Dussault R, Sevick R.  Arachnoiditis ossificans: MR imaging features in five patients. AJR Am J Roentgenol. 2001;177:461–4. https://doi.org/10.2214/ajr.177.2.1770461. Kaufman AB, Dunsmore RH.  Clinicopathological considerations in spinal meningeal calcification and ossification. Neurology. 1971;21:1243–8. https://doi.org/10.1212/wnl.21.12.1243. Kriaa S, Hafsa C, Zbidi M, Laifi A, Golli M, Gannouni A. Arachnoiditis ossificans of the lumbar spine: a case report. Jt Bone Spine. 2006;73:765–7. https://doi.org/10.1016/j.jbspin.2006.01.024. Liu LD, Zhao S, Liu WG, Zhang SK.  Arachnoiditis ossificans after spinal surgery. Orthopedics. 2015;38:e437–42. https://doi. org/10.3928/01477447-­20150504-­91. Maulucci CM, Ghobrial GM, Oppenlander ME, Flanders AE, Vaccaro AR, Harrop JS. Arachnoiditis ossificans: clinical series and review of the literature. Clin Neurol Neurosurg. 2014;124:16–20. https:// doi.org/10.1016/j.clineuro.2014.06.024. Ng P, Lorentz I, Soo YS.  Arachnoiditis ossificans of the cauda equina demonstrated on computed tomography scanogram. A case report. Spine (Phila Pa 1976). 1996;21:2504–7. https://doi. org/10.1097/00007632-­199611010-­00020. Scalia G, Certo F, Maione M, Barbagallo GMV.  Spinal arachnoiditis ossificans: report of quadruple-triggered case. World Neurosurg. 2019;123:1–6. https://doi.org/10.1016/j.wneu.2018.11.203. Urits I, Chesteen G, Viswanath O. Arachnoiditis ossificans of the lumbosacral spine. Turk J Anaesthesiol Reanim. 2019;47:427–8. https:// doi.org/10.5152/TJAR.2019.63239. Varughese G.  Lumbosacral intradural periradicular ossification. Case report. J Neurosurg. 1978;49:132–7. https://doi.org/10.3171/ jns.1978.49.1.0132. Wang L, Wang YP.  Arachnoiditis ossificans of lumbosacral spine: a case report and literature review. Chin Med Sci J. 2014;29:125–7. https://doi.org/10.1016/s1001-­9294(14)60042-­0. Ward M, Mammis A, Barry MT, Heary RF. Novel association between intrathecal drug administration and arachnoiditis ossificans. World Neurosurg. 2018;115:400–6. https://doi.org/10.1016/j. wneu.2018.04.196.

Bertolotti’s Syndrome

57.1 Generalities and Relevance Bertolotti’s syndrome is the eponymous name of the congenital lumbosacral transitional vertebra (LSTV) that is liable for low back pain. (See also Chap. 3 about Sacralization and Lumbarization). Classically, there are varying degrees of fusion, unilateral or bilateral, between the last lumbar vertebra and the first sacral segment. In most cases, there is an unusual enlargement of the transverse process of L5 that either fuses or articulates with the sacrum or ilium bone and causes adjacent disc abnormalities (Table 57.1; Fig. 57.1). Consequently, this spinal anatomical variation may cause lower back pain (lumbalgia) along with buttock pain. Radicular pain and especially sciatica are unusual with Bertolotti’s syndrome, unlike other causes of lumbosacral extraforaminal stenosis (c.f. Chap. 38 about Lumbosacral Extraforaminal Stenosis [Far-outSyndrome]). However, sciatica associated with Bertolotti’s syndrome should be taken into consideration. Table 57.1  Castellvi classification for lumbosacral transitional vertebra (Fig. 57.1) Types Description I Dysplastic transverse process (triangular in shape, enlarged, measuring at least 19 mm in width) II Incomplete sacralization/ lumbarization (pseudo and neoarticulation between the transverse process and the sacrum) III Complete sacralization/ lumbarization (total bony fusion between the transverse process and the sacrum) IV Mixed

Subtypes I A unilateral I B bilateral II A unilateral II B bilateral III A unilateral III B bilateral Coexistence of type II A on one side and type III A on the opposite side

57

Mario Bertolotti (1876–1957) was an Italian radiologist, best recognized for his work regarding the articulation between the fifth lumbar vertebra and the sacrum. In 1917, he was the first to describe the assimilation of L5 into the sacrum. Bertolotti is considered the father of neuroradiology in Italy. The incidence of Bertolotti’s syndrome is expected between 4 and 18% in adult patients with low back pain, but this incidence seems to be higher in the adult population who are aged under 30. The occurrence of LSTV is higher in men than in women; however, lumbarization of S1 seems more frequent in women, while sacralization of L5 is more frequent in men. The modification or reduction of mobility at the lumbosacral level will be compensated at segments superior to the LSTV resulting in faster degeneration and straining over the superjacent disc and/or facet joint that may become symptomatic and interact with the adjacent nerve root (L4, L5, or S1) occasioning a “sciatic” pain. LSTV is associated with significantly more adjacent lumbar disc herniation, facet degeneration, osteophytes, sacroiliac joint dysfunction, and nerve root canal stenosis. However, for many authors, Bertolloti’s syndrome should be separated from extraforaminal stenosis at the lumbosacral junction and far-out-syndrome (c.f. Chap. 38 about Lumbosacral Extraforaminal Stenosis [Far-out-Syndrome]). Regarding LSTV, there are sometimes some variations in lumbosacral nerve distribution, particularly with L5, S1, and S2 nerve roots. Furthermore, there is a problem in the literature about the exact numbering of the lumbosacral vertebrae. For some authors, the spine is to be numbered from bottom to top, while it is top-down for others. For other clinicians, this problem has relatively low importance in clinical practice.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_57

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57  Bertolotti’s Syndrome

690 Fig. 57.1 Castellvi’s classification for lumbosacral transitional vertebra. Type I: Dysplastic transverse process (arrows). Type II: Incomplete sacralization/lumbarization. Type III: Complete sacralization/lumbarization. Type IV: Mixed (II and III). (a) Unilateral. (b) Bilateral

a

b

57.2 Clinical Presentations Many cases with LSTV will remain asymptomatic and the congenital anomaly will be found only incidentally on spinal imaging. The majority of symptomatic patients present with nonspecific back pain with or without facet joint pain. Lumboradicular pain is unusual as well as neurogenic claudication. Neurological deficits are rare and may include mild sensory and/or motor deficits with or without reflex abnormalities. Scoliosis  may be found to be associated. A work-up of low-back pain beginning with palpation, active and passive range of motion, and the straight leg raise test should be performed. In some cases, separating lumbosacral radiculopathy from sciatic peripheral mononeuropathy or lumbosacral plexopathy on clinical grounds can be difficult. Therefore, in such cases electrodiagnostic studies are decisive.

57.3 Paraclinic Features Lumbosacral antero-posterior and lateral standard radiographs are usually sufficient for identifying skeletal abnormality (Figs.  57.2, 57.3, 57.4, 57.5 and 57.6). Additional dynamic plain radiography including flexion, extension views, and even oblique views can be required if there is a potential preoperative instability. Both computed tomography (CT) scan (with reconstructed 3D images) and magnetic resonance imaging (MRI)

are more accurate for classifying LSTV than standard radiographs (Figs. 57.7, 57.8, 57.9 and 57.10). Besides the LSTV, certain associated spinal lesions should receive particular attention during neuroimaging assessment, in particular lumbar disc herniations, facet joint arthrosis, spinal canal, foraminal stenosis, osteophytosis, spondylolysis, and spondylolisthesis as well as sacroiliac joint disorders. MRI is useful when sciatic pain with lumbar disc herniations coexist. Coronal T2-weighted images are the most effective for diagnosing LSTV in addition to a concomitant pathology like far-out-syndrome in which the exiting nerve root is entrapped between the transverse segment of the last lumbar vertebra and the sacral alar or ilium (Figs. 57.9 and 57.10). In addition to other classic spinal imaging, bone scintigraphy may help detect potential sources of pain in Bertolotti patients. Local degenerative and metabolic changes in LSTV pseudoarticulation and sacroiliac joint can be detected as increased uptake in bone scintigraphy. Local anesthetic infiltration of the abnormal articulation or facet joint (block with lidocaine 2% and bupivacaine 0.5%) under fluoroscopic guidance can be used as a diagnostic tool to define the origin of pain in a patient with LSTV. Pain decreases in about 80% of cases following this percutaneous block infiltration, but it appears that the injection did not provide long-lasting relief. To prevent wrong-level lumbosacral spine surgery, it is imperative to correlate CT scan and/or MRI with preoperative and intraoperative radiographs. Effective communication between the spinal surgeon and the radiologist is crucial regarding the numbering of vertebral segments before surgery.

57.3  Paraclinic Features

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Fig. 57.2  Lumbosacral antero-posterior plain radiographs showing Type I A (a), Type II A (b), Type III A (c), and Type IV (d) of Castellvi’s classification

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Fig. 57.3  Lumbosacral antero-posterior plain radiographs showing Type I B (a), Type II B (b), and Type III B (c) of Castellvi’s classification

Fig. 57.4  Type II A of Castellvi’s classification (arrowheads) as seen on lumbosacral antero-posterior plain X-ray

57.3  Paraclinic Features

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Fig. 57.5  Type III A of Castellvi’s classification as seen on lumbosacral antero-posterior (a) and lateral (b) plain radiographs. Note the complete unilateral sacralization of L5 on the right side (arrows)

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Fig. 57.6  Type II B of Castellvi’s classification as seen on lumbosacral antero-posterior (a) and lateral (b) plain radiographs. Note the incomplete bilateral sacralization of L5 (arrows)

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Fig. 57.7  Type II A of Castellvi’s classification (arrows) as seen on lumbosacral antero-posterior plain X-ray (a), axial CT scan (b, c), and coronal reconstructions CT scan (d, e)

694 Fig. 57.8  Type III B of Castellvi’s classification (arrowheads) as seen on lumbosacral antero-posterior plain X-ray (a) and coronal reconstructions CT scan (b, c). Note the complete bilateral sacralization of L5 and the morphology of L5–S1 foramina (dotted circles). The L5 nerve roots are seen inside the foramina (arrows)

57  Bertolotti’s Syndrome

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Fig. 57.9  The same case as Fig. 57.8. Type III B Castellvi’s classification (arrowheads) on coronal T2-weighted MRI (a, b). Note the exiting L5 nerve roots inside the foramina (arrows)

57.4  Treatment Options and Prognosis Fig. 57.10  Type II B of Castellvi’s classification as seen on coronal T2-weighted MRI (a, b) and STIR MR sequences (c, d). Note the exiting L5 nerve roots inside the foramina (dotted circles)

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57.4 Treatment Options and Prognosis

Direct local anesthetic (e.g., lidocaine) and steroid injection (e.g., triamcinolone acetate) in the abnormal transitional Treatment of patients with Bertolotti’s syndrome ranges articulation and/or the facet joint produce successful relief of from conservative, nonsurgical treatment (including steroid pain, but did not provide long-lasting relief. Patients with and local anesthetic infiltration into the anomalous lumbosa- sciatic pain may require transforaminal or interlaminar epicral articulations) to surgical resection of the accessory joint dural steroid injections. with or without posterolateral fusion of the transitional The main surgical intervention includes pseudo-­ segment. articulation resection (AKA transverse processectomy) with Conservative management includes activity modification, nerve decompression. Sometimes, associated lesions may pharmacologic therapy (analgesics, nonsteroidal anti-­ need a further surgical procedure such as herniectomy, disinflammatory drugs, and muscle relaxants), and physical cectomy, foraminotomy, or lumbosacral fusion. Different therapy interventions. Posture-modifying exercises can treatment strategies have been offered, from classic posterior improve symptoms by improving muscle strength, coordina- open surgery to minimally invasive microendoscopy tion, and flexibility. technic.

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The nerve decompression requires the translocation of the nerve medially and the resection of the pseudoarticulation. A classic complication from this surgical procedure is transient hypesthesia. Initially, patients are treated conservatively before testing more invasive treatment options such as steroid and anesthetic injections. If conservative treatment is unsuccessful, surgery can be considered. For some authors, surgical resection of the LSTV should be performed in younger patients, who do not present with spine degeneration or disc herniation, and in only those with Castellvi Type I and II. Fusion may be indicated in patients with LSTV coexisted with increased motion, instability, and adjacent segment problems. Complications associated with surgical treatment include the risks of any spine surgery such as neurovascular injury, dural tear, cerebrospinal fluid fistula, thromboembolism, infection, anesthesia complication, persistent pain, iatrogenic spinal instability, and recurrence. Finally, radio-frequency ablation or denervation, using a high-frequency alternating current, is another potential treatment option and provided more or less a period of pain relief. Most patients (about 85% of cases) presented with Bertolotti’s syndrome had good results after the surgery without recurrence; however, some fair or poor results were reported (less than 15%). Although surgical outcomes are mostly positive, no randomized studies have recognized their efficiency versus conservative treatment.

Further Reading Abe E, Sato K, Shimada Y, Okada K, Yan K, Mizutani Y.  Anterior decompression of foraminal stenosis below a lumbosacral transitional vertebra. A case report. Spine (Phila Pa 1976). 1997;22:823– 6. https://doi.org/10.1097/00007632-­199704010-­00023. Bertolotti M.  Contribution to the knowledge of the vices of regional differentiation of the spine with special regard to the assimilation of the fifth lumbar vertebrae into the sacrum. La Radiologia Medica (Torino). 1917;4:113–44. Castellvi AE, Goldstein LA, Chan DP.  Lumbosacral transitional vertebrae and their relationship with lumbar extradural defects. Spine (Phila Pa 1976). 1984;9:493–5. https://doi. org/10.1097/00007632-­198407000-­00014. Chang CJ, Chiu YP, Ji HR, Chu CH, Chiu CD. Surgical interventions for Bertolotti’s syndrome: case report and review of unsatisfactory cases in the literature. BMC Surg. 2022;22:36. https://doi. org/10.1186/s12893-­022-­01498-­y. Crane J, Cragon R, O'Neill J, Berger AA, Kassem H, Sherman WF, Paladini A, Varrassi G, Odisho AS, Miriyala S, Kaye AD. A comprehensive update of the treatment and management of Bertolotti’s syndrome: a best practices review. Orthop Rev (Pavia). 2021;13:24980. https://doi.org/10.52965/001c.24980. Iwasaki M, Akiyama M, Koyanagi I, Niiya Y, Ihara T, Houkin K. Double crush of L5 spinal nerve root due to L4/5 lateral recess stenosis and bony spur formation of lumbosacral transitional vertebra pseudoarticulation: a case report and review. NMC Case Rep J. 2017;4:121– 5. https://doi.org/10.2176/nmccrj.cr.2016-­0308.

57  Bertolotti’s Syndrome Ju CI, Kim SW, Kim JG, Lee SM, Shin H, Lee HY. Decompressive L5 transverse processectomy for Bertolotti’s syndrome: a preliminary study. Pain Physician. 2017;20:E923–32. Kanematsu R, Hanakita J, Takahashi T, Minami M, Tomita Y, Honda F.  Extraforaminal entrapment of the fifth lumbar spinal nerve by nearthrosis in patients with lumbosacral transitional vertebrae. Eur Spine J. 2020;29:2215–21. https://doi.org/10.1007/ s00586-­020-­06460-­1. Kawtharani S, Bsat SA, El Housheimy M, Moussalem C, Halaoui A, Sunna T. A case of Bertolotti’s syndrome as a cause of sciatica. Surg Neurol Int. 2021;12:516. https://doi.org/10.25259/SNI_756_2021. Knopf J, Lee S, Bulsara K, Moss I, Choi D, Onyiuke H. Onyiuke grading scale: a clinical classification system for the diagnosis and management of Bertolotti syndrome. Neurochirurgie. 2021;67:540–6. https://doi.org/10.1016/j.neuchi.2021.05.002. Konin GP, Walz DM. Lumbosacral transitional vertebrae: classification, imaging findings, and clinical relevance. AJNR Am J Neuroradiol. 2010;31:1778–86. https://doi.org/10.3174/ajnr.A2036. Kumar J, Ali S, Zadran N, Singh M, Ahmed Z. A rare case of Bertolotti’s syndrome in a young patient: a case report and literature review. Cureus. 2020;12:e10957. https://doi.org/10.7759/cureus.10957. Leonardi M.  A history of neuroradiology in Italy. AJNR Am J Neuroradiol. 1996;17:721–30. Lian J, Levine N, Cho W. A review of lumbosacral transitional vertebrae and associated vertebral numeration. Eur Spine J. 2018;27:995– 1004. https://doi.org/10.1007/s00586-­018-­5554-­8. Liebrand B, Brakel K, Boon A, van der Weegen W, Wal SV, Vissers KC. Diagnostic treatment-level discrepancies in patients with lumbosacral radicular pain and lumbar spine anomalies. Reg Anesth Pain Med. 2022;47:177–82. https://doi.org/10.1136/rapm-­2021-­103174. Louie CE, Hong J, Bauer DF. Surgical management of Bertolotti’s syndrome in two adolescents and literature review. Surg Neurol Int. 2019;10:135. https://doi.org/10.25259/SNI-­305-­2019. Lupo M. Prof. Mario Bertolotti. Minerva Med. 1958;49:840–6. Matsumoto M, Watanabe K, Ishii K, Tsuji T, Takaishi H, Nakamura M, et  al. Posterior decompression surgery for extraforaminal entrapment of the fifth lumbar spinal nerve at the lumbosacral junction. J Neurosurg Spine. 2010;12:72–81. https://doi.org/10.3171/2009.7 .SPINE09344. McGrath K, Schmidt E, Rabah N, Abubakr M, Steinmetz M. Clinical assessment and management of Bertolotti syndrome: a review of the literature. Spine J. 2021;21:1286–96. https://doi.org/10.1016/j. spinee.2021.02.023. O'Driscoll CM, Irwin A, Saifuddin A. Variations in morphology of the lumbosacral junction on sagittal MRI: correlation with plain radiography. Skelet Radiol. 1996;25:225–30. https://doi.org/10.1007/ s002560050069. Quinlan JF, Duke D, Eustace S. Bertolotti’s syndrome. A cause of back pain in young people. J Bone Jt Surg Br. 2006;88:1183–6. https:// doi.org/10.1302/0301-­620X.88B9.17211. Shibayama M, Ito F, Miura Y, Nakamura S, Ikeda S, Fujiwara K.  Unsuspected reason for sciatica in Bertolotti’s syndrome. J Bone Jt Surg Br. 2011;93:705–7. https://doi. org/10.1302/0301-­620X.93B5.26248. Takata Y, Sakai T, Higashino K, Goda Y, Mineta K, Sugiura K, et al. Minimally invasive microendoscopic resection of the transverse process for treatment of low back pain with Bertolotti’s syndrome. Case Rep Orthop. 2014;2014:613971. https://doi. org/10.1155/2014/613971. Weber J, Ernestus RI. Transitional lumbosacral segment with unilateral transverse process anomaly (Castellvi type 2A) resulting in extraforaminal impingement of the spinal nerve: a pathoanatomical study of four specimens and report of two clinical cases. Neurosurg Rev. 2010;34:143–50. https://doi.org/10.1007/s10143-­010-­0300-­7.

De Anquin’s Disease (Spinous Engagement Syndrome)

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58.1 Generalities and Relevance De Anquin’s disease (DAS), also known as “spinous engagement syndrome”, “engaged spina bifida”, or “clasp-knife deformity”, is a rare congenital anomaly found at the posterior lumbosacral spine and characterized by: • Hypertrophy (overgrowth) of the spinous process of the last lumbar vertebra (usually L5) • A posterior midline defect of the first sacral vertebra (usually S1) • The spinous process of the upper vertebra intrudes into the posterior defect of the lower vertebra causing reduction of the midsagittal diameter of the upper sacral canal as well as compression of the dural sac and its radicular contents (Fig. 58.1) This phenomenon may remain asymptomatic for a long time, but under certain conditions (e.g., lumbar lordosis) will appear spinal and/or lumbosacral radicular pain. This atypical anatomical and biomechanical entity was first described in 1934 by the American radiologist Albert Ferguson (1896–1976), whereas the term “clasp-knife deformity” was coined by GW Henry in 1958 as a similarity to the blade (representing the spinous process of L5) of a pocket knife folding into its handle (representing the spina bifida of S1) (Fig. 58.2). However, it was the Argentinian orthopedic surgeon Carlos de Anquin (1916–1999) who reported the first detailed series of DAS. Since then, about 30 cases were published in the literature. There are sometimes some variations from this previous “classic” description like the possibility of the existence of a free/mobile remnant of the sacral spinous process or a single enlarged and hooked (long tongue) lumbar spinous process. In

Fig. 58.1  In lumbar spine hyperextension, the spinous process of the upper vertebra (L5) intrudes into the posterior defect of the lower vertebra (S1), causing reduction of the midsagittal diameter of the upper sacral canal as well as compression of the dural sac and its nerve roots (arrow)

one case, hypertrophy of the spinous process of L4 was pressing on the posterior arch defect of L5. Rarely, there is a more extensive osseous defect over multiple sacral segments. DAS can be associated with other spinal and intraspinal disorders such as degenerative disc disease and variable degrees of intradural congenital malformations. The overall incidence of DAS is not known with certainty among individuals with spina bifida occulta. However, symptomatic forms are rare and the majority of reported cases are males in their 30s or 40s.

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Neurological evaluation should include testing for normal and abnormal reflexes, examination of rectal tone, and perianal sensation. The straight leg-raising test is often not present. Potential associated degenerative and other congenital diseases should be taken into consideration. It is important to determine if patients have other spinal signs and symptoms more typical of degenerative or congenital spondylolisthesis, spinal stenosis, or even lumbar disc disorder. If needed, a positive diagnostic test with local anesthetic injection may be used to confirm DAS. Certainly, many patients with clasp-knife deformity will remain asymptomatic and the disorder will be found only incidentally on spinal imaging. Fig. 58.2  The blade (representing the spinous process of L5) of a pocket knife folding into its handle (representing the spina bifida of S1)

58.2 Clinical Presentations Typically, DAS results in chronic low back pain that may radiate towards one or both legs following lumbar extension or some spinal hyperlordotic position and is relieved during spinal flexion. The expression “dynamic type of stenosis” was suggested to explain the pain-producing mechanism. About one-third of patients have lumbosacral radicular pain; however, neurologic deficits of the affected roots are unusual. Occasionally, some patients could notice a deterioration of their sexual function as well as disorders in their bowel and urinary habits. In only one patient, there was even an intermittent cauda equina syndrome secondary to a severe S1 spina bifida engagement syndrome and a bilateral L5 spondylolysis resulting in an important lower lumbar spinal stenosis. During clinical examination, the localized midline back pain is reproduced upon finger pressure at the level of the posterior lumbosacral junction and upper part of the sacrum. Neurological examination may demonstrate signs of nerve root compression. Some patients could present motor and sensory deficits in one or rarely multiple dermatomes.

58.3 Imaging Features The results of plain radiographs show a reduction in the normal lumbar lordosis. The L5 spinous process looked enlarged and elongated with its close approximation to the adjacent posterior arch of S1 (Fig. 58.3). Sometimes, there is the existence of a free remnant of the S1 spinous process or a hooked spinous process of L5. DAS can be accompanied by other degenerative spinal lesions such as facet joint degenerations, loss of intervertebral disc height, spinal stenosis, bilateral spondylolysis, or changes in sacroiliac joints. Dynamic lateral flexion-extension radiographs may be used to show the impingement of the L5 spinous process on the S1 spina bifida. Lumbosacral computed tomography (CT) studies including 3-dimensional reconstruction delineate the precise morphology of the lumbosacral junction. CT scan can demonstrate the lamina defects and the impinging cranial spinous process (Fig. 58.4). In some patients, additional disc protrusions might be associated. Magnetic resonance imaging (MRI) can be useful in the evaluation of potential lumbar disc herniation or other lumbosacral intradural congenital lesions. In addition, neurophysiologic studies could assess sensorimotor conductivity originating from L4 to S1 nerve roots.

58.4  Treatment Options and Prognosis Fig. 58.3 Antero-posterior (a) and lateral (b) plain radiographs showing a reduction in the normal lumbar lordosis. The L5 spinous process looked enlarged and elongated with its close approximation to the adjacent posterior arch of S1 (dotted frames)

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58.4 Treatment Options and Prognosis

Fig. 58.4  Axial lumbosacral CT scan revealing the S1 lamina defect and the adjacent cranial spinous process (L5)

Therapies for DAS range from conservative measures to interventional radiology and surgical intervention. Initially, and outside any neurologic emergency, the pain may be managed conservatively. Conservative therapy includes bed rest, pain control medications, physiotherapy (mainly lumbar flexion exercises), and other physical modalities resulting in more or less control of the patient’s pain. If there is a failure of pain reduction following conservative treatments, percutaneous injections are then considered. Under fluoroscopy or CT-guided, local anesthesia and ­corticosteroid injection can be applicated below the hypertrophic spinous process (often L5). Posterior decompressive surgery is indicated for cases that failed to improve under conservative therapy or percutaneous interventional radiology. The common procedure includes surgical resection of the concerned lumbar spinous process. The intervention must be completed by removing the membrane that replaces the bone defect and taking care of the dissection of the adherent dura to avoid any CSF leak.

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The gap that remains may be filled with adipose tissue or a flap of muscle to prevent postoperative adhesions in the area of the spina bifida. Potential symptomatic-associated degenerative lesions will be treated accordingly. If needed, arthrodesis could be performed if there is an abnormal degree of lumbosacral mobility (i.e., segmental instability). About half of the symptomatic cases may need decompressive surgery with an immediate and complete postoperative release of pain and a good clinical outcome. No serious postoperative complications were reported. Some rare patients complained of remaining lumbosacral pain which was attributed to other lumbosacral degenerative disorders.

Further Reading Agrawal A, Rao GM.  Asymptomatic spina bifida occulta involving sacrum in an elderly female. Rom Neurosurg. 2014;21:227–9. https://doi.org/10.2478/romneu-­2014-­0029. Barbera J, Gonzalez J, Broseta J, Barcia JL.  Espina bífida sacra con incrustación de la apófisis espinosa de la quinta lumbar. Rev Esp de Cir Ost. 1978;13:259–63. Bellerose MN.  Low-back pain caused by lumbosacral abnormalities. N Engl J Med. 1935;213:177–81. https://doi.org/10.1056/ NEJM193507252130409.

58  De Anquin’s Disease (Spinous Engagement Syndrome) Boone D, Parsons D, Lachmann SM, Sherwood T. Spina bifida occulta: lesion or anomaly? Clin Radiol. 1985;36:159–61. https://doi. org/10.1016/s0009-­9260(85)80100-­8. Bruns J, Rehder U, Dahmen GP, Behrens P, Meiss L. Morbus de Anquin or spinous engagement syndrome. A rare cause of low-back pain syndrome and sciatica. Eur Spine J. 1994;3:265–9. https://doi. org/10.1007/BF02226577. de Anquin CE. Spina bifida occulta with engagement of the fifth lumbar spinous process. J Bone Jt Surg (Br). 1959;41:486–90. Dieckmann C, Nicolas V, Bruns J.  De Anquin disease or spinous engagement syndrome. Aktuelle Radiol. 1995;5:212–5. Ferguson AB.  The clinical and roentgenographic interpretation of lumbosacral anomalies. Radiology. 1934;22:548–58. https://doi. org/10.1148/22.5.548. Goobar JE, Erickson F, Pate D, Sartoris DJ, Resnick D.  Symptomatic clasp-knife deformity of the spinous processes. Spine (Phila Pa 1976). 1988;13:953–6. https://doi. org/10.1097/00007632-­198808000-­00021. Henry GW, Larsen IJ, Stewart SF.  The roentgenologic criteria for appraising the human back as an economic asset or liability. Am J Roentgenol Radium Ther Nucl Med. 1958;79:658–72. Kattan KR, Pais MJ.  The spinous process: the forgotten appendage. Skelet Radiol. 1981;6:199–204. https://doi.org/10.1007/ BF00347187. Spasov MS, Todorov IP, Stojkovska Pemoska EM.  De Anquin syndrome-­rare cause of low back pain: a case report with review of the literature. Sanamed. 2016;11:145–9. https://doi.org/10.24125/ sanamed.v11i2.125. Stark WA.  Spina bifida occulta and engagement of the fifth lumbar spinous process. Clin Orthop Relat Res. 1971;81:71–2. https://doi. org/10.1097/00003086-­197111000-­00009.

Lumbosacral Conjoined Nerve Roots

59.1 Generalities and Relevance A conjoined nerve root (CNR) is a type of developmental/ embryological anomaly involving two adjacent nerve roots which share a common root sleeve at some part during their running course from the dural sac. The concerning neural exit foramina may be empty or sometimes contain two nerve roots instead of one. Sometimes, there is also an abnormal anastomosis between these conjoined nerve roots. CNR is most commonly observed in the lumbosacral region, mainly unilateral at L5 and S1 vertebral segments. CNR is the most frequent nerve root congenital anomaly of the cauda equina.  The incidence of CNR varies from 0.3 to 17% in imaging studies without gender preference; however, this incidence reaches 30% in autopsy studies.

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Since the first anatomical description of CNR by the Italian Zagnoni in 1949, various classifications were suggested. The classification by Neidre and MacNab is the most commonly used. According to this classification, there are three fundamental types of CNR (Fig. 59.1). The most frequent anomaly is the conjoint nerve roots with two nerve roots derived from a common dural sheath (Type 1) followed by two nerve roots in one lateral spinal foramina (Type 2). In type 3 anomaly, two adjacent nerve roots are connected by a connecting root (AKA nerve root anastomosis) (Fig. 59.1). Occasionally, there is a combination of two of the three types previously mentioned. CNR should be distinguished from the furcal nerve, an independent nerve found in the lumbosacral trunk (most commonly at the level of the fourth lumbar vertebra) that links the lumbar plexus to the sacral plexus.

Fig. 59.1  Conjoined nerve roots according to Neidre and MacNab’s classification. Type 1: Two nerve roots derived from a common dural sheath. Type 2: Two nerve roots in one lateral spinal foramina. Type 3: Two adjacent nerve roots are connected by a connecting root (AKA nerve root anastomosis)

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Isolated CNR may be either asymptomatic or cause spontaneous lumbosacral radicular pain. The presence of additional spinal congenital lesions or degenerative changes is an important factor in diagnostic confusion. Furthermore, the lack of preoperative awareness of CNR may be associated with surgical failure due to iatrogenic manipulation or retraction with little mobility of these particular nerve roots. Concomitant vertebral anomalies are not rare including spina bifida, spondylolisthesis, and hypoplastic ipsilateral pedicle or facet joints. Spontaneous radicular pain (particularly sciatic pain) may be related to nerve root stretching or tethering in the lateral recess or in the same foramen. Additionally, the CNR is predisposed to be compressed by the facet joint or the pedicle during regular activities. Recently, there has been growing interest in this phenomenon as a possible causative factor of Failed back surgery syndrome. There is no gender predominance reported and no age of predilection. No special risk factors have been recognized.

59.2 Clinical Presentations For many authors, isolated conjoined nerve roots remain asymptomatic for a long time until further degenerative changes occur. The majority of symptomatic patients with CNR present with isolated L5 and/or S1 lumbosacral radicular pain even without mechanical impingement of the lumbosacral nerve roots. Neurogenic claudication is less frequent. Neurological deficits are rare and include sensory and/or motor deficits with or without reflex abnormalities. Additional low back pain may be related to other concomitant spinal degenerative lesions. There are two important clinical clues suggested to be indicative of conjoined nerve roots, taking into consideration the presence of potential underlying pathologies: • Involvement of both dermatomes of the conjoined nerve root. • A negative straight leg raising sign (Lasègue sign) despite the radiculopathy due to the absence of root conflict. When a CNR is present, even a small herniated disc may present with relatively more severe radicular symptoms. This is explained by a decrease in the epidural space available for lumbosacral nerve roots at the lateral recess in the lumbar spinal canal. Traditional electromyography may also provide signs of radiculopathy.

59  Lumbosacral Conjoined Nerve Roots

Finally, many cases will remain asymptomatic and CNR will be found only incidentally on neuroimaging or when a coexisting spinal disease occurs.

59.3 Imaging Features Preoperative identification of CNR is based on a high degree of suspicion. The presence of lumbosacral radiculopathy or neurological claudication in a setting of a relatively small disc compression should increase the suspicion of the diagnosis of CNR. Computed tomography (CT) scan may show the anomaly, but the diagnosis is habitually missing if there is a combined lumbar herniated disc or spinal stenosis especially when the radiologist is unaware. A comparison of the two sides helps recognize this radicular malformation. Intravenous contrast injection does not seem very useful. Sometimes there is also a subtle widening of the lateral recess of the spinal canal on the side of the CNR. CT scan may show associated vertebral anomalies or malformations. Magnetic resonance imaging (MRI) is the technique of choice to identify the CNR (Figs. 59.2, 59.3, 59.4, 59.5, 59.6, 59.7 and 59.8). Coronal MR images provide definite data about the course of each nerve root. Axial and sagittal T1and T2-weighted images in addition to gadolinium injection allow the identification of other concurrent lesions. There is no pathognomonic sign of CNR; however, the following MRI signs are highly suggestive: (a) The “sagittal shoulder sign”: a vertical structure connecting two consecutive nerve roots was identified on both T1- and T2-weighted parasagittal MRI (Fig. 59.2). (b) The “corner sign”: an asymmetric structure of the anterolateral corner of the dural sac on T1-weighted axial MRI. (c) The “Parallel sign”: a nerve root running parallel to the disc plane at the disc level (Fig. 59.3). (d) The “Fat crescent sign”: the extradural fat between the asymmetric dura and the CNR (Fig. 59.3). Asymmetry of the subarachnoid space on the axial MRI was suggestive of a conjoined nerve root and could relate to the “corner sign”. Unfortunately, T1-weighted axial MRI which allows an excellent contrast between the dural sac and the adjacent epidural fat is not routinely used in some hospitals. Misdiagnoses are still possible because there is no pathognomonic sign (present beyond any doubt) of CNR. Additional lumbar myelo-radiculography with or without a complementary CT scan (post-myelo-CT scan) may be useful in some doubtful cases; however, this complement is rarely used.

59.4  Treatment Options and Prognosis

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Fig. 59.2  Conjoined nerve roots (arrows) as seen on axial (a) and parasagittal (b) T2-weighted MRI. Note the “sagittal shoulder sign” identified on T2-weighted parasagittal MRI (b)

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Fig. 59.3  Conjoined nerve roots (arrows) as seen on axial T2-weighted MRI (a, b). Note the “Parallel sign”: a nerve root running parallel to the disc plane at the disc level (a). Note the “Fat crescent sign”: the extradural fat between the asymmetric dura and the conjoined nerve roots (b)

If not correctly interpreted, CNR could be mistaken for other possible diagnoses in the lumbosacral region such as: • Lumbar disc herniation (Fig. 59.9) • Migration or sequestration of lumbar disc fragment

• Foraminal lumbar disc herniation • Post-arachnoiditis adhesions of the  cauda equina  nerve roots • Swollen/inflamed nerve root • Enlarged epidural venous plexus

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Fig. 59.4  Lumbosacral nerve root anomalies. Axial MRI (a, b) on STIR sequences at the level of S1: asymmetrical appearance of thecal sac due to conjoined L5 and S1 nerve root on the left side. Note the scalloping of the posterior wall of the S1 vertebrae

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Fig. 59.5  Asymmetrical lumbosacral nerve root anomalies (arrows) on L5 vertebral level as seen on axial T2-weighted MRI (a, b)

59.4  Treatment Options and Prognosis

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Fig. 59.6  Double nerve roots (arrows) on left-sided L5–S1 vertebral level as seen on axial T2-weighted MRI

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Fig. 59.7  Double nerve roots (arrows) on left-sided S1–S2 vertebral level as seen on axial T2-weighted MRI (a, b)

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59  Lumbosacral Conjoined Nerve Roots

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Fig. 59.8  Double nerve roots (arrows) on left-sided L5–S1 vertebral level as seen on axial MRI STIR sequences (a, b). (Courtesy of Pr. El Mehdi Atmane)

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Fig. 59.9  Conjoined nerve roots (arrows) could be mistaken for a lumbar disc herniation as seen on axial CT scan (a) and T2-weighted MRI (b)

59.4 Treatment Options and Prognosis The majority of symptomatic patients with isolated lumbosacral CNR are managed conservatively. Conservative therapy includes pain control medications, physiotherapy, and other

physical modalities resulting in more or less control of the patient’s pain. Attempting a routine microdiscectomy or endoscopic discectomy in the existence of CNR can be challenging because it raises the risk of inadvertent neural injuries during the pro-

Further Reading

cedure or can be the cause of neuropathic pain due to too much manipulation or retraction. When the CNR is associated with a large disc herniation, the recommendation is to approach the disc via the axilla area. After the axillary herniated disc is removed, the CNR can be mobilized medially to approach the disc through the shoulder region. Surgical treatment is rarely recommended even in cases with intractable pain. When required, surgical procedures comprise radicular decompression through a hemilaminectomy and foraminotomy to relieve the lateral recess stenosis. If needed, a more extensive approach will be used such as laminectomy, facetectomy, and even pediculectomy. A concomitant spinal fusion may be suggested if there is a supposed instability, particularly in patients with associated lumbar spondylolisthesis. Possible associated degenerative lesions will be treated consequently. Surgical results of CNR patients showed a tendency to have mildly worse long-term outcomes in comparison with patients operated on for a simple lumbar disc herniation. It seems that patients with CNR may have other negative factors that affect recovery like the long period of compression and/or lack of nerve mobility (tethering). The surgical success of patients undergoing a discectomy in the setting of a conjoined root anomaly is often less than satisfactory.

Further Reading Artico M, Carloia S, Piacentini M, Ferretti G, Dazzi M, Franchitto S, et al. Conjoined lumbosacral nerve roots: observations on three cases and review of the literature. Neurocirugia (Astur). 2006;17:54–9. https://doi.org/10.1016/s1130-­1473(06)70370-­0. Böttcher J, Petrovitch A, Sörös P, Malich A, Hussein S, Kaiser WA.  Conjoined lumbosacral nerve roots: current aspects of diagnosis. Eur Spine J. 2004;13:147–51. https://doi.org/10.1007/ s00586-­003-­0634-­8. Bouchard JM, Copty M, Langelier R.  Preoperative diagnosis of conjoined roots anomaly with herniated lumbar disks. Surg Neurol. 1978;10:229–31. Can H, Kircelli A, Kavadar G, Civelek E, Cansever T, Aydoseli A, et al. Lumbosacral conjoined root anomaly: anatomical considerations of exiting angles and root thickness. Turk Neurosurg. 2017;27:617–22. https://doi.org/10.5137/1019-­5149.JTN.16490-­15.1. Epstein JA, Carras R, Ferrar J, Hyman RA, Khan A. Conjoined lumbosacral nerve roots. Management of herniated discs and lateral recess stenosis in patients with this anomaly. J Neurosurg. 1981;55:585–9. https://doi.org/10.3171/jns.1981.55.4.0585. Gomez JG, Dickey JW, Bachow TB.  Conjoined lumbosacral nerve roots. Acta Neurochir. 1993;120:155–8. https://doi.org/10.1007/ BF02112035. Haijiao W, Koti M, Smith FW, Wardlaw D.  Diagnosis of lumbosacral nerve root anomalies by magnetic resonance

707 imaging. J Spinal Disord. 2001;14:143–9. https://doi. org/10.1097/00002517-­200104000-­00009. Harshavardhana NS, Dabke HV. The furcal nerve revisited. Orthop Rev (Pavia). 2014;6:5428. https://doi.org/10.4081/or.2014.5428. Kang CH, Shin MJ, Kim SM, Lee SH, Kim HK, Ryu JA, et al. Conjoined lumbosacral nerve roots compromised by disk herniation: sagittal shoulder sign for the preoperative diagnosis. Skelet Radiol. 2008;37:225–31. https://doi.org/10.1007/s00256-­007-­0421-­4. Kikuchi S, Hasue M, Nishiyama K, Ito T.  Anatomic features of the furcal nerve and its clinical significance. Spine (Phila Pa 1976). 1986;11:1002–7. https://doi. org/10.1097/00007632-­198612000-­00006. Lightsey HM, Xiong GX, Schoenfeld AJ, Simpson AK.  Microendoscopic decompression of conjoined lumbosacral nerve roots. BMJ Case Rep. 2022;15:e248680. https://doi. org/10.1136/bcr-­2021-­248680. Lotan R, Al-Rashdi A, Yee A, Finkelstein J. Clinical features of conjoined lumbosacral nerve roots versus lumbar intervertebral disc herniations. Eur Spine J. 2010;19:1094–8. https://doi.org/10.1007/ s00586-­010-­1329-­6. Maiuri F, Gambardella A. Anomalies of the lumbosacral nerve roots. Neurol Res. 1989;11:130–5. https://doi.org/10.1080/01616412.198 9.11739877. Neidre A, MacNab I. Anomalies of the lumbosacral nerve roots. Review of 16 cases and classification. Spine (Phila Pa 1976). 1983;8:294–9. https://doi.org/10.1097/00007632-­198304000-­00010. Oh CH, Park JS, Choi WS, Choi E, Ji GY.  Radiological anatomical consideration of conjoined nerve root with a case review. Anat Cell Biol. 2013;46:291–5. https://doi.org/10.5115/acb.2013.46.4.291. Popa I, Poenaru DV, Oprea MD, Andrei D.  Intraoperative conjoined lumbosacral nerve roots associated with spondylolisthesis. Eur J Orthop Surg Traumatol. 2013;23(Suppl 1):S115–9. https://doi. org/10.1007/s00590-­013-­1185-­2. Schmidt CK, Rustagi T, Alonso F, Loukas M, Chapman JR, Oskouian RJ, Tubbs RS.  Nerve root anomalies: making sense of a complicated literature. Childs Nerv Syst. 2017;33:1261–73. https://doi. org/10.1007/s00381-­017-­3457-­3. Scuderi GJ, Vaccaro AR, Brusovanik GV, Kwon BK, Berta SC.  Conjoined lumbar nerve roots: a frequently underappreciated congenital abnormality. J Spinal Disord Tech. 2004;17:86–93. https://doi.org/10.1097/00024720-­200404000-­00002. Sharma A, Singh V, Agrawal R, Mangale N, Deepak P, Savla J, et al. Conjoint nerve root an intraoperative challenge in minimally invasive tubular discectomy. Asian Spine J. 2021;15:545–9. https://doi. org/10.31616/asj.2020.0250. Song SJ, Lee JW, Choi JY, Hong SH, Kim NR, Kim KJ, et al. Imaging features suggestive of a conjoined nerve root on routine axial MRI.  Skelet Radiol. 2008;37:133–8. https://doi.org/10.1007/ s00256-­007-­0403-­6. Taghipour M, Razmkon A, Hosseini K.  Conjoined lumbosacral nerve roots: analysis of cases diagnosed intraoperatively. J Spinal Disord Tech. 2009;22:413–6. https://doi.org/10.1097/ BSD.0b013e31818f00a0. Trimba R, Spivak JM, Bendo JA.  Conjoined nerve roots of the lumbar spine. Spine J. 2012;12:515–24. https://doi.org/10.1016/j. spinee.2012.06.004. White JG, Strait TA, Binkley JR, Hunter SE. Surgical treatment of 63 cases of conjoined nerve roots. J Neurosurg. 1982;56:114–7. Witzmann A, Hammer B, Fischer J.  Free sequestered disc herniation at the S2 level misdiagnosed as neuroma. Neuroradiology. 1991;33:92–3. https://doi.org/10.1007/BF00593349.

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Tethered Spinal Cord Syndrome

60.1 Generalities and Relevance

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Tethered spinal cord syndrome (TSCS) is an umbrella term covering a wide group of  neurological manifestations  secondary to abnormal attachment and traction of the  spinal cord within the spinal canal. Spinal cord tethering can occur at any point in the spinal canal; however, most forms involve the lower spinal cord at the lumbosacral region. TSCS is associated with various conditions, mainly congenital with low conus medullaris (below L2 vertebral level). Table 60.1 shows different etiologies of tethered spinal cord reported in the literature (Table 60.1). The first diagnosed and operated cases of TSCS were reported by Johnson from London in 1857. The lesion was described as a spinal lipoma. A clinical disorder with the distinct term “tethered cord syndrome” was described in 1976 by Harold Joseph Hoffman (1932–2004) and colleagues. This Canadian neurosurgeon reported a series of 31 children Table 60.1  Main etiologies of tethered spinal cord reported in the literature Congenital • Soina bifida (occulta, meningocele, myelomeningocele) • Thickened/tight filum terminale (Figs. 60.1, 60.2, 60.3 and 60.4) • Lipoma, dermoid, epidermoid, neurenteric, or arachnoid cysts (Figs. 60.5 and 60.6) • Split spinal cord malformation (diastematomyelia and diplomyelia) (Figs. 60.7 and 60.8) •  Dermal sinus tract Tumoral No congenital intraspinal tumors (e.g., ependymoma) Acquired Arachnoid adhesions secondary to spinal trauma, surgery, infection, or inflammation

Fig. 60.1  Case 1. Thickened/tight filum terminale (arrows) with spina lipoma (stars) as seen on lumbosacral sagittal T2-weighted MRI (a, b)

with neurologic symptoms associated with low conus medullaris and/or thick filum diagnosed on  myelography.  Previously, TSCS has termed the filum terminale syndrome in 1953. Since Hoffman’s description, the concept of the tethered cord syndrome has extended beyond the notion of tight filum terminale.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_60

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60  Tethered Spinal Cord Syndrome

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Fig. 60.2  Case 2. Fatty filum terminal in an adult (arrows) as seen on axial CT scan (a, b) and T1-weighted MRI (c, d)

60.1  Generalities and Relevance Fig. 60.3  Case 2. Fatty filum terminal in the same case (arrows) as seen on lumbosacral sagittal T1- (a) and T2-weighted MRI (b)

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Fig. 60.4  Case 3. Fatty filum terminal (arrows) in an adult as seen on lumbosacral sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T1-weighted MR imaging (c, d)

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60  Tethered Spinal Cord Syndrome

Fig. 60.5  Case 4. Tethered spinal cord with posterior spina lipoma on L3–L4 (arrows). Sagittal (a) and axial CT scan (b, c)

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Fig. 60.6  Case 5. Sagittal T2-weighted MRI (a, b) showing a tethered spinal cord syndrome (arrows) with a concomitant epidermoid cyst on T12–L1 (stars)

Patients with TSCS will present with a wide spectrum of presenting signs and progressive symptoms including low back pain, neurologic and urologic abnormalities as well as orthopedic deformities and cutaneous disorders. Sometimes lumbosacral radicular pain may occur in isolation or most often associated with other concomitant neurologic and extra-neurologic manifestations. The majority of TSCS are congenital and occur in the pediatric population; however, some forms go undiagnosed until later in life. Acquired forms are rare and often develop near the site of an injury to the spinal cord. It has been suggested that abnormal spinal cord traction leads to chronic ischemic vascular damage and neuronal disorders to explain the clinical symptoms of TSCS.  In addition, some associated lesions may compress the conus medullaris and/or cauda equina roots. Then neurological manifestations can include a mixed picture of upper and lower motor neuron findings (both central and peripheral neural symptoms) (Figs.  60.1, 60.2, 60.3, 60.4, 60.5, 60.6, 60.7 and 60.8).

60.1  Generalities and Relevance

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Fig. 60.7  Case 6. Axial CT scan showing split cord malformation on L2–L3 (diastematomyelia) (a, b). Note the bony septum (arrowhead) and the tethered spinal cord (arrow). The diastematomyelia is best visualized on axial T1-weighted MRI (arrows) (c, d)

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60  Tethered Spinal Cord Syndrome

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Fig. 60.8  Case 7. Lumbar split cord malformation (stars) in an adult as seen on axial CT scan (a, b). Note the posterior bony septum on L2–L3 (arrow) (a) and the anterior part of the bony septum on L3–L4 (arrow) (b)

60.2 Clinical Presentations Patients with congenital TSCS may present with a great variety of symptoms and clinical signs including: (a) Cutaneous findings: hypertrichosis (hairy patches), dimples, dermal sinus, hemangiomatous discoloration, fatty tumors (e.g., lipoma) on the lumbosacral area (Figs. 60.9 and 60.10) (b) Spinal deformities: congenital kyphosis and/or scoliosis (Fig. 60.9a) (c) Foot deformities:  pes cavo-varus (AKA high arch or clubfoot) with or without trophic ulcerations (d) Low back pain (e) Lumbar and/or sacral radicular pain (e.g., sciatica) especially with flexion (f) Abnormal or gait difficulty (g) Sphincter dysfunctions: mainly urinary incontinence or retention (h) Chronic recurrent urinary infection (i) Motor deficit: mainly lower extremities weakness (j) Sensory deficit: sensory loss on the perineal area and/or the lower extremities (k) Other orthopedic disorders: lower limb muscle atrophy, short limb In some patients, clinical signs and symptoms can include varied peripheral and central disorders in the same lower limbs such as amyotrophy, hyperreflexia/hyporeflexia,

Babinski sign (pathologic plantar response), and a positive Lasègue’s test (straight leg raising). Unlike in pediatric TSCS, the majority of adult patients present urologic disorders while spinal and foot deformities are rarely seen. In the child, aggravating factors are related to growth spurts, whereas in adults triggering factors are related to physical activity (e.g., sports), trauma, pregnancy, or lumbosacral degenerative disorders. Severe cases can present with more serious neurologic conditions such as complete cauda equina syndrome or paraplegia and even end-stage kidney disease. Sometimes, separating lower-level myelopathy from lumbosacral plexopathy or lumbosacral radiculopathy on clinical grounds can be challenging. Consequently, in such cases electrodiagnostic studies are decisive. In addition, patients with sphincter disorders might be evaluated with various combinations of urodynamic studies (e.g., uroflowmetry and cystometry). Clinicians should take into consideration that TSCS may be associated with other potential congenital diseases whether vertebra-medullary or craniocerebral and even extra-neurologic. Adult patients without orthopedic or cutaneous disorders may be confused with those presenting conus medullaris syndrome secondary to other etiologies (c.f. Chap. 43 about Conus Medullaris Lesions). Finally, many patients with tethering spinal cord will remain asymptomatic and the disorder will be found only incidentally on spinal imaging.

60.3  Imaging Features

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Fig. 60.9  Case 7. Hypertrichosis (hairy patch) (a, b), on the lumbosacral area. Note the thoracolumbar scoliosis (a)

60.3 Imaging Features

Fig. 60.10  Case 8. Hypertrichosis on the lumbosacral area

Plain radiography (Figs.  60.7a, 60.8, and 60.11) and bony computed tomography (CT) scan may be useful for identifying secondary bone changes related to congenital and developmental abnormalities of the vertebrae. Spinal curvature is best assessed on plain radiography by measuring the degree of kyphosis, lordosis, or scoliosis. Magnetic resonance imaging (MRI) remains the gold standard for diagnosing a tethered spinal cord. The lower termination of the spinal cord (namely conus medullaris) usually terminates at or above L1–L2 vertebral level after about 3  months after birth. The tethered spinal cord is often encountered when the conus medullaris is below the L2 vertebral level (Figs. 60.12, 60.13 and 60.14). However, TSCS is conceivable in the location of a normal conus medullaris position. MRI examination must search for thickened filum terminal which has a diameter superior to 2 mm. Causative lesions, whether they are congenital, tumoral, or acquired, should be identified as well as potential associated musculoskeletal dysraphisms. In patients with contraindications of MRI, a myelogram followed by a CT scan (i.e., mylo-CT scan) may be used to define the anatomy and to visualize any abnormalities causing traction/compression of the spinal cord and/or the cauda equina.

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60  Tethered Spinal Cord Syndrome

Fig. 60.11  Case 9. Antero-posterior plain radiograph revealing a lumbar congenital scoliosis with spina bifida of L3–L4–L5 (dotted frame)

Fig. 60.12  Case 10. Tethered spinal cord (arrows) with intrasacral lipoma (arrowhead) on S3–S4 as seen on sagittal (a) and axial (b, c) T2-weighted MR imaging

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60.4  Treatment Options and Prognosis

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Fig. 60.13  Case 11. Lumbar split cord malformation in an adult manifesting as sciatica. Axial T2-weighted MRI (a, b) and axial CT scan (c). Note the bony septum (arrows). (Courtesy of Pr. Hatim Belfquih) Fig. 60.14  Case 11. Besides the split cord malformation (arrows), there is a terminal epidermoid cyst (stars) arising from the right-sided hemicord in L3–L4 vertebral level as seen on magnetic resonance imaging (a–c). (Courtesy of Pr. Hatim Belfquih)

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Posterior spinal ultrasonography may be useful in children below the age of 5 years with a large bony defect (spina bifida).

60.4 Treatment Options and Prognosis Asymptomatic or pauci-symptomatic patients with TSCS can be managed conservatively with regular clinical and MRI follow-ups. However, early surgery is recommended

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when symptoms and clinical signs start to get worse because neurological impairments are often irreversible. The goal of surgery is generally to stabilize or prevent additional neurological or urological disorders. However, postoperative improvement is never assured. Clinicians should always consider spinal growth and the timing of spinal maturity when managing the pediatric spine. Thickened and shortened filum need to be sectioned. The filum terminalis is identifiable by its fatty appearance, its midline location, and its superficial vessel. Some authors

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recommend intraoperative neurophysiologic monitoring. In addition, monopolar nerve stimulators can help identify the nerves. For split cord malformations, it is imperative to remove the septum without damaging the spinal cord through unintentional traction. The dermal sinus tract should be explored and excised intradural. Intramedullary cysts and tumors should be removed completely “if possible” to avoid recurrence. Patients with spinal deformities should be carefully monitored for progression because an early surgical procedure may be necessary to prevent severe deformity and more serious neurologic and/or bladder complications. Surgical complications are not rare. Up to 15% of patients may present at least one of the following complications: • CSF Leak. A careful watertight dural closure after neurologic release is critical to avoid this potential ­complication as well as iatrogenic pseudomeningocele, and meningitis. • Retethering. The diagnosis of retethering usually is based on clinical examination and history rather than postoperative MRI features. Complex cases and those with transitional lipoma have a high risk of symptomatic retethering. Any new or considerably progressive neurologic, urologic, or orthopedic manifestations should be assessed for the possibility of retethering. However, MRI has only a limited diagnostic value. Up to 20% of children will need a repeated surgical procedure for retethering, especially during the period of growth. • Iatrogenic neurologic damage. • Bleeding. • Wound healing problems. Neurophysiologic monitoring during surgery and the use of navigational tools are crucial to reduce the occurrence of new neurologic deficits or neurologic worsening. Recovery from lower limb weakness and sphincter dysfunction depends upon the degree and length of preoperative manifestations. Overall, patients who present only a fatty filum might have a more favorable outcome compared with those who have more anatomically complex lesions. Unlike in children, sphincter disturbance has less good results in adults. However, lower limb pain improves better in the adult population. Also, prognosis should always consider the underlying etiology and associated lesions. Interdisciplinary care including neurosurgery, paediatry, orthopedics, urology, psychiatry, physiotherapy, and social work may be required for this vulnerable population. The importance of school education and social development is significant, especially in children.

60  Tethered Spinal Cord Syndrome

Further Reading Agarwalla PK, Dunn IF, Scott RM, Smith ER. Tethered cord syndrome. Neurosurg Clin N Am. 2007;18:531–47. https://doi.org/10.1016/j. nec.2007.04.001. Akay KM, Erşahin Y, Cakir Y.  Tethered cord syndrome in adults. Acta Neurochir. 2000;142:1111–5. https://doi.org/10.1007/ s007010070038. Akhaddar A. Caudal regression syndrome (spinal thoraco-lumbo-sacro-­ coccygeal agenesis). World Neurosurg. 2020;142:301–2. https:// doi.org/10.1016/j.wneu.2020.07.055. Akhaddar A. Differential diagnosis of intraspinal arachnoid cysts. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: state-of-the-art concepts. Cham: Springer International Publishing; 2022. p. 26. Akhaddar A, Gourinda H, El Alami FZ, El Madhi T, Miri A. Scoliosis and diastematomyelia: four cases and a review of the literature. Rev Chir Orthop Reparatrice Appar Mot. 2000;86:300–5. Apaydin M.  Tethered cord syndrome and transitional vertebrae. Surg Radiol Anat. 2020;42:111–9. https://doi.org/10.1007/ s00276-­019-­02341-­5. Begley K, Sergides Y.  Giant sacral dural ectasia causing ureteric obstruction in Marfan syndrome. ANZ J Surg. 2021;92:1930. https://doi.org/10.1111/ans.17397. Böker T, Vanem TT, Pripp AH, Rand-Hendriksen S, Paus B, Smith HJ, et  al. Dural ectasia in Marfan syndrome and other hereditary connective tissue disorders: a 10-year follow-up study. Spine J. 2019;19:1412–21. https://doi.org/10.1016/j.spinee.2019.04.010. Da Silva LF, Robin S, Guégan-Massardier E, Krzanowska K, Mejjad O, Vittecoq O, et  al. Peripheral neurological involvement as the first manifestation of spina bifida occulta. Rev Rhum Engl Ed. 1997;64:839–42. de Kleuver M, van Jonbergen JP, Langeloo DD.  Asymptomatic massive dural ectasia associated with neurofibromatosis type 1 threatening spinal column support: treatment by anterior vascularized fibula graft. J Spinal Disord Tech. 2004;17:539–42. https://doi. org/10.1097/01.bsd.0000117544.88865.f0. Fattori R, Nienaber CA, Descovich B, Ambrosetto P, Reggiani LB, Pepe G, et  al. Importance of dural ectasia in phenotypic assessment of Marfan’s syndrome. Lancet. 1999;354:910–3. https://doi. org/10.1016/s0140-­6736(98)12448-­0. Ferreira Furtado LM, Da Costa Val Filho JA, Dantas F, Moura de Sousa C.  Tethered cord syndrome after myelomeningocele repair: a literature update. Cureus. 2020;12:e10949. https://doi.org/10.7759/ cureus.10949. Garceau GJ.  The filum terminale syndrome (the cord-traction syndrome). J Bone Jt Surg Am. 1953;35-A:711–6. Hoffman HJ, Hendrick EB, Humphreys RP. The tethered spinal cord: its protean manifestations, diagnosis and surgical correction. Childs Brain. 1976;2:145–55. https://doi.org/10.1159/000119610. Johnson A. Fatty tumour from the sacrum of a child, connected with the spinal membranes. Trans Pathol Soc Lond. 1857;8:16–8. Lee GY, Paradiso G, Tator CH, Gentili F, Massicotte EM, Fehlings MG.  Surgical management of tethered cord syndrome in adults: indications, techniques, and long-term outcomes in 60 patients. J Neurosurg Spine. 2006;4:123–31. https://doi.org/10.3171/ spi.2006.4.2.123. Lew SM, Kothbauer KF.  Tethered cord syndrome: an updated review. Pediatr Neurosurg. 2007;43:236–48. https://doi. org/10.1159/000098836. Liu CC, Lin YC, Lo CP, Chang TP. Cauda equina syndrome and dural ectasia: rare manifestations in chronic ankylosing spondylitis. Br J Radiol. 2011;84:e123–5. https://doi.org/10.1259/bjr/45816561.

Further Reading Lundby R, Rand-Hendriksen S, Hald JK, Lilleås FG, Pripp AH, Skaar S, et al. Dural ectasia in Marfan syndrome: a case control study. AJNR Am J Neuroradiol. 2009;30:1534–40. https://doi.org/10.3174/ajnr. A1620. Meester JAN, Verstraeten A, Schepers D, Alaerts M, Van Laer L, Loeys BL.  Differences in manifestations of Marfan syndrome, Ehlers-­ Danlos syndrome, and Loeys-Dietz syndrome. Ann Cardiothorac Surg. 2017;6:582–94. https://doi.org/10.21037/acs.2017.11.03. Naffaa L, Irani N, Saade C, Sreedher G. Congenital anomalies of lumbosacral spine: a pictorial review. J Med Imaging Radiat Oncol. 2017;61:216–24. https://doi.org/10.1111/1754-­9485.12499. Nallamshetty L, Ahn NU, Ahn UM, Nallamshetty HS, Rose PS, Buchowski JM, et  al. Dural ectasia and back pain: review of the literature and case report. J Spinal Disord Tech. 2002;15:326–9. https://doi.org/10.1097/00024720-­200208000-­00012. Nguyen HS, Lozen A, Doan N, Gelsomin M, Shabani S, Maiman D. Marsupialization and distal obliteration of a lumbosacral dural

719 ectasia in a nonsyndromic, adult patient. J Craniovertebr Junct Spine. 2015;6:219–22. https://doi.org/10.4103/0974-­8237.167887. Polster SP, Dougherty MC, Zeineddine HA, Lyne SB, Smith HL, MacKenzie C, et  al. Dural ectasia in neurofibromatosis 1: case series, management, and review. Neurosurgery. 2020;86:646–55. https://doi.org/10.1093/neuros/nyz244. Schonauer C, Tessitore E, Frascadore L, Parlato C, Moraci A. Lumbosacral dural ectasia in type 1 neurofibromatosis. Report of two cases. J Neurosurg Sci. 2000;44:165–8. Terai T, Henmi T, Kanematsu Y, Fujii K, Mishiro T, Sakai T, et  al. Adult onset tethered cord syndrome associated with intradural dermoid cyst. A case report. Spinal Cord. 2006;44:260–2. https://doi. org/10.1038/sj.sc.3101817. Weigang E, Ghanem N, Chang XC, Richter H, Frydrychowicz A, Szabó G, et al. Evaluation of three different measurement methods for dural ectasia in Marfan syndrome. Clin Radiol. 2006;61:971–8. https://doi.org/10.1016/j.crad.2006.05.015.

Ventriculus Terminalis (Fifth Ventricle)

61.1 Generalities and Relevance Ventriculus terminalis (VTER), also known as “fifth ventricle”, persistent terminal ventricle, or terminal ventricle of Krause, is an intramedullary ependymal-lined cavity in continuity with the central canal of the conus medullaris. VTER is formed between days 43 and 48 of embryogenesis, via canalization and retrogressive differentiation of the caudal end of the developing spinal cord. Classically, the cyst regresses completely during the first weeks or months after birth. The causes that determine the dilatation of the VTER are not completely understood. Various phenomenons have been postulated including inflammatory, traumatic, compressive, or vascular events. The cyst is usually small and filled with cerebrospinal fluid (CSF). Unlike syringomyelia, arachnoid cysts, and intramedullary cystic tumors, persistent terminal ventricle develops exclusively in the conus medullaris. Clinical symptoms of VTER can be explained by abnormal conus medullaris damage and/or cauda equina root compression leading to chronic ischemic vascular damage and neuronal. Subsequently, neurological manifestations may include a mixed picture of both central and peripheral neural symptoms. This rare residual ependymal cyst may persist in adults causing neurological and/or sphincter disturbances. About 20% of patients may present lumboradicular symptoms mimicking those encountered in discogenic sciatica. VTER should be distinguished from “filar cyst” which is a rare asymptomatic small cyst situated within the filum terminalis. German anatomist Benedikt Stilling (1810–1879) was the first to describe a VTER in 1859, but the term “ventriculus terminalis” was coined by another German anatomist named Johann Friedrich Wilhelm Krause (1833–1910) in 1875. Since then, about 70 surgically managed cases were reported in the literature. In 2008, de Moura Batista et al. suggested a simple clinical classification of cystic lesions of the VTER, later modi-

61

fied by Ganau et al. Patients with sciatica could be included in type I, because of the presence of nonspecific symptoms. The fifth ventricle may present in pediatric and adult populations without distinct gender predilection. However, women in their fifties seem to be the most affected. Curiously, patients with this supposed congenital malformation rarely present other developmental anomalies.

61.2 Clinical Presentations The clinical presentation is variable, ranging from an insidious onset to a rapidly worsening form. However, the majority of presentations are chronic and develop progressively. Symptoms are also variable and depend principally on the cyst size, duration of symptoms, and the patient’s age. Some patients manifest simple low back pain and sciatica, while others present with severe clinical manifestations such as progressive spastic or flaccid paralysis, lower limb weakness, bladder/bowel incontinence, or even complete cauda equina syndrome. However, many patients will remain asymptomatic and the cysts discover only incidentally on spinal imaging. The following classification distinguishes four main types of clinical presentations: • Type Ia: Stable nonspecific symptoms without a clear relation to ventriculus terminalis. • Type Ib: Nonspecific but progressing (worsening) symptoms. • Type II: Focal neurological deficits. • Type III: Bowel and bladder dysfunctions. Patients with sciatic pain could be included in type I, because of the presence of nonspecific symptoms. Rarely, possible concomitant malformations may be encountered such as scoliosis or kyphoscoliosis.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_61

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722

61  Ventriculus Terminalis (Fifth Ventricle)

61.3 Imaging Features Magnetic resonance imaging (MRI) is now the main imaging modality that may specify the exact topography of the cysts and their inner structures, define the exact margins of the collections, and determine the relationship of the cysts with contiguous anatomic structures. On MRI, the ventriculus terminalis is usually described as a rounded or oval, solitary lesion with regular borders. This fluid-filled lesion demonstrates similar signal characteristics to CSF in all pulse sequences: hypointense on T1-weighted images and hyperintense on T2-weighted images with no perilesional edema (Fig. 61.1). Classically, the cyst does not enhance after gadolinium injection. In regard to cyst extension, no more than one or two vertebral segments are habitually involved in the conus medullaris area. Spinal imaging examination must also seek the potential coexistence of other spinal or intraspinal congenital lesions (e.g., Chiari type I malformation or spinal cord lipoma). MRI on T1-post-gadolinium sequences helps distinguish VTER from other types of conus medullaris cystic lesions such as:

a

b

–– –– –– –– –– –– –– –– –– –– –– –– ––

Hydro-syringomyelia Arachnoid cyst Cystic schwannoma Hemangioblastoma Ependymoma Glioma (cystic astrocytoma) Dermoid and Epidermoid cysts Teratoma Enterogenous cyst Ependymal cyst Epithelial cyst Bronchogenic cyst Cysticercosis

Sometimes, diagnostic separation is difficult on neuroimaging, then the final diagnosis can only be done by histological examination. Radiologists should always consider that about 2.5% of children under 5 years of age might have an asymptomatic cyst localized corresponding to the VTER in the central conus medullaris region.

c

Fig. 61.1  Ventriculus terminalis (arrows) as seen on sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c)

Further Reading

61.4 Treatment Options and Prognosis

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Borius PY, Cintas P, Lagarrigue J. Ventriculus terminalis dilatation in adults: A case report and review of the literature. Neurochirurgie. 2010;56:386–90. https://doi.org/10.1016/j.neuchi.2009.12.006. The treatment for symptomatic ventriculus terminalis, Brisman JL, Li M, Hamilton D, Mayberg MR, Newell DW. Cystic dilation of the conus ventriculus terminalis presenting as an acute cauda whether conservative or surgical, remains unclear. equina syndrome relieved by decompression and cyst drainage: case Generally, no treatment is required for “asymptomatic” report. Neurosurgery. 2006;58:E585. https://doi.org/10.1227/01. VTER that causes no pain or neurological symptoms/signs neu.0000197486.65781.88. regardless of their volume. However, no or pauci-­ Ciappetta P, D’urso PI, Luzzi S, Ingravallo G, Cimmino A, Resta L. Cystic dilation of the ventriculus terminalis in adults. J Neurosurg symptomatic patients may need a follow-up MRI annually to Spine. 2008;8:92–9. https://doi.org/10.3171/SPI-­08/01/092. detect any cystic development or new abnormality. Then, de Moura BL, Acioly MA, Carvalho CH, Ebner FH, Tatagiba M. Cystic surgery is needed for “symptomatic” patients, especially lesion of the ventriculus terminalis: proposal for a new clinithose with uncontrolled persistent lumbosciatic pain, if neucal classification. J Neurosurg Spine. 2008;8:163–8. https://doi. org/10.3171/SPI/2008/8/2/163. rological signs/symptoms progress, or if there is a cyst extenDhillon RS, McKelvie PA, Wang YY, Han T, Murphy M.  Cystic sion (Ib). lesion of the ventriculus terminalis in an adult. J Clin Neurosci. The majority of authors recommend conservative treat2010;17:1601–3. https://doi.org/10.1016/j.jocn.2010.04.026. ment for patients with type Ia lesions, while surgery is rec- Domingo RA, Bohnen AM, Middlebrooks EH, Quinones-Hinojosa A, Abode-Iyamah K.  T10-L3 Cystic Lesion of the Ventriculus ommended for the remaining types (Ib, II, and III). Terminalis Presenting as Conus Medullaris Syndrome. Overall, a posterior approach is performed (laminectomy World Neurosurg. 2020;136:146–9. https://doi.org/10.1016/j. or laminotomy) and the cyst is usually fenestrated via a small wneu.2020.01.049. myelotomy to avoid further neurological damage for exci- Dullerud R, Server A, Berg-Johnsen J. MR imaging of ventriculus terminalis of the conus medullaris. A report of two operated patients sion of an adherent cyst wall. Some other alternative options and a review of the literature. Acta Radiol. 2003;44:444–6. https:// may be considered such as cyst diversion or shunting (espedoi.org/10.1034/j.1600-­0455.2003.00096.x. cially cysto-subarachnoid shunting). Following the intra Fletcher-Sandersjöö A, Edström E, Bartek J Jr, Elmi-Terander conus medullaris procedures, the dura matter should be A.  Surgical treatment for symptomatic ventriculus terminalis: case series and a literature review. Acta Neurochir (Wien). closed in a hermetic manner to avoid any postoperative CSF 2019;161:1901–8. https://doi.org/10.1007/s00701-­019-­03996-­0. fistula, pseudomeningocele, or potential meningitis. Ganau M, Talacchi A, Cecchi PC, Ghimenton C, Gerosa M, Faccioli Simple MRI-guided aspiration of the cyst contents has F. Cystic dilation of the ventriculus terminalis. J Neurosurg Spine. already been used in three previous patients without recur2012;17:86–92. https://doi.org/10.3171/2012.4.SPINE11504. rence; however, more long-term outcome data are needed to Helal A, Pirina A, Sorenson TJ, Palandri G. Fenestration of Symptomatic Ventriculus Terminalis: 2-Dimensional Operative Video. Oper validate this early good result. Neurosurg (Hagerstown). 2021;20:E293. https://doi.org/10.1093/ The majority of symptomatic patients (about 85%) ons/opaa372. showed good postoperative clinical results after surgical Kato M, Nakamura H, Suzuki E, Terai H, Wakasa K, Wakasa T, et  al. Ependymal cyst in the lumbar spine associated with cauda treatment. However, patients with less satisfactory results are equina compression. J Clin Neurosci. 2008;15:827–30. https://doi. the patients with greater cysts. Additionally, no patients org/10.1016/j.jocn.2006.12.020. developed complications attributed to the surgery. So when Kawanishi M, Tanaka H, Yokoyama K, Yamada M. Cystic dilation of indicated, surgical treatment for VTER appears to be both the ventriculus terminalis. J Neurosci Rural Pract. 2016;7:581–3. https://doi.org/10.4103/0976-­3147.185504. effective and safe. Regardless of the surgical technic, recurLotfinia I, Mahdkhah A.  The cystic dilation of ventriculus terminalis rence is rare. with neurological symptoms: Three case reports and a literature review. J Spinal Cord Med. 2018;41:741–7. https://doi.org/10.108 0/10790268.2018.1474680. Mastorakos P, Pomeraniec IJ, Shah S, Shoushtarizadeh A, Quezado Further Reading MM, Heiss J. Mobile Myxopapillary Ependymoma with Associated Filum Terminale Cyst. World Neurosurg. 2020;139:337–42. https:// Agrillo U, Tirendi MN, Nardi PV.  Symptomatic cystic dilatation of doi.org/10.1016/j.wneu.2020.04.095. V ventricle: case report and review of the literature. Eur Spine J. Matsubayashi R, Uchino A, Kato A, Kudo S, Sakai S, Murata S. Cystic 1997;6:281–3. https://doi.org/10.1007/BF01322453. dilatation of ventriculus terminalis in adults: MRI. Neuroradiology. Akhaddar A.  Differential Diagnosis of Intraspinal Arachnoid Cysts. 1998;40:45–7. https://doi.org/10.1007/s002340050537. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: State-of-the-art Concepts. Switzerland: Springer International Nagano S, Ijiri K, Kawabata R, Zenmyo M, Yone K, Kitajima S, et  al. Ependymal cyst in the conus medullaris. J Clin Neurosci. Publishing; 2022. p. 23. 2010;17:272–3. https://doi.org/10.1016/j.jocn.2009.05.026. Baig Mirza A, Visagan R, Boardman T, Murphy C, Al-Ali B, Kellett C, Pencovich N, Ben-Sira L, Constantini S.  Massive cystic dilatation et al. Recurrent terminal ventricle cyst: a case report. J Surg Case within a tethered filum terminale causing cauda equina compression Rep. 2021;2021:rjab498. https://doi.org/10.1093/jscr/rjab498. and mimicking syringomyelia in a young adult patient. Childs Nerv Bellocchi S, Vidale S, Casiraghi P, Arnaboldi M, Taborelli A. Multilobed Syst. 2013;29:141–4. https://doi.org/10.1007/s00381-­012-­1911-­9. cystic dilation of the ventriculus terminalis (CDVT). BMJ Seo K, Oguma H, Furukawa R, Gomi A. Filar cysts in rare cases may Case Rep. 2013;2013:bcr2013008654. https://doi.org/10.1136/ progress in size, particularly when associated with filar lipoma. bcr-­2013-­008654.

724 Childs Nerv Syst. 2019;35:1207–11. https://doi.org/10.1007/ s00381-­019-­04148-­6. Severino R, Severino P.  Surgery or not? A case of ventriculus terminalis in an adult patient. J Spine Surg. 2017;3:475–80. https://doi. org/10.21037/jss.2017.06.22. Shigekawa S, Matsui S, Inoue A, Shinohara N, Kunieda T. Usefulness of cyst-subarachnoid shunt using syringo-subarachnoid shunt tube for symptomatic enlarging ventriculus terminalis: A case report and review of the literature. Surg Neurol Int. 2023;14:165. https://doi. org/10.25259/SNI_120_2023. Sigal R, Denys A, Halimi P, Shapeero L, Doyon D, Boudghène F.  Ventriculus terminalis of the conus medullaris: MR imaging in four patients with congenital dilatation. AJNR Am J Neuroradiol. 1991;12:733–7. Suh SH, Chung TS, Lee SK, Cho YE, Kim KS. Ventriculus terminalis in adults: unusual magnetic resonance imaging features and review

61  Ventriculus Terminalis (Fifth Ventricle) of the literature. Korean J Radiol. 2012;13:557–63. https://doi. org/10.3348/kjr.2012.13.5.557. Weisbrod LJ, Liu C, Surdell D. Enlarging Ventriculus Terminalis in a Patient With Polyarteritis Nodosa. Cureus. 2021;13:e14460. https:// doi.org/10.7759/cureus.14460. Woodley-Cook J, Konieczny M, Spears J.  The Slowly Enlarging Ventriculus Terminalis. Pol J Radiol. 2016;81:529–31. https://doi. org/10.12659/PJR.895669. Zeinali M, Safari H, Rasras S, Bahrami R, Arjipour M, Ostadrahimi N.  Cystic dilation of a ventriculus terminalis. Case report and review of the literature. Br J Neurosurg. 2019;33:294–8. https://doi. org/10.1080/02688697.2017.1340585. Zhang L, Zhang Z, Yang W, Jia W, Xu Y, Yang J.  Cystic Dilation of the Ventriculus Terminalis: Report of 6 Surgical Cases Treated with Cyst-Subarachnoid Shunting Using a T-Catheter. World Neurosurg. 2017;104:522–7. https://doi.org/10.1016/j.wneu.2017.05.017.

62

Spinal Dural Ectasia

62.1 Generalities and Relevance

D

E

Dural ectasia, also recognized as an “enlarged dural sac”, refers to the ballooning or widening of the dural sac. This rare entity may be associated with herniation of spinal nerve root sleeves out of adjacent neural foramina, scalloping of the posterior vertebral body, bony erosion of pedicles and lamina, and widening of nerve root foramina. The lumbosacral area is by far the most often involved because the caudal portion of the spinal canal is the site of the highest cerebrospinal fluid (CSF) (hydrostatic) pressure in the upright posture (Figs. 62.1 and 62.2). Pathogenesis of dural ectasia is unknown. Classically, the disease is associated with Marfan syndrome. However, dural ectasia may exist with other generally weakened connective tissue disorders such as  Ehlers-Danlos syndrome, Loeys-­ Dietz syndrome,  type 1 neurofibromatosis, or ankylosing spondylitis. More rarely, the enlarged dural sac may be associated with acromegaly, trauma, post-surgery, scoliosis, or tumors. Sometimes, the exact cause is not known and the disease is then considered “idiopathic”. Fig. 62.1  Lumbosacral dural ectasia (double arrows) compared to norIn 1999, Fattori et  al. recommended a qualitative dural mal appearance (a) as seen in sagittal sections. Note the scalloping of the posterior vertebral body (b) ectasia grading system with 4 grades: • Grade 0: normal, with no dural ectasia. • Grade 1: mild dural ectasia, defined by bulging of the dural sac and lack of epidural fat at the posterior wall of one vertebral body, presence of radicular cysts, or both features. • Grade 2: moderate dural ectasia, defined by bulging of the dural sac and lack of epidural fat at the posterior wall of two or more vertebral body levels and presence of radicular cysts. • Grade 3: severe dural ectasia, defined by the presence of an anterior sacral meningocele.

Sciatica related to spinal dural ectasia may cause symptoms through a variety of mechanisms including: –– Vertebral bony erosions including foraminal widening leading to microfractures or spinal instability. –– Distortion and/or traction of neural roots. –– Compression of the lumbosacral nerve roots by concomitant meningeal cyst(s). –– Lumbosacral nerve root damage secondary to high CSF pressure.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_62

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726 Fig. 62.2  Lumbosacral dural ectasia compared to normal appearance (a) as seen in axial sections. Note the scalloping of the posterior vertebral body, the bony erosion of pedicles and lamina, and a lack of epidural fat (b). The nerve roots are placed on the periphery of the thecal sac (arrows)

62  Spinal Dural Ectasia

a

62.2 Clinical Presentations

b

a

b

Patients with dural ectasia may present with low back pain, radicular pain, rectal/genital pain, sciatica-like symptoms, urinary disturbances, or even postural headaches. Generally, the symptoms are worsened by upright position and often (but inconstantly) released by supine posture. However, many people will remain asymptomatic. Moderate to severe cases can present with more serious neurologic conditions such as lower limb weakness, bowel/ bladder/sexual dysfunctions, and even a complete cauda equina syndrome secondary to nerve root compression. Uncommonly, an abdominopelvic mass secondary to an anterior sacral  meningocele  may be encountered in some patients.

62.3 Imaging Features Radiography and bony computed tomography (CT) scan may be useful for identifying secondary bone changes especially posterior vertebral body erosion (scalloping) and sometimes vertebral fractures, angular deformities, and traumatic dislocations. On magnetic resonance imaging (MRI), there is typically an increase in the anteroposterior diameter of the dural sac with a lack of epidural fat. The signal content of the fluid inside the thecal sac is identical to that of CSF. The neuroimaging examination must seek the potential association of radicular cysts, anterior meningoceles, nerve root sleeve herniation, tethered spinal cord (Fig.  62.3), or other concomitant lesions. According to Lundby et al., the diagnosis of dural ectasia should be established on the existence of at least one of the following criteria: (a) Anterior meningocele. (b) Dural sac diameter at level S1 or below greater than at level L4.

Fig. 62.3  Sagittal T2-weighted MRI (a, b) showing a lumbosacral dural ectasia with low conus medullaris, tethered spinal cord (arrows), and spina-lipoma (stars)

(c) Dural sac ratio at S1 superior to 0.59. Occasionally, imaging appearances are atypical and may be confused with other possible differential diagnoses, especially in the lumbosacral region such as: –– –– –– –– –– –– ––

Arachnoid cyst. Tarlov cyst. Synovial cyst. Meningocele. Nerve sheath tumor. Hydatidosis. Some spinal metastases.

Further Reading

62.4 Treatment Options and Prognosis Lumbosacral dural ectasia can be managed conservatively or surgically. However, on most occasions, no specific treatment is required. Conservative therapy includes pain control medications, physiotherapy, and other physical modalities resulting in more or less control of the patient’s pain. Some authors have already tried to use acetazolamide with satisfactory results. Surgical procedures comprise radicular decompression and surgical repair of the dura which offers some neurologic and painful relief for some cases. The dura should be closed hermetically to avoid a postoperative CSF fistula, pseudomeningocele, and potential meningitis. Patients with spinal deformities should be carefully monitored for progression because an early surgical procedure may be necessary to prevent severe deformity, dislocation, and later more serious neurologic complications. Also, treatment options should always consider the underlying etiology and associated lesions.

Further Reading Akhaddar A. Differential diagnosis of Intraspinal arachnoid cysts. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: state-of-the-art concepts. Switzerland: Springer International Publishing; 2022. p. _26. Altman A, Uliel L, Caspi L.  Dural ectasia as presenting symptom of Marfan syndrome. Isr Med Assoc J. 2008;10:194–5. Begley K, Sergides Y.  Giant sacral dural ectasia causing ureteric obstruction in Marfan syndrome. ANZ J Surg. 2021;92(7-8):1930– 1. https://doi.org/10.1111/ans.17397. Böker T, Vanem TT, Pripp AH, Rand-Hendriksen S, Paus B, Smith HJ, et  al. Dural ectasia in Marfan syndrome and other hereditary connective tissue disorders: a 10-year follow-up study. Spine J. 2019;19:1412–21. https://doi.org/10.1016/j.spinee.2019.04.010. de Kleuver M, van Jonbergen JP, Langeloo DD.  Asymptomatic massive dural ectasia associated with neurofibromatosis type 1 threat-

727 ening spinal column support: treatment by anterior vascularized fibula graft. J Spinal Disord Tech. 2004;17:539–42. https://doi. org/10.1097/01.bsd.0000117544.88865.f0. Fattori R, Nienaber CA, Descovich B, Ambrosetto P, Reggiani LB, Pepe G, et  al. Importance of dural ectasia in phenotypic assessment of Marfan’s syndrome. Lancet. 1999;354:910–3. https://doi. org/10.1016/s0140-­6736(98)12448-­0. Foran JR, Pyeritz RE, Dietz HC, Sponseller PD.  Characterization of the symptoms associated with dural ectasia in the Marfan patient. Am J Med Genet A. 2005;134A:58–65. https://doi.org/10.1002/ ajmg.a.30525. Liu CC, Lin YC, Lo CP, Chang TP. Cauda equina syndrome and dural ectasia: rare manifestations in chronic ankylosing spondylitis. Br J Radiol. 2011;84:e123–5. https://doi.org/10.1259/bjr/45816561. Lundby R, Rand-Hendriksen S, Hald JK, Lilleås FG, Pripp AH, Skaar S, et al. Dural ectasia in Marfan syndrome: a case control study. AJNR Am J Neuroradiol. 2009;30:1534–40. https://doi.org/10.3174/ajnr. A1620. Meester JAN, Verstraeten A, Schepers D, Alaerts M, Van Laer L, Loeys BL.  Differences in manifestations of Marfan syndrome, Ehlers-­ Danlos syndrome, and Loeys-Dietz syndrome. Ann Cardiothorac Surg. 2017;6:582–94. https://doi.org/10.21037/acs.2017.11.03. Nallamshetty L, Ahn NU, Ahn UM, Nallamshetty HS, Rose PS, Buchowski JM, Sponseller PD. Dural ectasia and back pain: review of the literature and case report. J Spinal Disord Tech. 2002;15:326– 9. https://doi.org/10.1097/00024720-­200208000-­00012. Nguyen HS, Lozen A, Doan N, Gelsomin M, Shabani S, Maiman D. Marsupialization and distal obliteration of a lumbosacral dural ectasia in a nonsyndromic, adult patient. J Craniovertebr Junction Spine. 2015;6:219–22. https://doi.org/10.4103/0974-­8237.167887. Polster SP, Dougherty MC, Zeineddine HA, Lyne SB, Smith HL, MacKenzie C, et  al. Dural ectasia in Neurofibromatosis 1: case series, management, and review. Neurosurgery. 2020;86:646–55. https://doi.org/10.1093/neuros/nyz244. Schonauer C, Tessitore E, Frascadore L, Parlato C, Moraci A. Lumbosacral dural ectasia in type 1 neurofibromatosis. Report of two cases. J Neurosurg Sci. 2000;44:165–8. Smith MD.  Large sacral dural defect in Marfan syndrome. A case report. J Bone Joint Surg Am. 1993;75:1067–70. https://doi. org/10.2106/00004623-­199307000-­00013. Weigang E, Ghanem N, Chang XC, Richter H, Frydrychowicz A, Szabó G, et al. Evaluation of three different measurement methods for dural ectasia in Marfan syndrome. Clin Radiol. 2006;61:971–8. https://doi.org/10.1016/j.crad.2006.05.015.

Spinal Arachnoid Cysts

63.1 Definition and Relevance Arachnoid cysts, also known as “leptomeningeal cysts”, are nonneoplastic cerebrospinal fluid (CSF)-filled sacs lined with the arachnoid membrane composed of arachnoidal cells and collagen. The arachnoid membrane is one of the three meninges that envelop the spinal cord and the spinal nerve roots. Arachnoid cysts can be primary (congenital) or secondary (acquired). Primary arachnoid cysts are a common congenital disorder (more than 90%) present at birth. Whereas secondary arachnoid cysts are more unusual (less than 10%) and develop as a result of injury, meningitis, bleeding, tumors, or postsurgical procedures. The majority of arachnoid cysts form intracranially in relation to an arachnoid cistern. Intraspinal arachnoid cysts are rarer and may be intradural, extradural, or intramedullary. The degree of communication with the adjacent CSF space is variable with some arachnoid cysts freely communicating and others not. The mechanism of cyst expansion is not clearly understood. However, there are three proposed mechanisms: one-way ball-valve hypothesis, hyperosmotic, and secreting theories. The first description of a spinal arachnoid cyst was published in 1842 by François Magendie (1783–1855). While the first patient was operated on by Spiller in 1903. In 1988, Nabors et al. recommended a simplified classification of spinal “meningeal” cysts, comprising three main categories based on their topographic situation: Type I: Cysts are extradural without spinal nerve root fibers Type II: Cysts are extradural with spinal nerve root fibers (e.g., Tarlov cyst) Type III: Cysts are intradural. Type I was subdivided into extradural cysts (type IA) and sacral meningoceles (type IB). (For Tarlov Cysts, please refer to Chap. 64). Most primary spinal forms occur in the thoracic (70%) or cervical (20%) spinal regions. In the lumbosacral spinal canal, this rare (less than 10%) but benign pathologic entity

63

has the potential to cause serious neurologic damage by compressing the cauda equina nerve roots. Secondary arachnoid cysts can occur anywhere in the spinal canal, depending on the site of the causal factor. Primary spinal arachnoid cysts may be associated with other developmental anomalies such as neural tube defects, tethered cord, syringomyelia, dermoid/epidermoid cysts, or congenital lipoma. These congenital malformations are more common in the child and mainly among patients with intradural arachnoid cysts. Overall, spinal arachnoid cysts may present in pediatric and adult populations without distinct gender predilection. However, lumbar and sacral cysts more often develop among adults in their fifth decade with a slight predominance of males.

63.2 Clinical Presentations Clinical presentations are highly variable and depend principally on the exact anatomic site, cyst volume, duration of symptoms, and the patient’s age. Some patients manifest simple lumbosacral rachialgia, while others present with complete cauda equina syndrome. However, many patients will remain asymptomatic and the cysts discover incidentally through neuroimaging. Patients may present with low back pain, lumbosacral radicular pain, rectal/genital pain, sciatica-like symptoms, or urinary disturbances. Generally, the symptoms are worsened by postural changes and the Valsalva maneuver. Severe presentations may include progressive spastic or flaccid paralysis, lower limb weakness, bladder/bowel incontinence, or even cauda equina syndrome. However, sensory deficits are less noticeable. However, the course of lumbosacral arachnoid cysts is often progressive, long, and more indolent than in thoracic and cervical ones because the lumbar spinal canal is the largest in diameter and the spinal cord itself ends around the L1 vertebrae level.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_63

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730

In the pediatric population, most symptoms begin during infancy but onset may be delayed until adolescence. Indeed, the clinical symptoms develop over months or years knowing that many patients may present long-term remission extending for years. Interestingly, some patients with recurrent neurological symptoms have been misdiagnosed as having multiple sclerosis. Possible concomitant malformations may be encountered in some patients such as scoliosis and spinal midline skin lesions.

63.3 Imaging Features Plain radiography and bony computed tomography (CT) scan may be useful for identifying secondary bone changes especially posterior vertebral body erosion (scalloping) and sometimes vertebral fractures, or angular deformities; however, the arachnoid cyst itself was rarely diagnosed on CT scan. Most spinal arachnoid cysts opacify with contrast on myelo-CT, but it may be challenging to be diagnosed with certainty. Magnetic resonance imaging (MRI) is now the primary imaging modality of choice that may indicate the exact

a

63  Spinal Arachnoid Cysts

topography of the cysts and their inner structures, define the exact margins of the collections, and determine the relationship of the cysts with contiguous anatomic structures as well as any communication (known as a pedicle, fistula, or ostium) between the cyst and adjacent subarachnoid spaces. On MRI, these fluid-filled lesions demonstrate similar signal characteristics to CSF in all pulse sequences: low signal intensity on T1-weighted images and high intensity on T2-weighted images without gadolinium enhancement (Fig. 63.1). Classically, there is a decreased CSF flow within the cyst on phase-contrast imaging. In addition, there is no evidence of restricted diffusion on diffusion-weighted images. The vast majority of lumbosacral cysts are single and typically limited to 2 or 3 vertebral body levels craniocaudally. Arachnoid cysts with multiple septations are more often related to secondary etiologies, especially those resulting from delayed postinfectious meningitis. Overall, the diagnosis of a secondary arachnoid cyst will be highly evocative when there is a previous history of spinal surgery, traumatic injury, subarachnoid inflammation, or bleeding. The neuroimaging examination must also seek for the potential coexistence of other spinal or intraspinal congenital lesions.

b

Fig. 63.1  Extradural mid-thoracic arachnoid cyst (stars) as seen on axial (a) and sagittal (b) T2-weighted MRI

63.4 Treatment Options and Prognosis

Diffusion-weighted MRI helps distinguish spinal arachnoid cysts from other types of cystic lesions. However, occasionally, imaging appearances are atypical and may be confused with some differential diagnose in the lumbosacral region such as: –– –– –– –– –– –– ––

Synovial cyst  Tarlov cyst Meningocele Cystic tumors Nonneoplastic Cysts Dural ectasia Hydatidosis or cysticercosis

63.4 Treatment Options and Prognosis Many surgeons recommend no treatment for “asymptomatic” spinal arachnoid cysts that cause no pain or neurological symptoms/signs regardless of their volume and spinal localization. However, no or pauci-symptomatic patients may need a follow-up MRI yearly to detect any cystic development or new abnormality. Surgery is the treatment of choice for “symptomatic” patients, especially those with uncontrolled persistent pain, if neurological signs/symptoms progress, or if there is a spinal instability or cyst extension. The aim of surgical proce-

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dures is a spinal exploration and neurologic decompression via total/partial cyst excision, marsupialization, fenestration, ligation of the communication site, shunting, or a combination of these techniques. Overall, extradural arachnoid cysts are typically resected via a posterior approach with the closure of the dural defect (Fig. 63.2), while intradural or anterior cysts are usually fenestrated in order to avoid further neurological damage for excision of an adherent cyst wall. Some other alternative options may be considered such as cyst diversion or shunting. Simple CT-guided aspiration of the cyst contents may be useful, but provides only a temporary solution. In order to avoid some surgical complications such as nerve root injury, postoperative deficits, and kyphotic deformity, some authors encouraged the use of the endoscope. Following the intradural procedures, the dura matter should be closed in a hermetic manner to avoid a postoperative CSF fistula, pseudomeningocele, and potential meningitis. Also, treatment possibilities should always consider the secondary etiology and potentially associated lesions. The majority of patients showed good clinical results after surgical excision of the cyst. However, the recurrence rate was not rare (less than 15%), mainly encountered with intradural forms. Globally, intradural primary arachnoid cysts had a low incidence rate (12%) compared to the incidence rate of posthemorrhagic cysts (66%).

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Fig. 63.2  Operative view during cyst excision (a). The extradural cyst surgically removed (b)

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Further Reading Akhaddar A.  Surgical management of spinal arachnoid cysts. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: state-of-the-art concepts. Switzerland: Springer International Publishing; 2022. p. 29. Bond AE, Zada G, Bowen I, McComb JG, Krieger MD. Spinal arachnoid cysts in the pediatric population: report of 31 cases and a review of the literature. J Neurosurg Pediatr. 2012;9:432–41. https:// doi.org/10.3171/2012.1.PEDS11391. Cai Z, Hong X, Huang J, Hu H, Lu C, Ding X, et  al. Microsurgical treatment of symptomatic spinal extradural arachnoid cyst: a consecutive case series of 34 patients and literature review. Clin Neurol Neurosurg. 2021;210:107000. https://doi.org/10.1016/j. clineuro.2021.107000. Candy N, Young A, Devadass A, Dean A, McMillen J, Trivedi R. Dual lumbar bronchogenic and arachnoid cyst presenting with sciatica and left foot drop. Acta NeurochirActa Neurochir (Wien). 2017;159:2029–32. https://doi.org/10.1007/s00701-­017-­3284-­z. Fam MD, Woodroffe RW, Helland L, Noeller J, Dahdaleh NS, Menezes AH, et al. Spinal arachnoid cysts in adults: diagnosis and management. A single-center experience. J Neurosurg Spine. 2018;29:711– 9. https://doi.org/10.3171/2018.5.SPINE1820. Ido K, Matsuoka H, Urushidani H.  Effectiveness of a transforaminal surgical procedure for spinal extradural arachnoid cyst in the upper lumbar spine. J Clin Neurosci. 2002;9:694–6. https://doi. org/10.1054/jocn.2002.1138. Kadono Y, Yuguchi T, Ohnishi Y, Iwatsuki K, Yoshimine T.  A symptomatic spinal extradural arachnoid cyst with lumbar disc herniation. Case Rep Orthop. 2015;2015:250710. https://doi. org/10.1155/2015/250710.

63  Spinal Arachnoid Cysts Krstačić A, Krstačić G, Butković SS. Atypical cause of radiculopathy Intradural spinal arachnoid cyst. Acta Clin Belg. 2016;71:267–8. https://doi.org/10.1080/17843286.2016.1139288. Lee HG, Kang MS, Na YC, Jin BH. Spinal intradural arachnoid cyst as a complication of insertion of an interspinous device. Br J Neurosurg. 2023;37(4):811–5. https://doi.org/10.1080/02688697.2 019.1668541. Liu JK, Cole CD, Kan P, Schmidt MH.  Spinal extradural arachnoid cysts: clinical, radiological, and surgical features. Neurosurg Focus. 2007;22:E6. https://doi.org/10.3171/foc.2007.22.2.6. Nabors MW, Pait TG, Byrd EB, Karim NO, Davis DO, Kobrine AI, et al. Updated assessment and current classification of spinal meningeal cysts. J Neurosurg. 1988;68:366–77. https://doi.org/10.3171/ jns.1988.68.3.0366. Papagelopoulos PJ, Peterson HA, Ebersold MJ, Emmanuel PR, Choudhury SN, Quast LM. Spinal column deformity and instability after lumbar or thoracolumbar laminectomy for intraspinal tumors in children and young adults. Spine (Phila Pa 1976). 1997;22:442– 51. https://doi.org/10.1097/00007632-­199702150-­00019. Qi W, Zhao L, Fang J, Chang X, Xu Y. Clinical characteristics and treatment strategies for idiopathic spinal extradural arachnoid cysts: a single-center experience. Acta NeurochirActa Neurochir (Wien). 2015;157:539–45. https://doi.org/10.1007/s00701-­014-­2278-­3. Quinones-Hinojosa A, Sanai N, Fischbein NJ, Rosenberg WS. Extensive intradural arachnoid cyst of the lumbar spinal canal: case report. Surg Neurol. 2003;60:57–9. https://doi.org/10.1016/ s0090-­3019(03)00150-­2. Yoo KH, Kim MC, Ju CI, Kim SW. Extradural spinal arachnoid cyst as a cause of cauda Equina syndrome in a child. Korean J Neurotrauma. 2020;16:355–9. https://doi.org/10.13004/kjnt.2020.16.e35.

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Tarlov Cysts

64.1 Generalities and Relevance Tarlov cysts, also known as spinal “perineural cysts”, are cerebrospinal fluid-filled dilatations of the  nerve root sleeve  at the posterior  root ganglion  usually found in the lower lumbar spine and the sacrum (Figs.  64.1, 64.2, and 64.3). These cystic lesions may be solitary or multiple and

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correspond to type II of Nabors’s classification of spinal meningeal cysts (Table 64.1). Tarlov cysts were first described in 1938 by Isadore Max Tarlov (1905–1977). This American neurosurgeon observed these benign cystic lesions in a cadaveric study. Ten years later, he defined the clinical consequence of this new sacral cystic entity. Also, he distinguished the menin-

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Fig. 64.1  L5-S1 Tarlov cyst on the right side (arrows). Lumbosacral sagittal T1- (a) and T2-weighted (b) MRI. Axial STIR sequence (c) and T2-weighted (d) MRI

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_64

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Fig. 64.2  S1-S2 large Tarlov cyst. Lumbosacral sagittal T1- (a) and T2-weighted (b) MRI. Axial T2-weighted MRI (c) and on axial CT scan (d). Note the position of the adjacent S2 nerve roots (arrows) (c) and posterior vertebral scalloping (posterior vertebral body mass effect) (d)

geal diverticula (without neural elements in their wall) from the Tarlov cysts which have nerve root fibers within the cyst wall. The majority of the cysts are asymptomatic (about 80% of cases) and found incidentally on routine neuroimaging especially in young and middle-aged adult populations (up to 9%) with a female predominance. Symptomatic cases are unusual (less than 20%). Indeed, initiated by certain factors, some cysts progressively expand

in size over time and can begin to compress the nerve roots resulting in lumbosacral radicular pain in a good number of symptomatic patients. The etiology of Tarlov cysts is not clearly understood. There are three supposed theories: • Congenital (developmental) • Inflammatory • Traumatic

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64.3 Imaging Features

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Fig. 64.3  S2 Tarlov cyst (stars). Lumbosacral sagittal T1- (a), T2-weighted (b) MRI, and on CT scan (c). Note the sacral bone erosion (c)

Table 64.1  Nabors simplified classification of spinal “meningeal” cysts Types Type I Type II Type III

Descriptions Cysts are extradural without spinal nerve root fibers Cysts are extradural with spinal nerve root fibers (e.g., Tarlov cyst) Cysts are intradural

64.2 Clinical Presentations The clinical presentations of symptomatic Tarlov cysts are unspecific and may be confused with other usual degenerative lumbar spine diseases. Classically, symptoms include low-back pain, sacrococcygeal pain (coccygodynia), perineal (including vaginal and rectal) pain, lumbosacral nerve root pain (sciatic pain), leg weakness, neurogenic claudication, bowel and bladder dysfunction, and sexual dysfunction. Cysts larger than 10 mm are more expected to be symptomatic. However, symptoms don’t seem to be correlated with cystic size for many authors. The course of symptoms is often progressive, long, and more indolent than those of other classic arachnoid cysts. Usually, the symptoms are worsened by postural changes

and the Valsalva maneuver. These can be explained by the increase in CSF pressure. Acute and severe presentations are rarely encountered and may include progressive spastic or flaccid paralysis, lower limb weakness, urinary/rectal incontinence, or even complete cauda equina syndrome. However, as with other meningeal cysts, many cases will remain asymptomatic and the cyst will be found only incidentally on MRI.

64.3 Imaging Features On computed tomography (CT) scan, Tarlov cysts have the same hypodensity as normal CSF. A bony CT scan may be useful for identifying secondary bone changes especially sacral foramina widening and sometimes posterior vertebral body erosion (scalloping) (Figs.  64.2d and 64.3c). When needed, myelography or CT myelography will show delayed cystic filling (Fig. 64.4). Magnetic resonance imaging (MRI) allows a better assessment. It may specify the exact topography of the cysts and their inner structures, define the exact margins of the collections, and determine the relationship of the cysts with contiguous anatomic structures. Most Tarlov cysts are a sim-

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64  Tarlov Cysts

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Fig. 64.4  Antero-posterior lumbosacral myelography (a) and on the posterior oblique view (b) showing a Tarlov cyst of the S2 nerve root on the left side (arrows) Fig. 64.5  Multiple bilateral foraminal perineural cysts (arrows) as seen on axial (a, b) and anteroposterior MR myelography (c). (Courtesy of Pr. Abad Cherif El Asri)

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ple rounded cyst mass developing near the lower lumbar or sacral nerves adjacent to the posterior root ganglion (Figs. 64.1, 64.2, 64.3, 64.4, 64.5, 64.6, 64.7, 64.8, 64.9, and 64.10). But sometimes, Tarlov cysts may present as a complex multiloculated cystic collection with intraluminal septations (Figs. 64.11, 64.12, and 64.13). Typically, these fluid-filled lesions demonstrate similar signal characteristics to CSF in all pulse sequences: low signal intensity on T1-weighted images and high intensity on T2-weighted images with no gadolinium enhancement. Classically, there is no evidence of restricted diffusion on diffusion-weighted images. A Tarlov cyst may be associated with another disease that is causing symptoms (e.g., lumbar disc herniation or lumbar foraminal stenosis) (Fig. 64.6), but the majority of the cysts themselves are asymptomatic. Occasionally, imaging appearances are atypical and may be confused with some differential diagnoses in the lumbosacral region such as: –– Synovial cyst –– Arachnoid cyst

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64.3 Imaging Features

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Fig. 64.6  Small L5-S1 Tarlov cyst (arrows) with concomitant adjacent lumbar disc herniation on the right side. Sagittal (a) and axial (b) T2-weighted MRI

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Fig. 64.7  Bilateral L5-S1 Tarlov cysts as seen on sagittal (a, b) and axial (c, d) T2-weighted MRI (arrows)

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64  Tarlov Cysts

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Fig. 64.8  Tarlov cyst of right-sided S1 nerve root (arrows) as seen on sagittal T1- (a), T2-weighted (b) MRI, and on STIR sequence (c)

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Fig. 64.9  Tarlov cyst of right-sided L5 nerve root (arrows) as seen on sagittal T1- (a), T2-weighted (b) MRI, as well as on axial T2-weighted MRI (c, d)

64.3 Imaging Features

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Fig. 64.10  Bilateral L5-S1 Tarlov cysts causing posterior vertebral body erosion (scalloping) (arrows). Axial T2-weighted MRI (a-c). (Courtesy of Pr. Hatim Belfquih)

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Fig. 64.11  Coronal T1-weighted MRI (a) and on STIR sequence (b) showing multiple sacral Tarlov cysts (C) presenting as a complex multiloculated cystic collection adjacent to the thecal sac (T)

–– –– –– –– –– ––

Meningocele Conjoined nerve root Cystic tumors Nonneoplastic Cysts Dural ectasia Hydatidosis or cysticercosis

Sometimes, electromyography can be used to identify axonal damage in symptomatic patients. Also, standard urodynamic tests can be required to define if the patient has a neurogenic bladder.

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Fig. 64.12  Complex multiple bilateral S1-S2 Tarlov cysts. Sagittal T1- (a) and T2-weighted (b) MRI. Axial T2-weighted MRI (c, d). Note the position of the sacral nerve roots (arrows) in the periphery of the thecal sac

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Fig. 64.13  The same case as in Fig. 64.12. Complex multiple S1-S2 Tarlov cysts (arrows) as seen in coronal T2-weighted MRI (a, b)

Further Reading

64.4 Treatment Options and Prognosis Overall, “asymptomatic” Tarlov cysts do not require treatment regardless of their volume and spinal localization. Symptomatic cases can be managed conservatively or surgically. Conservative therapy includes pain control medications, physiotherapy, and other physical modalities resulting in more or less control of the patient’s pain. Surgery is indicated for “symptomatic” patients with uncontrolled persistent pain, those with the progression of neurological signs/symptoms, and those with evolving cysts. Surgical procedures aim to explore spinal and neurologic decompression via total/partial cyst excision, marsupialization, fenestration, imbrication, ligation of the communication site, shunting, or a combination of these techniques. Direct microsurgical approach, through posterior exposing of the lumbosacral region will allow the cyst to open and drain the fluid. The cyst can be occluded with fibrin glue or other substance such as autologous muscle and fat to prevent any recurrence. If nerve root fibers are found within the cystic cavity, the cyst wall could be removed but the nerve roots should be preserved. Therefore, a duraplasty technic will be required to reconstruct the nerve root sheath. Some other alternative options may be considered such as cyst diversion or shunting. Simple CT-guided aspiration of the cyst contents with or without fibrin glue injection may be useful. Unfortunately, none of these techniques prevent symptomatic cyst recurrence. On another side, some authors recommend percutaneous drainage before any more invasive surgical approaches. More recently, some authors published their experience of endoscopic-assisted resection and fenestration of a series of sacral Tarlov cysts. Postoperative CSF leak is the most common complication with potential meningitis. Also, iatrogenic neurological deficits, chronic neuropathic pain, urinary disturbances, and spinal headaches are not insignificant complications. The majority of patients operated on via a direct surgical excision showed good clinical results. However, the recurrence rate was not rare (up to 12%).

Further Reading Akhaddar A.  Surgical Management of Spinal Arachnoid Cysts. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: state-of-the-art concepts. Switzerland: Springer International Publishing; 2022. https://doi.org/10.1007/978-­3-­031-­22701-­1_29.

741 Burke JF, Thawani JP, Berger I, Nayak NR, Stephen JH, Farkas T, et al. Microsurgical treatment of sacral perineural (Tarlov) cysts: case series and review of the literature. J Neurosurg Spine. 2016;24:700– 7. https://doi.org/10.3171/2015.9.SPINE153. Cantore G, Bistazzoni S, Esposito V, Tola S, Lenzi J, Passacantilli E, et al. Sacral Tarlov cyst: surgical treatment by clipping. World Neurosurg. 2013;79:381–9. https://doi.org/10.1016/j.wneu.2012.06.015. Fletcher-Sandersjöö A, Mirza S, Burström G, Pedersen K, Kuntze Söderqvist Å, Grane P, et  al. Management of perineural (Tarlov) cysts: a population-based cohort study and algorithm for the selection of surgical candidates. Acta Neurochir. 2019;161:1909–15. https://doi.org/10.1007/s00701-­019-­04000-­5. Kleib AS, Salihy SM, Hamdi H, Carron R, Soumaré O. A rare cause of thoracic spinal cord compression by multiple large Tarlov cysts. Korean J Neurotrauma. 2018;14:35–8. https://doi.org/10.13004/ kjnt.2018.14.1.35. Klepinowski T, Orbik W, Sagan L. Global incidence of spinal perineural Tarlov’s cysts and their morphological characteristics: a meta-­ analysis of 13,266 subjects. Surg Radiol Anat. 2021;43:855–63. https://doi.org/10.1007/s00276-­020-­02644-­y. Lee JY, Impekoven P, Stenzel W, Löhr M, Ernestus RI, Klug N.  CT-guided percutaneous aspiration of Tarlov cyst as a useful diagnostic procedure prior to operative intervention. Acta Neurochir. 2004;146:667–70. https://doi.org/10.1007/s00701-­004-­0274-­8. Lucantoni C, Than KD, Wang AC, Valdivia-Valdivia JM, Maher CO, La Marca F, et al. Tarlov cysts: a controversial lesion of the sacral spine. Neurosurg Focus. 2011;31:E14. https://doi.org/10.3171/2011 .9.FOCUS11221. Potts MB, McGrath MH, Chin CT, Garcia RM, Weinstein PR.  Microsurgical fenestration and Paraspinal muscle pedicle flaps for the treatment of symptomatic sacral Tarlov cysts. World Neurosurg. 2016;86:233–42. https://doi.org/10.1016/j. wneu.2015.09.055. Prashad B, Jain AK, Dhammi IK.  Tarlov cyst: case report and review of literature. Indian J Orthop. 2007;41:401–3. https://doi. org/10.4103/0019-­5413.37007. Sharma M, Velho V, Mally R, Khan SW.  Symptomatic lumbosacral perineural cysts: a report of three cases and review of literature. Asian J Neurosurg. 2015;10:222–5. https://doi. org/10.4103/1793-­5482.161177. Stella L, Gambardella A, Maiuri F.  Giant sacral perineurial cyst. A case report. Clin Neurol Neurosurg. 1989;91:343–6. https://doi. org/10.1016/0303-­8467(89)90012-­7. Sugawara T, Higashiyama N, Tamura S, Endo T, Shimizu H.  Novel wrapping surgery for symptomatic sacral perineural cysts. J Neurosurg Spine. 2021;36:185. https://doi.org/10.3171/2021.5.SP INE21179. Tarlov IM.  Perineural cysts of the spinal roots. Arch Neurol Psychiatr. 1938;40:1067–74. https://doi.org/10.1001/ archneurpsyc.1938.02270120017001. Wang Z, Jian F, Chen Z, Wu H, Wang X, Duan W, et al. Percutaneous spinal endoscopic treatment of symptomatic sacral Tarlov cysts. World Neurosurg. 2021;S1878-8750(21):01720–4. https://doi. org/10.1016/j.wneu.2021.11.019. Xu J, Sun Y, Huang X, Luan W.  Management of symptomatic sacral perineural cysts. PLoS One. 2012;7:e39958. https://doi.org/10.1371/ journal.pone.0039958.

Lumbosacral Spine Fractures and Dislocations

65.1 Generalities and Relevance Fractures and dislocations of the lumbosacral spine involve breaks and/or subluxations in one or more bones of the lumbar and  sacral regions  of the spine (from L1 through S5) resulting in lumbosacral nerve root damage. Their distinctive anatomy and biomechanical characteristics differentiate them from other traditional thoracolumbar spine injuries. In this chapter, we will focus mainly on lumbosacral spine fractures and dislocations (LSFD) involving L4, L5, S1, and S2 vertebral levels corresponding to sciatic nerve roots. The sacrum below S2 is less indispensable to locomotion or support of the entire spinal column. LSFDs are relatively uncommon compared with other more highly situated spine injuries. They represent less than 8% of all spinal injuries and can result in a variety of neurological symptoms ranging from simple lumbosacral radicular pain such as sciatica to complete paraplegia secondary to cauda equina syndrome. About 10% to 30% of adults with LSFD are reported to have associated neurologic damage. Up to 45% of sacral fractures occur with a simultaneous pelvic ring injury. The majority of these lumbosacral lesions are related to blunt trauma and are caused by motor vehicle accidents (40%), followed by falls (20%) and sporting accidents. A high percentage of LSFDs occur in injured men younger than 30 years. Penetrating (open) lumbosacral spine injuries, which are mainly dominated by gunshot wounds, are discussed in Chap. 68 of the present book. Pathologic fractures are seen in individuals with osteoporosis or other disease conditions that compromise bone strength (c.f. Chap. 66 about Spinal Pathologic Fractures). Sacral lesions of a less serious nature, fatigue fractures, and insufficiency fractures should not be left out (c.f. Chap. 67 about Sacral Stress Fractures). In the lumbosacral spine, fractures and dislocations may be classified according to the mechanism of injury and the

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degree of  instability.  The forces responsible for LSFD are variable including compression, flexion, extension, rotation, shear, distraction, or a combination of one or more of these forces. However,  compression fractures  are the most common acute fractures encountered. Rarely, some thoracolumbar burst fractures may induce lumbosacral radicular pain secondary to post-traumatic conus medullary syndrome (c.f. Chap. 43 about Conus Medullaris Lesions). According to the classification system of the AO Foundation and the Orthopaedic Trauma Association published in 2018, lumbar spinal injuries are categorized into three main types as follows: (a) Compression injury of the vertebral body (including burst fracture). (b) Tension band injury (e.g., Chance fracture). (c) Displacement/translational injury. Some fracture-dislocations of L5 are also considered traumatic spondylolistheses (c.f. Chap. 36 about Lumbar Spondylolisthesis). Most burst fractures of the lower lumbar spine are the result of an axial compressive force which can be responsible for the posterior displacement of bony fragments into the spinal canal, as well as lumbosacral kyphotic deformity. Lumbosacral junction injury is a rare type often associated with a pelvic injury and mainly occurred in high-energy trauma accidents. Regarding sacral spine injuries, sacral fractures are a major component of determining the stability of a pelvic ring injury. Overall, there are three principal types of fractures: –– Fractures of the lower segments not associated with sacroiliac joint. –– Fractures involving the upper sacral segments associated with the sacroiliac joint (Table 65.1; Fig. 65.1). –– Injuries resulting in spino-pelvic instability.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_65

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744 Table 65.1  Denis classification system related to traumatic sacral fractures (Fig. 65.1) Zone involved Zone I Zone II

Zone III

Descriptions Transalar fractures lateral to the foramina or spinal canal (can be associated with partial L5 nerve root injury) Transforaminal fractures involving the foramina but not the spinal canal (can be associated with unilateral L5-S1-S2 radiculopathies but sphincter dysfunctions are rare) Isolated central fractures (vertical or transverse) medial to the foramina involving the spinal canal (habitually associated with bowel and bladder dysfunction. High occurrence of cauda equina syndrome)

Fig. 65.1  Denis classification system related to traumatic sacral fractures. The sacral bone is divided into 3 zones: Zone I: Region of ala. Zone II: Region of sacral foramina. Zone III: Region of the central sacral canal

In some complex lumbosacral spine trauma, neurologic symptoms may be accompanied by various degrees of pelvic ring lesions as well as vascular and intrapelvic damage. Furthermore, lumbosacral plexus injuries are not rare. Management of patients is completely different from other traditional forms of spinal traumatic injuries. Sometimes, patients are multi-injured and various medical specialties may be involved in their management. Sciatica related to LSFD may result from lumbosacral nerve root damage (injury, elongation, avulsion, or compression) secondary to different mechanisms including: • • • • • • •

Foraminal and/or central spinal stenosis Injured nerve roots or intradural rootlets Retropulsed bony fragments Intervertebral instability Secondary lumbar disc herniation Secondary spondylolisthesis Concomitant spinal epidural or subdural hematoma

65.2 Clinical Presentations As soon as the injured patient is admitted to the emergency room, it is mandatory to ensure stabilization (medical and spinal), resuscitation measures, and control of pain. The initial evaluation should include a sufficient and detailed history (mechanism of injury, loss of consciousness, leg weakness, tingling and numbness, urinary retention) and a physical exam. Clinical symptoms following such post-traumatic damages include severe pain, spinal or pelvic deformity, and neurologic deficits related to compression of neural structures. Lower lumbar fractures may cause solitary or multiple root deficits. However, massive post-traumatic disc herniations, lumbosacral dislocations, and burst fractures in the lumbar region can cause  cauda equina syndroma  (CES) with variable degrees of paraparesis and sphincter disturbances. In the context of a violent road traffic accident or fall from a very high place, lumbosacral nerve root damage rarely exists in isolation, but is often associated with other neurologic and extraspinal-neurologic symptoms. Sometimes, patients are multi-injured and various medical and surgical specialties may be involved in their management. The physical examination is often limited by pain severity. In the spinal and pelvic examination, inspect the overlying skin for abrasions or contusions. It is important to assess spine curves by looking for muscle spasms, kyphotic, or scoliotic deformity. Furthermore, the spine needs to be palpated for points of tenderness or fractured or displaced spinous processes. In addition, a detailed neurologic evaluation should include motor and sensory level assessment, testing for normal and abnormal reflexes (including sacral reflexes), and examination of rectal tone and perianal sensation. The perineal and pelvic examination must be executed accurately. S1 and S2 nerve root damages lead to motor deficits in hip abduction and ankle plantar flexion, as well as sensory changes in the posterior thigh, leg, and sole/lateral part of the foot. Overall, injury of S3-S5 nerve roots has little impact on lower limb motility and sensation.

65.3 Paraclinic Features Imaging assessment with or without neurophysiologic studies enhances the clinical evaluation with functional and anatomic details that determine localization, extent, and degree of spinal instability and neurologic damage (Figs. 65.2, 65.3, 65.4, 65.5, 65.6, 65.7, 65.8, 65.9, 65.10, 65.11, and 65.12).

65.3  Paraclinic Features

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Fig. 65.2  Case 1. Burst fracture of L4 with canal compromise (arrows) as seen on sagittal reconstructions (a, b) and axial (c, d) CT scan on both bone (b, d) and soft-tissue (a, c) windows

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Fig. 65.3  Case 2. Fracture of the antero-inferior part of the vertebral body of L4 as seen on sagittal (a) and coronal reconstructions (b) CT scan as well as on axial view (c) (bone windows)

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Fig. 65.4  Case 3. Post-­ traumatic fracture of the vertebral body of L3 (arrow) with vertebral canal compromise (stars). Sagittal reconstruction (a) and axial (b, c) CT scan

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Fig. 65.5  Case 3. Intraoperative view showing posterior decompression and L1-L5 fusion using a polyaxial screw-rod system (a). Postoperative sagittal reconstruction CT scan (b) showing the L3 vertebral body height correction (arrow)

In addition, to classify the type of lumbosacral lesions, these investigations may help decisions regarding therapeutic management.

Plain radiographies represent the most important initial imaging examination, including anteroposterior, lateral, and oblique views. Most kyphotic angulations are associated with misalignment and bony fractures. Disruption of the posterior vertebral body line and widening of the interpediculate distance are important signs of a burst fracture. Narrowing of an intervertebral disc space frequently goes with a flexion injury. Widening of the posterior facet joint or the interspinous distance and complete exposing of the facet surfaces point to a severe posterior ligamentous injury. Oblique radiographs are useful in looking for pars interarticularis fractures and posterior facet joint subluxation. However, plain radiographs are often inadequate for visualizing subtle sacral fractures. Dynamic active flexion-extension views may be obtained, at best, 2  weeks post-injury to evaluate spinal instability from ligamentous injuries in some cases. On computed tomography (CT) scan, both bone and soft-­ tissue windows should be obtained with coronal and sagittal reconstructions (Figs. 65.2, 65.3, and 65.4, 65.8, and 65.11). Tridimensional (3D) reconstructions can be used to better describe the extent of canal compromise and posterior element fractures (Fig.  65.8). The presence of a “naked facet sign” on the axial plane [L5 facets passing superiorly over the facets of S1] is indicative of facet dislocation. The complexities of the sacral fractures are much more visualized on a CT scan. Furthermore, air on pelvic CT imaging should increase suspicion of concomitant intrapelvic soft tissue injuries.

65.3  Paraclinic Features

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Fig. 65.6  Case 4. Lumbosacral axial CT scan (a–d) showing fracture of the posterior wall of the vertebral body of L5 (arrow) as well as fracture of the left-sided transverse processes of L5 and S1 ala (double arrows)

Magnetic resonance imaging (MRI) allows better visualization of ligamentous and neurologic structures. Indeed, MRI will be useful in demonstrating associated disc herniation, dural tears, root compression, and degree of musculo-­ ligamentous damage (Fig. 65.9). Further imaging investigations such as complete abdominopelvic CT scan, ultrasonography, or angiographic studies may be needed for specific cases in the search for concomitant bony, vascular, or soft tissue lesions.

Sometimes physiologic tests such as electromyography (EMG) and nerve conduction studies can show evidence of denervation in the lower limb muscles or disorders in the sphincter muscles. Examination of the paraspinal muscles can distinguish lesions on the cauda equina from lumbosacral plexopathies. In addition, nerve conduction studies are an essential part of the assessment of suspected ­radiculopathy. Patients with sphincter disturbances might be evaluated with various combinations of urodynamic studies (e.g., uroflowmetry, cystometry, and sphincteric EMG).

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65  Lumbosacral Spine Fractures and Dislocations

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Fig. 65.7  Case 4. Pelvic axial CT scan (a–d) showing fracture of the left-sided region of ala from S1 to S3 (arrows) [Zone I fracture]

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Fig. 65.8  Case 5. Post-traumatic burst fracture of L3 (arrows) with vertebral canal compromise (stars) as seen on 3D (a, b) and sagittal reconstructions (c, d) CT scan. (Courtesy of Pr. Badr Slioui)

65.3  Paraclinic Features

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Fig. 65.9  Case 5. Lumbosacral sagittal T1- (a) and T2-weighted (b) MRI as well as axial T2-weighted MRI (c, d) showing the thecal sac and cauda equina nerve roots compression (arrows)

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Fig. 65.10  Case 5. Postoperative sagittal reconstructions (a, b) and axial CT scan (c, d) showing the L3 vertebral body height correction (arrow) using a polyaxial L2-L4 screw-rod system

750 Fig. 65.11  Case 6. Post-­ traumatic complex fracture of L3 (arrows) with significant vertebral canal compromise as seen on sagittal reconstructions (a, b) and axial (c, d) CT scan. Note the retropulsed intracanalar bony fragments

65  Lumbosacral Spine Fractures and Dislocations

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65.4  Treatment Options and Prognosis

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Fig. 65.12  Case 7. Right-sided sciatica in a child sustained a penetrating lumbosacral injury. There are multiple bony fragments at the level of right L5-S1 foramen (arrows) as seen on axial CT scan on parenchymal (a, b) and bony (c, d) windows

65.4 Treatment Options and Prognosis

Transiliac-transsacral screw stabilization is a surgical technique that may offer rapid and complete pain relief for The goal of the treatment of LSFD is controlling pain, elimi- the patient’s refractory to conservative management. nating the aggressive cause, restoring the neural and sphincOverall, surgical procedure is often necessary for patients ter functions, performing nervous decompression in case of with unstable fractures or those with neurologic deficits incomplete neurological deficit related to intracanalar related to compression of the neural radicular elements by lesions, and stabilizing any spinal and even pelvic post-­ bony lesions or hematomas, or cases with non-compressive traumatic instability. However, the treating surgeon should partial cauda equina injuries. consider some factors including but not limited to the mechPhysical therapy including early active mobilization, with anism of injury, spinal canal compromise, degree of neuro- or without bracing, seems appropriate for stable fractures logic damage, biomechanical deficiencies, patient’s general without significant vertebral body damage, lumbosacral condition, and further concurrent disorders. fractures with reasonable alignment, and those without neuMany therapeutic tools have been proposed such as medica- rologic deficit. It would also seem appropriate for isolated tion and conservative measures including bracing, surgery, and process fractures without major pelvic trauma. physical therapy. Regarding spinal surgery, various ­operative Patients with neurologic injuries are predisposed to multechniques are used including posterior, posterolateral anterior, tiple complications, including  decubitus ulcers,  pulmonary or combined approach with or without fusion. Some more problems, urinary sepsis, and new fractures. Sometimes, complex lumbosacroiliac procedures should be considered. patients develop delayed progressive neurologic deteriora-

752

tion months to years after sustaining spinal trauma because of instability and progressive spinal deformity. Intraoperative complications include: • Neurologic deterioration (secondary to neural traction, compression, or interruption of the vascular supply to the neurologic elements) • Graft displacement • Dislocation of the hardware • Blood loss • Major vessels or viscera injury • Dural tears resulting in cerebrospinal fluid CSF leaks Main postoperative complications are related to: –– –– –– –– –– –– –– –– –– –– ––

Spinal infections Neurologic pain Progressive neurologic deficit Malplaced instrumentation Failure of the fusion (pseudarthrosis) Spinal deformity Thromboembolic disease Pulmonary embolism Stress ulcers Ogilvie syndrome (AKA colonic pseudo-obstruction) Genitourinary complications

Further underlying diseases and disorders should be adequately managed and monitored in a multidisciplinary perspective involving neurosurgeons, orthopedists, urologists, gynecologists, and even visceral and vascular surgeons. The outcome and prognosis of patients with LSFD depend on their neurologic condition and biomechanics stability. Patients with no neurologic deficits or partial deficits generally have a good prognosis, whereas those with complete injuries remain paraplegic. Other factors (e.g., age, comorbidities, patient’s general condition, concurrent injuries, and related complications) also have an impact on the outcome. Generally, patients with preoperative neurological deficits managed nonoperatively reported the highest rate of complications and poor results.

Further Reading Butler JS, Fitzpatrick P, Ni Mhaolain AM, Synnott K, O'Byrne JM. The management and functional outcome of isolated burst fractures of the fifth lumbar vertebra. Spine (Phila Pa 1976). 2007;32:443–7. https://doi.org/10.1097/01.brs.0000255076.45825.1e. Cavagnaro MJ, Tavolaro C, Orenday-Barraza JM, Farhardi D, Baaj AA, Bransford R. Burst fractures of the fifth lumbar vertebra: case series

65  Lumbosacral Spine Fractures and Dislocations and systematic review. J Clin Neurosci. 2022;103:163–71. https:// doi.org/10.1016/j.jocn.2022.07.017. Denis F, Davis S, Comfort T.  Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop Relat Res. 1988;227:67–81. Ebot J, Bohnen AM, Abode-Iyamah K.  Bilateral acute osteoporotic lumbar pedicle fracture presenting with associated neurological deficit: a case report and review of literature. Cureus. 2020;12:e7273. https://doi.org/10.7759/cureus.7273. Finn CA, Stauffer ES. Burst fracture of the fifth lumbar vertebra. J Bone Joint Surg Am. 1992;74:398–403. Grivas TB, Papadakis SA, Katsiva V, Koufopoulos G, Mouzakis V. Unilateral lumbosacral dislocation: case report and a comprehensive review. Open Orthop J. 2012;6:473–7. https://doi.org/10.2174/ 1874325001206010473. Herrera AJ, Berry CA, Rao RD. Single-level transforaminal interbody fusion for traumatic lumbosacral fracture-dislocation: a case report. Acta Orthop Belg. 2013;79:117–22. Likhachev SV, Zaretskov VV, Arsenievich VB, Ostrovskij VV, Shchanitsyn IN, Shulga AE, et al. Treatment tactics for patients with isolated injuries of the fifth lumbar vertebra. Sovrem Tekhnologii Med. 2021;13:31–9. https://doi.org/10.17691/stm2021.13.5.04. Liu HC, Chen YZ, Sang XG, Qi L.  Management of lumbosacropelvic fracture-dislocation using lumbo-iliac internal fixation. Injury. 2012;43:452–7. https://doi.org/10.1016/j.injury.2011.08.036. Meyer M, Noudel R, Farah K, Graillon T, Prost S, Blondel B, et  al. Isolated unstable burst fractures of the fifth lumbar vertebra: functional and radiological outcome after posterior stabilization with reconstruction of the anterior column: about 6 cases and literature review. Orthop Traumatol Surg Res. 2020;106:1215–20. https://doi. org/10.1016/j.otsr.2020.03.014. Moon AS, Atesok K, Niemeier TE, Manoharan SR, Pittman JL, Theiss SM. Traumatic lumbosacral dislocation: current concepts in diagnosis and management. Adv Orthop. 2018;2018:6578097. https://doi. org/10.1155/2018/6578097. Pascal-Moussellard H, Hirsch C, Bonaccorsi R.  Osteosynthesis in sacral fracture and lumbosacral dislocation. Orthop Traumatol Surg Res. 2016;102:S45–57. https://doi.org/10.1016/j.otsr.2015.12.002. Ramieri A, Domenicucci M, Cellocco P, Raco A, Costanzo G. Neurological L5 burst fracture: posterior decompression and lordotic fixation as treatment of choice. Eur Spine J. 2012;21(Suppl 1):S119–22. https://doi.org/10.1007/s00586-­012-­2226-­y. Rizzi L, Castelli C. Open pelvic fracture associated with lumbosacral dislocation and extensive perineal injury. Injury. 2015;46(Suppl 7):S44–7. https://doi.org/10.1016/S0020-­1383(15)30045-­0. Safaie Yazdi A, Omidi-Kashani F, Baradaran A. Intrapelvic lumbosacral fracture dislocation in a neurologically intact patient: a case report. Arch Trauma Res. 2015;4:e25439. https://doi.org/10.5812/ atr.25439. Santolini E, Kanakaris NK, Giannoudis PV.  Sacral fractures: issues, challenges, solutions. EFORT Open Rev. 2020;5:299–311. https:// doi.org/10.1302/2058-­5241.5.190064. Schmid R, Reinhold M, Blauth M. Lumbosacral dislocation: a review of the literature and current aspects of management. Injury. 2010;41:321–8. https://doi.org/10.1016/j.injury.2009.06.008. Scott KW, Arias J, Tavanaiepour K, Tavanaiepour D, Rahmathulla G. Combined posterior-anterior interbody fusion in the Management of Traumatic Lumbosacral Dissociation: a case report and review of literature. Cureus. 2020;12:e7089. https://doi.org/10.7759/ cureus.7089. Seybold EA, Sweeney CA, Fredrickson BE, Warhold LG, Bernini PM.  Functional outcome of low lumbar burst fractures. A mul-

Further Reading ticenter review of operative and nonoperative treatment of L3-L5. Spine (Phila Pa 1976). 1999;24:2154–61. https://doi. org/10.1097/00007632-­199910150-­00016. Spine. J Orthop Trauma. 2018;32(Suppl 1):S145–60. https://doi. org/10.1097/BOT.0000000000001075. Tender GC. Caudal vertebral body fractures following lateral interbody fusion in nonosteoporotic patients. Ochsner J. 2014;14:123–30.

753 Thongtrangan I, Le H, Park J, Kim DH.  Cauda equina syndrome in patients with low lumbar fractures. Neurosurg Focus. 2004;16:e6. Xu R, Solakoglu C, Kretzer RM, McGirt MJ, Witham TF, Bydon A.  Bilateral traumatic dislocation without fracture of the lumbosacral junction: case report and review of the literature. Spine (Phila Pa 1976). 2011;36:E662–8. https://doi.org/10.1097/ BRS.0b013e318207814c.

Spinal Pathologic Fractures

66.1 Generalities and Relevance Spinal pathologic fractures (SPF) occur in the setting of pathologic weakening of the vertebra secondary to an underlying disease. This condition is also called “secondary spinal fracture,” “spontaneous spinal fracture,” or “vertebral compression fracture.” These fractures are unique in that they are usually non-traumatic in nature. Most SPF concern thoracic and thoracolumbar spines. Sacral and lower lumbar columns are unusually involved. Progressive collapse of the sacral or lumbar vertebral body may induce spinal deformation (mainly kyphosis), low back pain, and lumbosacral radicular pain with or without neurological deficits. In some cases, delayed onset of radiculopathy is observed after conservative therapy for benign SPF due to advanced vertebral collapse. SPF has various etiologies (Table  66.1); however, the majority of cases are secondary to bone failure related to osteoporosis (benign) and metastatic cancer (malignant). In this chapter, we will focus mainly on osteoporotic and metastatic lumbosacral pathologic fractures which are the most common subtypes associated with vertebral compression fractures. Clinically, an SPF secondary to osteoporosis may be categorized as a benign fracture whereas an SPF caused by bone metastasis is usually considered a malignant fracture. Differentiating between benign and malignant vertebral fractures is fundamental for the diagnosis and treatment of the patient, especially in the acute and subacute stages. Osteoporosis is the most common cause of SCF, but unlike malignant fractures, most osteoporotic fractures are stable and could be managed conservatively. Indeed, current therapeutic options are often limited by the nature of the lesions and the underlying disease. Sciatica related to SPF may result from different mechanisms including: –– Foraminal stenosis

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Table 66.1  Different etiologies of spinal pathologic fractures –  Osteoporotic compression fracture – Secondary osteolytic metastasis (mainly from breast, prostate, lung, and thyroid) –  Bone marrow neoplasm (e.g., multiple myeloma, lymphoma) –  Primary malignant neoplasm of bone (e.g., sarcoma, chordoma) – Benign bone neoplasm (e.g., giant cell tumors, aneurysmal bone cyst) –  Aggressive vertebral hemangioma –  Eosinophilic granuloma –  Paget’s disease –  Rheumatoid arthritis – Hyperparathyroidism – Osteomalacia –  Osteogenesis imperfect –  Renal osteodystrophy –  Giant Schmörl’s node –  Kummell disease (AKA avascular necrosis) –  Steroid-induced fractures –  Vertebral osteomyelitis (e.g., tuberculosis and brucellosis)

Central spinal stenosis Retropulsed bony fragments Intervertebral instability Secondary lumbar disc herniation Secondary spondylolisthesis Direct neural compression due to intraspinal expansion of epidural neoplasms or granulomatous lesions –– Concomitant spinal epidural hematoma –– –– –– –– –– ––

Osteoporotic SPF commonly occurs in elderly patients following a minimal trauma or spontaneously, particularly in postmenopausal women. The lifetime risk of symptomatic osteoporotic SPF is 16% for women and 5% for men. Although the exact prevalence of osteoporotic vertebral compression fracture and neurological symptoms remains unknown, it seems that 5.5% of patients present with neurological symptoms. The elderly population has also a higher incidence and prevalence of metastatic SPF. Spinal metastases are the most common tumors of the spine and about two-thirds of all bone

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_66

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metastases are located in the spine. Both osteoporotic and metastatic SPF frequently affect the same age group of patients and may be indistinguishable clinically and radiographically.

66.2 Clinical Presentations Patients with lumbosacral SPF may present with various clinical presentations, including spinal, neurologic, and extraspinal manifestations. Anamnestic data about trauma, infection, or preexisting disease could be very helpful to identify the expected cause of vertebral compressive fracture. Unfortunately, the experience of spinal trauma (even minimal trauma) is rarely found in the clinical history. The majority of patients complain of unspecific pain in the lower back associated with radicular symptoms with or without neurological impairment. Overall, clinical data regarding the onset of low back pain, the presence or absence of lower limb weakness, and acute or progressive neurological symptoms may give only little benefit in differentiating between the different causes of SPF.  However, it seems that patients with malignant SPF tend to have more rapid gradual symptoms than those with benign forms. In addition, fatigue and weight loss should point toward malignancy. Fig. 66.1 Pathologic osteoporotic vertebral fracture at L1 and L4 (arrows) in a woman as seen on lumbosacral sagittal reconstruction CT scan on bone windows (a, b)

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The physical exam may show localized pain and tenderness, spinal stiffness and postural changes, spinal deformity or angulation, and decreased range of motion, with or without neurologic deficits. Bilateral lumbosacral radicular pain with or without neurogenic claudication is correlated to large involvement with bilateral extension. Cauda equina syndrome is not rare and is often related to severe compressive lesions. Many other concomitant symptoms related to underlying etiologies or systemic diseases should be considered in clinical presentations. Finally, in almost all cases, identifying the nature of the disease by examining the signs and symptoms is often impossible without additional imaging explorations.

66.3 Paraclinic Features In the face of suspicion of a lumbar vertebral fracture, the main objective of the radiologist is to distinguish osteoporotic (benign) insufficiency fractures from malignant metastatic fractures, especially in the acute and subacute stages. Plain radiography shows some difficulties in differentiating causative lesions. Computed tomography (CT) scan is one of the most suitable imaging techniques for the assessment of bone structure and fragments and to establish the degree of cortical bone destruction (Figs.  66.1, 66.2, 66.3,

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66.3  Paraclinic Features

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Fig. 66.2  Lumbosacral sagittal (a, b), coronal (c), and axial (d) CT scan showing a pathologic fracture on L5 vertebral level (arrows) causing central spinal stenosis

66.4, 66.5, and 66.6). However, magnetic resonance imaging (MRI) is the most helpful imaging modality in order to provide the basis for the distinction between metastatic and acute osteoporotic compression fractures. Radiography can identify and localize the fracture, estimate the duration of the fracture, define the fracture anatomy, and assess for posterior vertebral body wall deficiency should be part of preoperative planning for vertebroplasty or vertebral augmentation surgery. Lateral radiographs are essential for planning the trajectory of any percutaneous procedure such as spinal biopsy, vertebroplasty, or vertebral augmentation technic. On MRI, malignant fractures are associated with additional paraspinal masses, involvement of the posterior element, involvement of the pedicle, complete replacement of normal bone marrow, potential intracanalar epidural mass (“double-bag” configuration), and diffuse convexity of the posterior vertebral border. On the contrary, coexisting healed benign vertebral fractures, fluid signs, focal posterior vertebral border retropulsion, and a band-like abnormal signal (a band pattern that appears as areas of low signal intensity on

T1-weighted and high signal intensity on STIR sequence) are with benign fractures. Furthermore, diffusion-weighted imaging (DWI) is reported to be a useful exploration of MRI. Generally, the apparent diffusion coefficient (ADC) in benign compression fractures is higher than in malignant compression fractures. Aggressive vertebral hemangioma appears as an expansile lytic lesion associated with a “polka dot” or “spotted” pattern on axial CT scan and a “corduroy” or “jail bar” shape on sagittal or coronal CT-scan imaging. Plasmacytoma has a mini-brain appearance. Lymphoma is characterized by an epidural part that is hypointense on T1and iso-hyperintense on T2-weighted images. Chordoma can look very similar to aggressive hemangioma on T2 and post-gadolinium imaging; however, chordoma is not hyperintense on T1-weighted images. There are also frequent peripheral calcifications on CT imaging. Vertebral collapse associated with paravertebral and epidural cystic collections (abscesses) can be related to vertebral osteomyelitis with or without discitis.

758 Fig. 66.3 Pathologic osteoporotic vertebral fracture of L4 (arrows) in a woman as seen on lumbosacral sagittal reconstruction CT scan on bone windows (a, b)

66  Spinal Pathologic Fractures

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Bone scintigraphy is not always conclusive. However, a fluorodeoxyglucose positron emission tomography (FDG-­ PET) scan is another useful modality in differentiating benign from malignant compression fractures. Malignant SPF demonstrated significantly increased FDG uptake compared with benign fractures (Fig. 66.5c). High FDG uptake is also a characteristic of inflammatory processes. Biologic findings could help in differentiating between benign and malignant SPF and may be sometimes appropriate for the final diagnosis. In this perspective, the following biologic tests could be used as blood count, sedimentation

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rate, C-reactive protein, creatinemia, calcemia, phosphoremia, 25-hydroxyvitamin D, alkaline phosphatase, liver function, serum protein electrophoresis, hormonology, ­ microbiology, and some tumor markers. Concerning osteoporosis and osteopenia, many techniques can measure bone mineral density, but dual-energy X-ray absorptiometry (DEXA) represents the gold standard. Sometimes, a percutaneous vertebral biopsy is necessary to diagnose the underlying causative lesions before continuing a more extensive evaluation and/or planning a final treatment (Fig. 66.7).

66.3  Paraclinic Features

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Fig. 66.4  S1 vertebral localization of solitary plasmacytoma with pathologic fracture (arrow) as seen on axial (a), sagittal (b), and coronal (c, d) reconstructions CT scan

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Fig. 66.5  L5 and S1 vertebral localization of prostatic acinar adenocarcinoma (arrows) as seen on sagittal reconstruction CT scan (a), STIR sequence (b), and PET scan (c)

Fig. 66.6  L5 vertebral localization of prostatic acinar adenocarcinoma with bony invasion as seen on axial CT scan on both parenchymatous (a) and bony windows (b)

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66.4  Treatment Options and Prognosis

Fig. 66.7  Microscopic image showing vertebral localization of prostatic acinar adenocarcinoma (Gleason 4 + 3 = 7). The tumor cells are arranged in glandular and cribriform structures (arrows) (Hematoxylin and eosin stain, original magnification × 100). (Courtesy of Pr. Mohamed Amine Azami and Pr. Issam Rharrassi)

66.4 Treatment Options and Prognosis Treatment of vertebral compressive fracture-inducing sciatic pain is not well established and depends on many factors including but not limited to causative factors and underlying disease, lesion extension, patient’s general condition, and degree of neurological disorders. Rheumatologists and oncologists may assist in a formal diagnosis, management, and monitoring. The aim of the treatment is to relieve pain, maintain axial spine motion and functional ability, prevent the progression of the disease, and avoid spinal complications. Medication, conservative measures, physical therapy programs, bracing, surgery, radiotherapy, hormone therapy, and chemotherapy have been proposed. Several open surgical approaches have been proposed whether they are anterior, posterior, posterolateral, or mixed approaches depending on the location and the size of the damage. However, when surgery is indicated, most patients underwent decompression and short fusion surgery with rigid pedicle screw fixation and bone graft via a posterior lumbar approach. Treating practitioners should always take into account that many patients present advanced age, spinal fragility, poor bone quality, and other comorbidities. Furthermore, the rate of postoperative complications related to the instrumentation is not insignificant in this aged popu-

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lation. Sometimes, less invasive surgery may be indicated such as transforaminal full-endoscopic lumbar for aminoplasty with or without discectomy if needed. Conservative measures can be considered when osteoporotic SPF is stable without neurological complications. Nonsurgical treatments are recommended for other less severe pathological fractures. The efficacy of transforaminal epidural steroid injection has been demonstrated in patients with radicular symptoms. In some cases with a vertebral compression fracture, a vertebroplasty via a percutaneous transpedicular approach can be considered. The goal of this minimally invasive procedure is to restore height to the collapsed lumbar vertebral body, reduce kyphosis, and improve the patient’s pain and function. Regarding the sacrum, sacroplasty is a variation of vertebroplasty, in which cement is injected into the sacrum to improve its structural integrity and alleviate symptoms. Sacroplasty was first introduced as a treatment for pelvic lesions resulting from metastasis with a good outcome. However, the long-term results of sacroplasty remain unknown. Overall, surgery may be considered if the spine is unstable or where there is significant compression of the nerve roots. Etiological treatment should be undertaken afterward whether the cause is benign, malignant, or other underlying diseases. Regarding their origins, malignancy should be correctly managed by chemotherapy, surgery, and/or radiation therapy. Infectious disease should be treated with anti-infectious agents depending on the pathogenic species. Surgery to remove the infected tissues may be needed when the infection creates spinal instability and serious neurological impairment due to bony compression. Sometimes, correction osteotomy and long fusion were performed in a few cases to restore spinal alignment. Complications are especially related to prolonged bed rest (e.g., pneumonia, deep venous thrombosis with the associated risk of pulmonary embolism), underlying disease, and spinal instrumentation. The prognosis is variable depending on causative factors, underlying disease, tumor nature and aggressiveness, initial neurological disorders, treatment response, delay of treatment, and the patient’s general condition. Prognosis is better for patients with osteoporosis, infectious disease, and benign neoplasm as well as for those without severe and longtime neurologic impairment. Progressive clinical deterioration is common in patients with SPF secondary to malignancy with life-threatening consequences. Whatever the results be, careful clinical and paraclinical follow-up should be needed.

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Further Reading

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in patients with osteoporotic sacral insufficiency fractures or pathologic sacral lesions. J Neurointerv Surg. 2013;5:461–6. https://doi. org/10.1136/neurintsurg-­2012-­010347. Arpitha A, Rangarajan L.  Computational techniques to segment and Li Y, Zhang Y, Zhang E, Chen Y, Wang Q, Liu K, et al. Differential diagclassify lumbar compression fractures. Radiol Med. 2020;125:551– nosis of benign and malignant vertebral fracture on CT using deep 60. https://doi.org/10.1007/s11547-­020-­01145-­7. learning. Eur Radiol. 2021;31:9612–9. https://doi.org/10.1007/ Azevedo-Marques PM, Spagnoli HF, Frighetto-Pereira L, Menezes-­ s00330-­021-­08014-­5. Reis R, Metzner GA, Rangayyan RM, et al. Classification of ver- Li Z, Guan M, Sun D, Xu Y, Li F, Xiong W. A novel MRI- and CT-based tebral compression fractures in magnetic resonance images using scoring system to differentiate malignant from osteoporotic vertespectral and fractal analysis. Annu Int Conf IEEE Eng Med Biol Soc. bral fractures in Chinese patients. BMC Musculoskelet Disord. 2015;2015:723–6. https://doi.org/10.1109/EMBC.2015.7318464. 2018;19:406. https://doi.org/10.1186/s12891-­018-­2331-­0. Bortoletto A, Rodrigues LC, Matsumoto MH. Pathological fracture of Lin GX, Sun LW, Jhang SW, Ou SW, Chang KS, Tsai RY, et  al. A lumbar vertebra in children with acute neurological deficit: case pilot study of radiculopathy following osteoporotic vertebral fracreport. Rev Bras Ortop. 2015;46:315–7. https://doi.org/10.1016/ ture in elderly patients: an algorithmic approach to surgical manageS2255-­4971(15)30202-­0. ment. Geriatr Orthop Surg Rehabil. 2021;12:21514593211044912. Bredella MA, Essary B, Torriani M, Ouellette HA, Palmer WE.  Use https://doi.org/10.1177/21514593211044912. of FDG-PET in differentiating benign from malignant compression Mattei TA, Rehman AA. Schmorl’s nodes: current pathophysiological, fractures. Skelet Radiol. 2008;37:405–13. https://doi.org/10.1007/ diagnostic, and therapeutic paradigms. Neurosurg Rev. 2014;37:39– s00256-­008-­0452-­5. 46. https://doi.org/10.1007/s10143-­013-­0488-­4. Cho WI, Chang UK. Comparison of MR imaging and FDG-PET/CT in Nakajima H, Uchida K, Honjoh K, Sakamoto T, Kitade M, Baba the differential diagnosis of benign and malignant vertebral comH. Surgical treatment of low lumbar osteoporotic vertebral collapse: pression fractures. J Neurosurg Spine. 2011;14:177–83. https://doi. a single-institution experience. J Neurosurg Spine. 2016;24:39–47. org/10.3171/2010.10.SPINE10175. https://doi.org/10.3171/2015.4.SPINE14847. Chung SK, Lee SH, Kim DY, Lee HY.  Treatment of lower lumbar Nakase T, Fujiwara K, Kohno J, Owaki H, Tomita T, Yonenobu K, et al. radiculopathy caused by osteoporotic compression fracture: the role Pathological fracture of a lumbar vertebra caused by rheumatoid of vertebroplasty. J Spinal Disord Tech. 2002;15:461–8. https://doi. arthritis--a case report. Int Orthop. 1998;22:397–9. https://doi. org/10.1097/00024720-­200212000-­00005. org/10.1007/s002640050286. Cicala D, Briganti F, Casale L, Rossi C, Cagini L, Cesarano E, et al. Oh E, Kim HJ, Kwon JW, Yoon YC, Kim HS. Differentiation between Atraumatic vertebral compression fractures: differential diagspinal subchondral bone metastasis with focal pathologic endplate nosis between benign osteoporotic and malignant fractures by fracture and oedematous Schmorl’s node. J Med Imaging Radiat MRI. Musculoskelet Surg. 2013;97(Suppl 2):S169–79. https://doi. Oncol. 2021;66:913. https://doi.org/10.1111/1754-­9485.13365. org/10.1007/s12306-­013-­0277-­9. Omidi-Kashani F, Parsa A, Madarshahian D.  Impending cauda Curtis JR, Taylor AJ, Matthews RS, Ray MN, Becker DJ, Gary LC, et al. equina syndrome due to Kummell disease; a case report and lit“Pathologic” fractures: should these be included in epidemiologic erature review. Int J Surg Case Rep. 2021;83:106041. https://doi. studies of osteoporotic fractures? Osteoporos Int. 2009;20:1969–72. org/10.1016/j.ijscr.2021.106041. https://doi.org/10.1007/s00198-­009-­0840-­2. Sattari A, Quillard A, Laredo JD. Benign nontraumatic osteolytic verDimar JR 2nd, Nathan ST, Glassman SD. The spectrum of traumatic tebral collapse simulating malignancy. Eur Radiol. 2008;18:631–8. Schmorl’s nodes: identification and treatment options in 3 patients. https://doi.org/10.1007/s00330-­007-­0807-­7. Am J Orthop (Belle Mead NJ). 2012;41:427–31. Sills AK. Lumbar stenosis with osteoporotic compression fracture and Doita M, Ando Y, Hirata S, Ishikawa H, Kurosaka M. Bilateral pedicle neurogenic claudication. J Spinal Disord. 1993;6:269–70. stress fracture in a patient with osteoporotic compression fracture. Takigawa T, Tanaka M, Sugimoto Y, Tetsunaga T, Nishida K, Ozaki Eur Spine J. 2009;18(Suppl 2):206–9. https://doi.org/10.1007/ T. Discrimination between malignant and benign vertebral fractures s00586-­008-­0816-­5. using magnetic resonance imaging. Asian Spine J. 2017;11:478–83. Frighetto-Pereira L, Rangayyan RM, Metzner GA, de Azevedo-­ https://doi.org/10.4184/asj.2017.11.3.478. Marques PM, Nogueira-Barbosa MH.  Shape, texture and sta- Thawait SK, Marcus MA, Morrison WB, Klufas RA, Eng J, Carrino tistical features for classification of benign and malignant JA. Research synthesis: what is the diagnostic performance of magvertebral compression fractures in magnetic resonance images. netic resonance imaging to discriminate benign from malignant verComput Biol Med. 2016;73:147–56. https://doi.org/10.1016/j. tebral compression fractures? Systematic review and meta-analysis. compbiomed.2016.04.006. Spine (Phila Pa 1976). 2012;37:E736–44. https://doi.org/10.1097/ Ishimoto Y, Yamada H, Curtis E, Cooper C, Hashizume H, Minamide BRS.0b013e3182458cac. A, et  al. Spinal endoscopy for delayed-onset lumbar radiculopa- Van den Brande R, Mj Cornips E, Peeters M, Ost P, Billiet C, Van de thy resulting from Foraminal stenosis after osteoporotic vertebral Kelft E.  Epidemiology of spinal metastases, metastatic epidural fracture: a case report of a new surgical strategy. Case Rep Orthop. spinal cord compression and pathologic vertebral compression 2018;2018:1593021. https://doi.org/10.1155/2018/1593021. fractures in patients with solid tumors: a systematic review. J Bone Jorge-Mora A, Amhaz-Escanlar S, Lois-Iglesias A, Leborans-Eiris Oncol. 2022;35:100446. https://doi.org/10.1016/j.jbo.2022.100446. S, Pino-Minguez J.  Surgical treatment in spine Paget’s disease: a Wallace MJ, Kruse RW, Shah SA. The spine in patients with osteogensystematic review. Eur J Orthop Surg Traumatol. 2016;26:27–30. esis imperfecta. J Am Acad Orthop Surg. 2017;25:100–9. https:// https://doi.org/10.1007/s00590-­015-­1659-­5. doi.org/10.5435/JAAOS-­D-­15-­00169. Kortman K, Ortiz O, Miller T, Brook A, Tutton S, Mathis J, et  al. Multicenter study to assess the efficacy and safety of sacroplasty

Sacral Stress Fractures

67.1 Generalities and Relevance A stress fracture is an overuse bone injury secondary to a mismatch of bone strength and chronic mechanical stress placed upon the bone. This condition is usually seen in the lower extremities and less often in the upper extremities. The pelvis and sacrum are unusually involved. Sacral stress fractures are traditionally divided into three types: • Fatigue fractures which are due to overuse of normal bone with usual elastic resistance, mainly seen following hard athletic and military training. • Insufficiency fractures which are secondary to everyday physiologic stress on the fragile bone with poor elastic resistance (Table 67.1). • Pathologic fractures which are due to bone weakness involving tumors or other diseases (c.f. Chap. 66 about Spinal Pathologic Fractures). In this chapter, we will focus on fatigue fractures and insufficiency fractures involving the sacrum. Sacral insufficiency-type fractures are often seen in elderly osteoporotic individuals while fatigue fractures are encountered in young active persons. Sacral insufficiency fracture was first described in 1982 by the American neurosurgeon Herbert Lourie (1929–1987) in three elderly patients who present spontaneous osteoporotic fracture of the sacrum. A few years later in 1989, the Israeli orthopedic surgeon Gershon Volpin (1946-) diagnosed the first case of fatigue fracture of the sacrum in three young military recruits following rigorous elite basic training. Most patients with sacral stress fractures (SSF) present with buttock, low back, hip, groin, and/or pelvic pain following minimal or no trauma. Radicular symptoms are uncommon but could be the cause of lumbosacral radiculopathy,

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Table 67.1  Main risk factors for sacral insufficiency fractures • Osteoporosis • Osteopenia • Hyperparathyroidism •  Diabetes mellitus •  Rheumatoid arthritis •  Corticosteroid use •  Radiation therapy •  Renal osteodystrophy • Osteomalacia •  Osteogenesis imperfecta •  Paget’s disease •  Lumbosacral fusion •  Joint arthroplasty •  Pregnancy and postpartum

lower limb paresthesias, and sphincter dysfunction. According to some recent studies, up to 28% of patients with sacral insufficiency fractures had corresponding radicular symptoms which could be secondary to both adjacent soft tissue periosteal thickening and/or callus formation that impinged or ventrally displaced the nerve roots. Sacral stress fractures often result from minimal or no significant trauma. Because of their relative paucity and heterogeneous nature, they are frequently underdiagnosed or misdiagnosed and consequently mistreated. In addition, the final diagnosis will be more difficult when SSF are associated with concomitant spinal degenerative disorders such as lumbar disc herniation, central or neural foraminal stenosis, spondylolisthesis, and even synovial cyst formations. SSF can be classified according to the classification system of Denis related to traumatic sacral fractures by dividing the sacrum into three zones (Fig. 67.1). • Zone I: Region of ala (unilateral sacral wing lateral to the sacral foramina). Sometimes, it is associated with partial L5 nerve root injury. • Zone II: Region of sacral foramina. The fracture occurs in a vertical fashion parallel to the sacroiliac joint and can be

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Fig. 67.1  The classification system of Denis related to traumatic sacral fractures. The sacral bone is divided into three zones. Zone I: Region of ala (unilateral sacral wing lateral to the sacral foramina). Zone II: Region of sacral foramina. The fracture occurs in a vertical fashion parallel to the sacroiliac joint and can be associated with unilateral L5-S1-S2 radiculopathies. Zone III: Region of the central sacral canal. The fracture may be vertical or horizontal (transverse)

associated with unilateral L5-S1-S2 radiculopathies. Sphincter dysfunctions are rare. • Zone III: Region of the central sacral canal. The fracture may be vertical or horizontal (transverse). It is habitually associated with Bowel and bladder dysfunction (high occurrence of cauda equina syndrome). Osteoporotic SSF is usually seen in elderly females in their 70  s. Both sides are affected in 60% of patients with sacral insufficiency fractures. Sacral osteoporotic fractures have a lumbosacral nerve root involvement between 2 and 28% of all individuals. On the contrary, fatigue SSF occurs in much younger individuals with a mean age between 20 s and 30 s but without sex predominance.

67.2 Clinical Presentations The majority of patients with SSF complain of nonspecific pain in the lumbar region rather than the sacrum rarely associated with radicular pain or neurological impairment. Anamnestic data about trauma or preexisting disease could be very helpful to identify the expected cause of the sacral fracture. The patient’s history usually reveals worsening pain with a history of minimal or no significant trauma. In fatigue SSF, there is usually a history of a recent alteration or increase in physical or athletic activity. Symptomatic pain is aggravated by weight-bearing movement and usually improves with rest. In addition, patients are habitually most reposeful in a supine position. Some patients can describe problems with walking, pain, and tenderness on palpation over the lower back, hip, groin, and/or diffusely over the sacral region, and pubic tenderness.

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Bilateral lumbosacral radicular pain, leg weakness, and cauda equina syndrome are less frequent but correlate rather to type III sacral fractures. Furthermore, gait is usually slow, with an antalgic pattern and limited low back range of motion. Classic sacroiliac joint provocative maneuvers such as Gaenslen’s, Yeoman’s, thigh trust, and compression tests, may be positive, although they are unspecific for SSF. Patients who have sacral insufficiency fractures may also have other pelvic fractures or concomitant lumbar degenerative diseases which may further confuse the symptomatology. Clinical presentations of SSF may be confused with other diseases such as: –– –– –– –– –– –– –– –– –– –– ––

Lumbar disc herniation Spinal stenosis Other lumbosacral pathologic fractures Facet arthropathy Trochanteric bursitis Sacroiliitis Gluteal and proximal hamstring muscle strains Ischial tuberosity bursitis Septic Sacroiliitis Gluteal bursitis Intrapelvic, intra-abdominal or retroperitoneal masses, inflammations, or infections –– Spondyloarthropathies –– Spondylolisthesis Many other concomitant symptoms related to underlying etiologies or systemic diseases should be considered in clinical presentations. Finally, in almost all cases, identifying the nature of the disease by examining the signs and symptoms is often impossible without additional imaging and/or biological explorations.

67.3 Paraclinic Features Imaging and biological studies may help to confirm the diagnosis, recognize the underlying etiology, and plan the therapeutic management of SSF. Plain radiographs, although considered inadequate for diagnosis, are usually the initial diagnostic imaging modality that assesses the integrity of the pelvic ring and rules out other more common entities such as lumbar spine pathology. Plain radiographs are inadequate for visualizing a subtle fracture line with or without sclerosis in the involved area. The most sensitive technique for detecting SSF is with technetium-99 m bone scan. Although this technique is not specific, a typical H-­sign or butterfly uptake pattern (AKA

67.4  Treatment Options and Prognosis

Honda sign) may be noted in up to 40% of cases and is considered diagnostic. Unilateral uptake patterns are less characteristic. Bone scan with single-photon emission computed tomography (SPECT) may also aid in the diagnosis. However, the increased uptake pattern found in the normal sacroiliac joint (SIJ) may hide potential sacral fractures. Computed tomography (CT) scan may show cortical disruptions and a fracture line along with sclerosis that is often parallel to the SIJ. Besides confirming the diagnosis, a CT scan can help exclude other diseases such as malignancy or osteomyelitis which are the most common differential diagnosis in this region. However, CT-scan imaging is less sensitive when compared to magnetic resonance imaging and bone scanning. Fat suppression and inversion recovery (STIR) sequences can greatly enhance the sensitivity of MRI in detecting bone marrow edema (up to 18  days after symptoms initiation), indicative of an acute fresh fracture. The sacral fracture appears hypointense on T1-weighted images and hyperintense on T2-weighted images. Coronal views can visualize the extent and site of the fracture, the neuroforamina, and the potential radicular abnormalities. In addition, MRI might be useful for diagnosing potentially associated disorders such as lumbar disc herniation, spinal stenosis, spondylolysis/listhesis, and even synovial cyst formations that could have caused nerve root impingement. Biological findings could help in diagnosing the cause of osteoporosis or recognizing other underlying diseases. In this context, the following laboratory studies could be used as thyroid function tests, parathyroid hormone levels, 25-hydroxyvitamin D, albuminemia, C-reactive protein, creatinemia, calcemia, phosphoremia, alkaline phosphatase, serum protein electrophoresis, blood count, liver function tests, and some tumor markers. Regarding osteoporosis and osteopenia, a number of techniques may measure bone mineral density, but dual-energy X-ray absorptiometry (DEXA) represents the gold standard.

67.4 Treatment Options and Prognosis Treatment options for SSF can be variable ranging from medical management, and rehabilitation, to sacroplasty and even more aggressive surgical procedures. However, management strategies differ according to etiology, the severity of the fractures, and the degree of neurological impairment. Rheumatologists and even orthopedists may assist in a formal diagnosis, management, and monitoring. Patients with SSF should have calcium and vitamin D supplementation daily. Those with insufficiency of SSF should have bisphosphonate and calcitonin in their medication.

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Pain management strategies include oral medications, various physical therapy modalities such as heat, gentle massage, transcutaneous electrical stimulation, ultrasound, as well as sacroplasty may be indicated in certain patients. Patients with fatigue-type SSF require a period time of relative rest between 4 and 6 weeks with activity modification and interruption of rigorous training. For many authors, early mobilization can decrease the decubitus complication rate (e.g., pneumonia, deep venous thrombosis with the associated risk of pulmonary embolism, urinary tract complications, gastrointestinal tract complications, and mental health symptoms) related to a long period of immobility and/or bed rest. In addition, early rehabilitation will stimulate osteoblastic activity and help conserve muscle mass and strength. Nonsteroidal anti-inflammatory drugs (NSAIDs) should generally be avoided for at least 3–4  weeks due to their potentially detrimental effect on bone healing. Sacroplasty, a variation of vertebroplasty, is a minimally invasive technique using percutaneous puncture of the sacrum and injection of polymethylmethacrylate cement for treatment of painful insufficiency fractures. The quality of life of most patients is improved, and the complications of immobility are avoided. In order to avoid cement leakage into the sacral foramen, sacroplasty should only be achieved in Zone I fractures. Further underlying diseases and disorders should be adequately managed. Under conservative measures, resolution of symptoms from sacral insufficiency fractures may require a period as long as 12 months. This time period could be shortened by using a sacroplasty procedure. Sometimes, open surgical approaches have been proposed for decompression and/or surgical reduction and fixation for highly unstable fractures and in order to improve radicular or sphincter deficits. Transiliac-transsacral screw stabilization is a surgical technique that may offer rapid and complete pain relief for patients refractory to conservative management. However, the majority of SSF does not require aggressive surgery. Treating practitioners should always be taken into account that many patients present advanced age, spinal fragility, poor bone quality, and other comorbidities. Furthermore, the rate of postoperative complications related to the instrumentation is not insignificant in this aged population. The prognosis of SSF is variable depending on causative factors, underlying disease, initial neurological disorders, treatment response, delay of treatment, and the patient’s general condition. Prognosis is better for patients with fatigue SSF and those without neurologic impairment compared to patients with insufficient SSF as well as for those with severe and longtime sphincter or neurologic disorders.

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Further Reading Bayley E, Srinivas S, Boszczyk BM. Clinical outcomes of sacroplasty in sacral insufficiency fractures: a review of the literature. Eur Spine J. 2009;18:1266–71. https://doi.org/10.1007/s00586-­009-­1048-­z. Blake SP, Connors AM.  Sacral insufficiency fracture. Br J Radiol. 2004;77:891–6. https://doi.org/10.1259/bjr/81974373. Boissonnault WG, Thein-Nissenbaum JM. Differential diagnosis of a sacral stress fracture. J Orthop Sports Phys Ther. 2002;32:613–21. https://doi.org/10.2519/jospt.2002.32.12.613. Deen HG, Nottmeier EW. Balloon kyphoplasty for treatment of sacral insufficiency fractures. Report of three cases. Neurosurg Focus. 2005;18:e7. Denis F, Davis S, Comfort T.  Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop Relat Res. 1988;227:67–81. Finiels PJ, Finiels H, Strubel D, Jacquot JM. Spontaneous osteoporotic fractures of the sacrum causing neurological damage. Report of three cases. J Neurosurg. 2002;97:380–5. https://doi.org/10.3171/ spi.2002.97.3.0380. Garant M. Sacroplasty: a new treatment for sacral insufficiency fracture. J Vasc Interv Radiol. 2002;13:1265–7. https://doi.org/10.1016/ s1051-­0443(07)61976-­9. Geannette C, Lee SC, Sneag DB.  Etiology of Lumbosacral Radiculoplexopathy: Sacral Insufficiency Fracture on Magnetic Resonance Imaging. HSS J. 2020;16:126–9. https://doi.org/10.1007/ s11420-­020-­09750-­y. Graul I, Vogt S, Strube P, Hölzl A.  Significance of Lumbar MRI in Diagnosis of Sacral Insufficiency Fracture. Global Spine J. 2021;11:1197–201. https://doi.org/10.1177/2192568220941821. Karataş M, Başaran C, Ozgül E, Tarhan C, Ağildere AM. Postpartum sacral stress fracture: an unusual case of low-back and buttock pain. Am J Phys Med Rehabil. 2008;87:418–22. https://doi.org/10.1097/ PHM.0b013e318164a8e6. Kortman K, Ortiz O, Miller T, Brook A, Tutton S, Mathis J, et  al. Multicenter study to assess the efficacy and safety of sacroplasty in patients with osteoporotic sacral insufficiency fractures or pathologic sacral lesions. J Neurointerv Surg. 2013;5:461–6. https://doi. org/10.1136/neurintsurg-­2012-­010347. Lapina O, Tiškevičius S. Sacral insufficiency fracture after pelvic radiotherapy: a diagnostic challenge for a radiologist. Medicina (Kaunas). 2014;50:249–54. https://doi.org/10.1016/j.medici.2014.09.006. Lin JT, Lutz GE. Postpartum sacral fracture presenting as lumbar radiculopathy: a case report. Arch Phys Med Rehabil. 2004;85:1358–61. https://doi.org/10.1016/j.apmr.2003.09.021. Lourie H. Spontaneous osteoporotic fracture of the sacrum. An unrecognized syndrome of the elderly. JAMA. 1982;248:715–7. Major NM, Helms CA. Sacral stress fractures in long-distance runners. AJR Am J Roentgenol. 2000;174:727–9. https://doi.org/10.2214/ ajr.174.3.1740727.

67  Sacral Stress Fractures Malherbe JAJ, Davel S.  An Atraumatic Sacral Fracture with Lumbosacral Radiculopathy Complicating the Early Postpartum Period: A Case Report. Am J Case Rep. 2019;20:794–9. https://doi. org/10.12659/AJCR.915764. Memetoğlu OG, Ozkan FU, Boy NS, Aktas I, Kulcu DG, Taraktas A.  Sacroiliitis or insufficiency fracture? Osteoporos Int. 2016;27:1265–8. https://doi.org/10.1007/s00198-­015-­3363-­z. Pentecost RL, Murray RA, Brindley HH.  Fatigue, Insufficiency, and Pathologic Fractures. JAMA. 1964;187:1001–4. https://doi. org/10.1001/jama.1964.03060260029006. Rickert MM, Windmueller RA, Ortega CA, Devarasetty VVNM, Volkmar AJ, Waddell WH, et al. Sacral insufficiency fractures. JBJS Rev. 2022;10 https://doi.org/10.2106/JBJS.RVW.22.00005. Schindler OS, Watura R, Cobby M.  Sacral insufficiency fractures. J Orthop Surg (Hong Kong). 2007;15:339–46. https://doi. org/10.1177/230949900701500320. Tamaki Y, Nagamachi A, Inoue K, Takeuchi M, Sugiura K, Omichi Y, et al. Incidence and clinical features of sacral insufficiency fracture in the emergency department. Am J Emerg Med. 2017;35:1314–6. 10.1016/j.ajem.2017.03.037 Thein R, Burstein G, Shabshin N. Labor-related sacral stress fracture presenting as lower limb radicular pain. Orthopedics. 2009;32:447. https://doi.org/10.3928/01477447-­20,090,511-­24. Thomas EN, Cyteval C, Herisson C, Leonard L, Blotman F. Osteoporotic fracture of the sacrum: sacroplasty and physical medecine. Ann Phys Rehabil Med. 2009;52:427–35. https://doi.org/10.1016/j. rehab.2009.01.003. Tsiridis E, Upadhyay N, Giannoudis PV. Sacral insufficiency fractures: current concepts of management. Osteoporos Int. 2006;17:1716– 25. https://doi.org/10.1007/s00198-­006-­0175-­1. Urits I, Orhurhu V, Callan J, Maganty NV, Pousti S, Simopoulos T, et  al. Sacral Insufficiency Fractures: a Review of Risk Factors, Clinical Presentation, and Management. Curr Pain Headache Rep. 2020;24:10. https://doi.org/10.1007/s11916-­020-­0848-­z. Volpin G, Milgrom C, Goldsher D, Stein H.  Stress fractures of the sacrum following strenuous activity. Clin Orthop Relat Res. 1989;243:184–8. Wagner D, Hofmann A, Kamer L, Sawaguchi T, Richards RG, Noser H, et al. Fragility fractures of the sacrum occur in elderly patients with severe loss of sacral bone mass. Arch Orthop Trauma Surg. 2018;138:971–7. https://doi.org/10.1007/s00402-­018-­2938-­5. Zaman FM, Frey M, Slipman CW.  Sacral stress fractures. Curr Sports Med Rep. 2006;5:37–43. https://doi.org/10.1097/01. csmr.0000306517.25172.68. Zhong X, Zhang L, Dong T, Mai H, Lu B, Huang L, et al. Clinical and MRI features of sacral insufficiency fractures after radiotherapy in patients with cervical cancer. BMC Womens Health. 2022;22:166. https://doi.org/10.1186/s12905-­022-­01758-­2.

Penetrating Lumbosacral Spine Injuries

68.1 Generalities and Relevance Penetrating spine injuries involves a wound in which an object breaches the spinal column with or without an exit wound. The majority of these injuries are serious  medical emergencies  and may cause permanent  disability or death. The management of these injured patients is completely different from other traditional forms of spinal traumatic injuries (c.f. Chap. 65 about Lumbosacral Spine Fractures and Dislocations). Penetrating injuries to the spine are unusual accounting for less than 15% of all spinal cord injuries, mainly represented by thoracic and cervical injuries. The lumbosacral column is rarely involved, representing less than 20% of all penetrating spine injuries. A penetrating injury can be caused by the following injuries: • Missile injuries such as gunshot wounds (GSWs), bullets, and shrapnel. • Non-missile injuries mainly stabbing using various instruments including a knife, pencil, and iron bar. Gunshot wounds are by far the most frequent penetrating injuries of the spine. The lesions can be multifactorial and comprise concussive, penetrating, and shearing trauma to the neural elements; however, the extent of damage is highly correlated to the type of weapon. Unlike civilian GSWs which produces direct injury from the bullet, military weapons may generate injury from shock wave and cavitation consequently, military GSWs induce more massive tissue injury than civilian ones. On the other hand, damage from non-missile penetrating injuries is restricted to the tract of the stab wound and often has fewer lesions than missile spinal injuries.

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Penetrating injuries to the spine though not commonly encountered can result in a range of neurological symptoms and deficits depending on the location and extent of foreign body injury. In the lumbosacral spine, some injured patients with incomplete damage may present lumbosacral radicular symptoms such as sciatica. Sciatic pain may be secondary to various conditions depending on the timing of onset and progression of the symptoms: –– In the early period, symptoms may be caused by compression (foreign objects, bone, disc material, and hematoma), blast effect (neurologic dysfunction), stretching, or cutting the nerve roots. –– Later, delayed presentations can be related to reactive epidural fibrosis around the retained foreign body, epidural scar, or migration of the bullet intrathecally (as a result of gravitational forces). In some complex GSW injuries, especially military injuries, lumbosacral radicular injuries are usually accompanied by vascular compromise as well as vertebral, joints, disco-­ ligamentous, and soft tissue damage. Furthermore, association with other spinal roots or even lumbosacral plexus injuries is not rare. Like other patients with a penetrating spine injury, the majority of victims with lumbosacral injuries are principally young males of lower socioeconomic status from urban areas. Most injuries are related to violent acts and criminal behaviors. In the lumbar spine, the most frequent neurological injury is at L1, and the most common impairment is incomplete motor function. About 70% of patients with GSW of the lumbosacral region have incomplete neurologic damage.

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68.2 Clinical Presentations

68.3 Paraclinic Features

As soon as the injured patient is admitted to the emergency room, it is mandatory to ensure the maintenance of the airway, breathing, and circulation (ABCs) and to control pain. The initial evaluation should include a sufficient and detailed history and physical exam. Recent injury, presence of signs of trauma, or existence of spinal, pelvic, or abdominal wound may help for the diagnosis of penetrating spine injury. The onset of symptoms related to lumbosacral radiculopathy may be instantaneous, acute, or delayed. Post-traumatic damages include neuropathic pain, paresthesia, and variable motor and/or sensory deficits. Delayed presentations are rare, more subtle, and often misdiagnosed. In the context of trauma, lumbosacral nerve root damage rarely exists in isolation but is often associated with other neurologic and/or non-­ neurologic symptoms, especially in the context of military injuries. Sometimes, patients are multi-injured and various medical specialties may be involved in their management. As for other types of spinal trauma, each spinous process must be palpated for painfulness and crepitus. An in-depth neurologic examination, including motor, sensory, reflexes, and anal sphincter tone must be executed accurately. Entrance and even exit wounds should be examined thoroughly. Very rarely, spinal gunshot injury does cause mild or no neurological symptoms. On the contrary, neurological symptoms may occur months to years later after the gunshot injury. Delayed presentation of neurological symptoms is likely the result of migration of the bullet intrathecally in the spinal canal (about 20 cases described in the lumbosacral region) or secondary to reactive epidural fibrosis around the retained foreign object. Lead toxicity is a rare but serious delayed complication that should be kept in mind. Symptoms of lead toxicity (AKA plumbism, lead poisoning, or saturnism) can include microcytic hypochromic anemia, peripheral paresthesia, chronic renal failure, high blood pressure, lassitude, malaise, abdominal pain, constipation, headache, joint pain, and impairment of higher cognitive functions (e.g., memory loss, attention deficit, and irritability). Sometimes, electromyography can be used to localize and evaluate the affected lumbosacral roots.

The imaging assessment with or without neurophysiologic studies enhances the clinical evaluation with functional and anatomic details that determine the extent and localization of the nerve root injury. These investigations may help decisions regarding the timing of surgical intervention as well as the type of surgical procedures. Both nerve conduction studies and needle electromyography can define the degree of neurological damage in the nerve. A repetitive surveillance program may be taken on to assess the possibility of re-innervation with time because the clinical-electrophysiological correlation is often unexploited or misinterpreted in the beginning. Two orthogonal plain radiographic views of the lumbosacral spine can help detect gunshot fractures and locate metallic fragments (Figs.  68.1 and 68.2). Dynamic active flexion-extension views may be obtained to evaluate spinal instability; however, this exploration must be done, at best, 2 weeks post-injury. Computed tomography (CT) scan is highly useful in assessing the location of ballistic fragments, bone destruction, canal compromise, and spinal stability (Fig.  68.3). However, images are often masked by artifacts when metallic foreign body fragments are present. Magnetic resonance (MR) imaging could give more information about soft-tissue damage, especially neurological lesions. However, if the ballistic fragment was not MR compatible, then there was the possibility of fragment movement or heating of the fragment aggravating the existing neurological damage. For this reason, CT myelography could be performed avoiding MRI. For some authors, MR imaging can be performed in patients with incomplete neurologic injuries or at a minimum of 2 months after the injury with no movement of the bullet on plain radiography or CT scan. Further paraclinic investigations such as abdominopelvic CT scan, ultrasonography, or angiographic studies may be needed for specific cases in the search for concomitant traumatic lesions.

68.3  Paraclinic Features Fig. 68.1  Anteroposterior (a) and lateral (b) plain radiographic views of the lumbosacral spine in an adult patient presenting with left-sided sciatic pain following a posterior lumbar penetrating injury. Note the position of the metallic fragment on L5-S1 (arrows)

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Fig. 68.2  Anteroposterior (a) and lateral (b) plain radiographic views of the lumbosacral spine showing an L2-L3 metallic fragment (c) on the right side (arrows)

68.4  Treatment Options

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Fig. 68.3  Right-sided sciatica in a child sustained a penetrating lumbosacral injury. There are multiple bony fragments at the level of right L5-S1 foramen (arrows) as seen on axial CT scan on parenchymal (a, b) and bony (c, d) windows

68.4 Treatment Options Management of penetrating spinal injury is an issue of controversy. For many treating surgeons, treatment needs to be individualized taking into account various parameters including: –– –– –– –– –– –– ––

Patient’s general condition Hemodynamic stability Additional concomitant disorders Degree and extension of neurological damage Spinal stability Causative agent Location of potential foreign bodies

The goal of the treatment of penetrating lumbosacral spinal injuries is variable (Table  68.1) and many therapeutic methods have been proposed such as medication, conservative measures, surgery, and physical therapy.

Table 68.1  The goal of the treatment of penetrating lumbosacral spine injuries (a) Maintenance of airway, breathing, and circulation (ABCs) if needed (b)  Pain control (c)  Eliminate the aggressive causative agent (d)  Restore neural function (e) Perform nervous decompression in case of incomplete neurological deficit related to intracanalar lesions (f)  Stabilize any post-traumatic instability (g)  Achieve watertight closure of the dura and avoid CSF leakage

In complete radicular nerve rupture, some surgeons have attempted to direct repair of the cauda equina rootlets with a microscope but seemed very difficult because of the retraction of the distal stumps. Regardless of the level of injury, corticosteroid infusion has little effect on neurologic improvement. Tetanus prophylaxis must be considered in all instances of penetrating spine injuries. About an obvious CSF consecutive to damage of the thecal sac, antibiotic prophylaxis against meningitis, as well as proper surgical repair of the dura, seems incontestable.

68  Penetrating Lumbosacral Spine Injuries

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Indications for surgery remain controversial. Most authors recommend decompression and foreign body removal in the following situations: • Incomplete injury • Lumbosacral radiculopathy or cauda equina syndrome attributable to nerve root compression • Neurologic deterioration suggesting the risk of an epidural hematoma • Nerve root compression (foreign objects, hematoma, bone fragments, disc material) • Cerebrospinal fluid leak • Vascular injuries • Lumbosacral spinal instability • Potential risk of infection (e.g., transabdominal or transpelvic trajectory) • Late complications: Migrating bullet, lead toxicity, and secondary spinal instability If large or complex dural defects are encountered, a lumbar drain can be used following the dural reparation. Overall, in cases of penetrating cauda equina injury by foreign objects, many authors have recommended emergent surgery to perform decompression by removing foreign objects, bone fragments, or blood clots, to prevent persistent infection and to stop drainage of the CSF if needed. Many studies demonstrated statistically significant motor improvement after surgical decompression below T12 vertebral levels compared with conservative management. Unlike military weapons which produce more massive tissue injuries needing debridement of the missile tract, most civilian GSWs do not require systematic surgical debridement. Sacral GSWs are most frequently complicated by bleeding. In hemodynamically unstable patients, emergent angiographic embolization can reduce or stop severe hemorrhage. The posterior approach is most commonly used for neurologic decompression and debridement. Sometimes, lateral and anterior approaches can be used for the removal of foreign bodies from the intervertebral disc and vertebral bodies. Compared to the standard open technique, minimally invasive and endoscopy procedures reduce the risk of infectious complications through minimal invasiveness. Intraoperative fluoroscopy is very helpful and leads to the correct localization of the ballistic fragments. The management of bullets that have migrated in the spinal canal remains controversial. Most authors advocate extracting the ballistic fragment from the spinal canal if there are progressive neurologic symptoms. However, delayed surgical decompression might encounter some difficulties during surgical dissection (neurolysis) of the roots with sometimes strong intrathecal root adhesions.

Any associated lesions will be treated appropriately. It is well known that military GSWs are associated with many regional and even general concomitant traumatic lesions that should be managed properly at a convenient time. Multidisciplinary specialist management is required for various and complex disorders.

68.5 Outcomes and Prognosis Unlike cervical and thoracic penetrating spinal injuries or complete neurologic damage, lumbar and incomplete neurologic lesions have shown that surgery provides the best chance for neurological recovery. Non-missile injuries may favor non-operative intervention as compared to military injuries which may favor surgical intervention. Most cases with lumbar or sacral radicular pain syndromes are reported to improve after the debridement and removal of a compressive structure such as a bullet or bone fragments. However, residual neuropathic pain is a common long-term sequel and can be commonly treated with neuropathic pain medications such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline) and some anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine). Physical therapy may be used to speed up the recovery of motor function. The most common causes of death after spinal GSW are exsanguination, hypoxemia, and infection. The highest-­ velocity injuries tend to have the worst associated damage and subsequently the worst prognosis. Lead intoxication and bullet migration are infrequent causes of late morbidity and require a high index of suspicion for accurate diagnosis and specific management.

Further Reading Aljuboori Z, Sieg E. Resolution of cauda equina syndrome after surgical extraction of the lumbar intrathecal bullet. Surg Neurol Int. 2020;11:214. https://doi.org/10.25259/SNI_400_2020. Avci SB, Açikgöz B, Gündoğdu S.  Delayed neurological symptoms from the spontaneous migration of a bullet in the lumbosacral spinal canal. Case report. Paraplegia. 1995;33:541–2. https://doi. org/10.1038/sc.1995.117. Baldawa S, Shivpuje V.  Migratory low velocity intradural lumbosacral spinal bullet causing cauda equina syndrome: report of a case and review of literature. Eur Spine J. 2017;26:128–35. https://doi. org/10.1007/s00586-­016-­4913-­6. Beucler N, Haikal C, Kaya JM. A penetrating lumbar spine injury with misleading neurological symptoms. Mil Med. 2021;188(1–2):e440– 4. https://doi.org/10.1093/milmed/usab137. Bono CM, Heary RF. Gunshot wounds to the spine. Spine J. 2004;4:230– 40. https://doi.org/10.1016/S1529-­9430(03)00178-­5.

Further Reading Bordon G, Burguet GS. Gunshot wound in lumbar spine with intradural location of a bullet. Case Rep Orthop. 2014;2014:698585. https:// doi.org/10.1155/2014/698585. Brash A, Halalmeh DR, Rajah G, Loya J, Moisi M. Operative intervention for lumbar Foraminal gunshot wounds: case report and review of the literature. Cureus. 2019;11:e5269. https://doi.org/10.7759/ cureus.5269. Cağavi F, Kalayci M, Seçkiner I, Cağavi Z, Gül S, Atasoy HT, et  al. Migration of a bullet in the spinal canal. J Clin Neurosci. 2007;14:74–6. https://doi.org/10.1016/j.jocn.2005.12.042. Crutcher CL, Wilson JM, DiGiorgio AM, Fannin ES, Shields JA, Morrow KD, et  al. Minimally invasive Management of Civilian Gunshot Wounds to the lumbar spine: a case series and technical report. Oper Neurosurg (Hagerstown). 2020;19:219–25. https://doi. org/10.1093/ons/opaa030. de Los CD, Powers A, Behrens JP, Mattei TA, Salari P. Surgical removal of a migrating intraspinal bullet: illustrative case. J Neurosurg Case Lessons. 2021;1:CASE21132. https://doi.org/10.3171/CASE21132. Dulou R, Delmas JM, Dagain A, Yordanova Y, Pernot P. Is it worth performing suture of the cauda equina roots after traumatic penetrating lumbar injury in a combat support hospital? Acta Neurochir. 2015;157:1087–8. https://doi.org/10.1007/s00701-­014-­2283-­6. Farrugia A, Raul JS, Géraut A, Ludes B.  Ricochet of a bullet in the spinal canal: a case report and review of the literature on bullet migration. J Forensic Sci. 2010;55:1371–4. https://doi. org/10.1111/j.1556-­4029.2010.01439.x. Ghori SA, Khan MS, Bawany FI. Delayed cauda Equina syndrome due to a migratory bullet. J Coll Physicians Surg Pak. 2014;24(Suppl 3):S219–20. Hakan T, Çerçi A, Gürcan S, Akçay S.  Firearm bullet settling into the lumbar spinal canal without causing neurological deficit: a report of two cases. Surg Neurol Int. 2016;7:S251–4. https://doi. org/10.4103/2152-­7806.181978. Harsha KJ, Thomas A. Penetrating injury to cauda Equina from a missile fragment, completely recovered after delayed surgical removal of ballistic fragment. Asian J Neurosurg. 2018;13:433–5. https:// doi.org/10.4103/1793-­5482.228565. Jun W, Yi-Jun K, Xiang-Sheng Z, Jing W.  Cauda equina syndrome caused by a migrated bullet in dural sac. Turk Neurosurg. 2010;20:566–9. https://doi.org/10.5137/1019-­5149.JTN.2247-­09.1. Kafadar AM, Kemerdere R, Isler C, Hanci M. Intradural migration of a bullet following spinal gunshot injury. Spinal Cord. 2006;44:326–9. https://doi.org/10.1038/sj.sc.3101808. Khorasanizadeh M, Yousefifard M, Eskian M, Lu Y, Chalangari M, Harrop JS, et al. Neurological recovery following traumatic spinal cord injury: a systematic review and meta-analysis. J Neurosurg

773 Spine. 2019;30(5):683–99. https://doi.org/10.3171/2018.10. SPINE18802. Karim NO, Nabors MW, Golocovsky M, Cooney FD.  Spontaneous migration of a bullet in the spinal subarachnoid space causing delayed radicular symptoms. Neurosurgery. 1986;18:97–100. https://doi.org/10.1227/00006123-­198601000-­00018. Kolur SS, Rathod TN, Prabhu RM, Yadav VK, Hadole BS, Rai AK. Isolated L5 nerve root injury without osseous disruption in a case of gunshot injury to the paediatric spine-a case report. Spinal Cord Ser Cases. 2022;8:45. https://doi.org/10.1038/s41394-­022-­00516-­8. Kravtsov MN, Manukovsky VA, Bulyshchenko GG, Mirzametov SD, Byvaltsev VA.  Case report: full-endoscopic surgery for bullet wounds of the spine: a report of three cases. Front Surg. 2022;9:873365. https://doi.org/10.3389/fsurg.2022.873365. Mariottini A, Delfini R, Ciappetta P, Paolella G.  Lumbar disc hernia secondary to gunshot injury. Neurosurgery. 1984;15:73–5. https:// doi.org/10.1227/00006123-­198407000-­00013. Moon E, Kondrashov D, Hannibal M, Hsu K, Zucherman J. Gunshot wounds to the spine: literature review and report on a migratory intrathecal bullet. Am J Orthop (Belle Mead NJ). 2008;37:E47–51. Morare N, Moeng MS. Unusual case of a migrating spinal bullet: an opportunity for reflection. Trauma Case Rep. 2020;27:100301. https://doi.org/10.1016/j.tcr.2020.100301. Platt A, Dafrawy MHE, Lee MJ, Herman MH, Ramos E.  Gunshot wounds to the lumbosacral spine: systematic review and meta-analysis. Global Spine J. 2022;12:1247–53. https://doi. org/10.1177/21925682211030873. Rentfrow B, Vaidya R, Elia C, Sethi A. Lead toxicity and management of gunshot wounds in the lumbar spine. Eur Spine J. 2013;22:2353– 7. https://doi.org/10.1007/s00586-­013-­2805-­6. Robertson DP, Simpson RK, Narayan RK.  Lumbar disc herniation from a gunshot wound to the spine. A report of two cases. Spine. 1991;Phila Pa 1976(16):994–5. https://doi. org/10.1097/00007632-­199108000-­00026. Siddiqui MI, Hawksworth SA, Sun DY.  Removal of migrating lumbar spine bullet: case report and surgical video. World Neurosurg. 2019;131:62–4. https://doi.org/10.1016/j.wneu.2019.07.151. Tani T, Ebira Y, Kamitani S, Kodama M.  Vertical stab wound to the lumbo-sacral spinal canal: report of a case. Surg Today. 1998;28:346–8. https://doi.org/10.1007/s005950050138. Thakur RC, Mittal RS, Khosla VK.  Spinal subarachnoid haematoma after stab injury of the cauda equina. S Afr J Surg. 1990;28(1):21–3. Vilela MD, Gelfenbeyn M, Bellabarba C. U-shaped sacral fracture and lumbosacral dislocation as a result of a shotgun injury: case report. Neurosurgery. 2009;64:E193–4. https://doi.org/10.1227/01.NEU.0 000336313.88450.5E.

Spinal Epidural Hematomas

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69.1 Generalities and Relevance A spinal epidural hematoma is a collection of blood in the intraspinal epidural space which is the potential space between the inner surface of the vertebral canal and the dura mater of the meninges that envelop the spinal cord and the spinal nerve roots (Figs. 69.1 and 69.2). The spinal epidural space is characterized by the presence of fat tissue, the internal vertebral venous plexuses, and the spinal nerve roots, contrary to the cranial one. However, the pathophysiology of spinal epidural hematoma remains unclear, in the lumbar spine epidural bleeding is best known as the consequence of internal rupture of the Batson vertebral venous plexus. Most spinal epidural hematomas occur in the cervico-­ thoracic and thoraco-lumbar spinal regions. In the lumbosa- Fig. 69.2  Lumbar epidural hematoma compressing the thecal sac and its contents as seen in sagittal section cral spinal canal, this unusual but serious pathologic entity has the potential to cause rapid and permanent neurologic damage by compressing the cauda equina nerve roots. Some factors or causes that can result in this type of hematoma are as follows: –– –– –– –– –– –– –– –– ––

Fig. 69.1  Lumbar epidural hematoma compressing the thecal sac and its contents as seen in axial section

Coagulopathy Hematologic disease Anticoagulation therapy Traumatic injury Lumbar puncture and other percutaneous iatrogenic procedures Spinal surgery Pregnancy Intraspinal vascular malformations Intratumoral bleeding

Sometimes, the exact cause of the bleeding is undetermined and the spinal epidural hematoma is then considered “idiopathic” (up to 40% of cases).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_69

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Intraspinal hematomas are an uncommon clinical entity. However, due to rich epidural venous plexuses, spinal epidural hematomas are considered the most usual type of intraspinal hematomas (75.2%) in comparison to subarachnoid (15.7%), subdural (4.1%), and intramedullary (0.82%) ones. Although rare, practitioners should consider the possibility of a mixed combination of different localizations of hematomas in the spinal canal (epidural, subdural, and/or subarachnoid).

69.2 Clinical Presentations Clinical signs and symptoms of spinal epidural hematoma are similar to those of other intraspinal hematomas. With the exclusion of post-traumatic forms, most patients will present with spontaneous acute onset of back pain and varying degrees of radicular pain of the extremities. Then, a progressive neurologic deficit is developed. Chronic clinical forms are less frequent and more subtle. Unlike acute forms, chronic spinal epidural hematomas typically show mild radicular pain and mild or no motor deficit. In the lumbosacral spine, patients may present with unilateral or bilateral sciatica followed by partial or complete cauda equina syndrome due to nerve root compression. Also, the development of neurologic symptoms tends to be more fulminant in patients with spinal epidural hematoma than in those with subdural ones. Whatever the clinical expression be, the diagnosis of spinal epidural hematoma is often unsuspected before a neuroimaging evaluation.

69.3 Imaging Features Like other intraspinal hematomas, magnetic resonance imaging (MRI) is considered the gold standard for suspected spinal epidural hematoma. MRI can visualize both the epidural collection, its exact location, the nerve root compression, and other concomitant soft-tissue injuries. In addition, MRI may help identify the potential underlying lesions such as vascular malformations or tumors. The appearance of the hematoma itself has a variable T1 and T2 signal depending on the chronicity of the bleeding (Table 69.1). Epidural hematomas are outside the dura and cause a mass effect with a local displacement of the thecal sac. Unlike subdural hematomas, the fat tissue of the epidural space will be obliterated and effaced when epidural hematomas develop. Most spinal epidural hematomas are located dorsally or dorsolaterally within the spinal canal. This is

Table 69.1  MRI findings of spinal hematomas according to Braun et al. Stage Hyperacute

Timing < 24 h

Acute

1–3 days

T1-weighted image T2-weighted image Isointense Slightly hyperintense Slightly Hypointense hypointense Hyperintense Hypointense

Early 3–7 days subacute Late subacute 7– Hyperintense 14 days Chronic > 14 days Slightly hypointense

Hyperintense Hypointense

because the dura mater is more closely adherent to the posterior longitudinal ligament than to the yellow ligaments. Also, peripheral enhancement may be seen following gadolinium injection. The axial images are particularly important for separating between subdural and epidural hematomas. The spinal epidural collection that has a convex lens-like shape, may extend into the neural foramina, is usually located dorsal to the thecal sac, and make direct contact with adjacent bony structures. However, a subdural collection is typically found ventral and lateral to and around the cauda equina nerve roots with a tri-radiate pattern called an “inverted Mercedes Benz sign” in the lumbar area due to the existence of the lateral denticulate ligaments and dorsal septum (c.f. Chap. 70 about Spinal Subdural Hematomas). When needed, MR angiography, CT scan angiography, or digital subtraction spinal angiography will be used for identifying potential vascular abnormalities and for assessment of the hemorrhagic source. However, these angiographic explorations should not waste the time required for appropriate surgical decompression of the hematoma. In many spinal injured patients, a CT scan is performed before MRI. A spinal epidural hematoma can be visualized classically as a biconvex, hyperdense mass lesion with sharp borders into the spinal canal. However, a subacute hematoma can present as an isodense lesion that is difficult to identify. On spinal imaging, some ENVT may be confused with a wide spectrum of other epidural lumbosacral pathologies such as: • Degenerative lesions (free/sequestered disc fragment, synovial cyst, ligamentum flavum lesions). • Tarlov cysts. • Vascular lesions (cavernous angioma, vascular malformations, varices). • Benign or malignant vertebro-epidural tumors. • Congenital lesions (arachnoid cyst, meningocele, lipoma, dermoid, epidermoid cysts). • Spinal epidural lipomatosis.

Further Reading

• Granulomatous lesions (tuberculoma, sarcoidosis). • Epidural abscesses. • Some rheumatologic diseases (gouty tophus, pigmented villonodular synovitis, rheumatoid nodules). Furthermore, patients should be assessed by appropriate biological and imaging studies to look for potential underlying disorders or concomitant lesions (Table 69.1).

69.4 Treatment Options and Prognosis A lumbosacral epidural hematoma can be managed conservatively or surgically. However, in most occasions, surgical evacuation should be given increased concern to prevent possible permanent neurologic damage induced by this bleeding. Surgical procedures typically comprise decompressive laminectomy and hematoma removal through careful aspiration and peeling off the organized blood clot from the dura and nerve roots. Any active bleeding should be stopped and controlled. Theoretically, percutaneous drainage, with or without neuroimaging guidance, may be considered in cases where the hematoma is situated dorsally, being well-liquefied, and without coagulopathy. However, percutaneous drainage is not always possible because most hematomas appear as a non-aspirable organized clot in the acute phase of the bleeding. Conservative management may be considered if no or mild deficits are present, the blood collection is small, or neurological symptoms are improving. Although the treatment is conservative, it is necessary to have attentive clinical monitoring. In patients presenting with rapid or severe neurological deterioration, surgical evacuation is indicated as soon as possible. Treatment success varies depending on several factors such as the patient’s conditions, the severity of neurological status at admission, the presence or absence of coagulopathies, the underlying etiologies of bleeding, the associated lesions, the craniocaudal localizations, and the timing of surgical evacuation. It seems that idiopathic cases, epidural hematomas located in the lumbosacral region, those with moderate neurological impairment, and those without coagulopathy are expected to have good results.

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Further Reading Akhaddar A, Albouzidi A, Boucetta M.  Sudden onset of paraplegia caused by hemorrhagic spinal epidural angiolipoma. A case report. Eur Spine J. 2008;17(Suppl 2):S296–8. https://doi.org/10.1007/ s00586-­008-­0591-­3. Al-Mutair A, Bednar DA.  Spinal epidural hematoma. J Am Acad Orthop Surg. 2010;18:494–502. https://doi. org/10.5435/00124635-­201008000-­00006. Braun P, Kazmi K, Nogués-Meléndez P, Mas-Estellés F, Aparici-­ Robles F.  MRI findings in spinal subdural and epidural hematomas. Eur J Radiol. 2007;64:119–25. https://doi.org/10.1016/j. ejrad.2007.02.014. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 14-1982. An 81-year-old woman with severe lumbar pain and sciatica. N Engl J Med. 1982;306:855–60. https://doi.org/10.1056/NEJM198204083061407. Domenicucci M, Mancarella C, Santoro G, Dugoni DE, Ramieri A, Arezzo MF, et al. Spinal epidural hematomas: personal experience and literature review of more than 1000 cases. J Neurosurg Spine. 2017;27:198–208. https://doi.org/10.3171/2016.12.SPINE15475. Fuster S, Castañeda S, Ferrer E, Wang J, Poblete J. Spontaneous chronic epidural hematoma of the lumbar spine mimicking an extradural spine tumour. Eur Spine J. 2013;22(Suppl 3):S337–40. https://doi. org/10.1007/s00586-­012-­2402-­0. Giri PJ, Sharma MS, Jaiswal AK, Behari S, Jain VK. Extruded lumbar disc associated with epidural hematoma. Case report. J Neurosurg. 2006;104:282–4. https://doi.org/10.3171/ped.2006.104.4.282. Giugno A, Basile L, Maugeri R, Iacopino DG. Emergency surgery in a patient with large spontaneous spinal epidural hematoma determining excellent neurological recovery: review of the literature. Spinal Cord. 2014;52(Suppl 3):S22–4. https://doi.org/10.1038/ sc.2014.156. Iliescu BF, Chiriţă BC, Poeată I. The pitfalls of differential diagnosis of lumbar spine epidural lesions--exemplification with two particular cases and a review of the literature. Rev Med Chir Soc Med Nat Iasi. 2013;117:947–53. Khalatbari MR, Abbassioun K, Amirjmshidi A.  Solitary spinal epidural cavernous angioma: report of nine surgically treated cases and review of the literature. Eur Spine J. 2013;22:542–7. https://doi. org/10.1007/s00586-­012-­2526-­2. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev. 2003;26:1– 49. https://doi.org/10.1007/s10143-­002-­0224-­y. Morse K, Weight M, Molinari R.  Extensive postoperative epidural hematoma after full anticoagulation: case report and review of the literature. J Spinal Cord Med. 2007;30:282–7. https://doi.org/10.10 80/10790268.2007.11753938. Pierce JL, Donahue JH, Nacey NC, Quirk CR, Perry MT, Faulconer N, et  al. Spinal hematomas: what a radiologist needs to know. Radiographics. 2018;38:1516–35. https://doi.org/10.1148/ rg.2018180099. van Veen JJ, Nokes TJ, Makris M. The risk of spinal haematoma following neuraxial anaesthesia or lumbar puncture in thrombocytopenic individuals. Br J Haematol. 2010;148:15–25. https://doi. org/10.1111/j.1365-­2141.2009.07899.x.

Spinal Subdural Hematomas

70

70.1 Generalities and Relevance

70.2 Clinical Presentations

A spinal subdural hematoma is a collection of blood in the intraspinal subdural space which is the potential space between the  arachnoid mater and the dura mater  of the meninges that envelop the spinal cord and the spinal nerve roots. The predominant location was the thoracic spine. In the lumbosacral spinal canal, this rare but serious pathologic entity has the potential to cause secondary neurologic damage by compressing the cauda equina nerve roots. There are various factors or etiologies that can predispose to this type of hematoma, including:

Clinical signs and symptoms of spinal subdural hematoma are similar to those of other intraspinal hematomas. Except for post-traumatic forms which are rare, most patients will present with spontaneous acute onset of back pain and varying degrees of radicular pain with or without sciatica. Then, rapidly progressive neurologic deficits developed. Chronic clinical forms are rare and more subtle. Unlike acute forms, chronic spinal subdural hematomas usually show mild radicular pain and mild or no motor deficit. In the lumbosacral spine, many patients will present with partial or complete cauda equina syndrome due to nerve root compression. Progression of neurologic symptoms tends to be faster in patients with spinal epidural hematoma than in those with subdural hematoma. Whatever the clinical expression be, the diagnosis of spinal subdural hematoma is often unpredictable before a neuroimaging study.

• • • • • • • •

Bleeding disorders Hematologic disease Anticoagulation therapy Lumbar puncture and other percutaneous iatrogenic procedures Spinal surgery Intraspinal vascular malformations Intraspinal tumors Traumatic injury (rarely)

Sometimes, the exact origin of the bleeding is unknown and the spinal subdural hematoma is then considered “idiopathic.” Spinal subdural hematomas, with about 260 cases reported in the literature, are much less frequent than those occurring in the epidural space because the spinal subdural space lacks the same number of blood vessels or bridging veins which could be a cause of subdural hemorrhage. Also, subdural hematomas are among the most unusual types of intraspinal hematomas in comparison to epidural ones. In a literature review of 613 intraspinal hematomas, only 4.1% were cited in the subdural space. Although rare, practitioners should consider the possibility of a combination of spinal and cranial subdural hematomas.

70.3 Imaging Features Like other intraspinal hematomas, magnetic resonance imaging is considered the gold standard in the diagnosis of spinal subdural hematoma. Magnetic resonance imaging (MRI) can visualize both the subdural hematoma, and its exact location, and may help identify the potential underlying lesions such as vascular malformations or tumors. The appearance of the hematoma itself has a variable T1 and T2 signal depending on the chronicity of the bleeding (Table 70.1). The axial images are particularly important for separating between subdural and epidural hematomas. The spinal epidural collection has a convex lens-like shape, may extend into the neural foramina, is usually located dorsal to the spinal cord, and make direct contact with adjacent bony structures. While a subdural collection is typically found ventral

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_70

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and lateral to and around the cauda equina nerve roots with a tri-radiate pattern called an “inverted Mercedes Benz sign” in the lumbar area due to the existence of the lateral denticulate ligaments and dorsal septum (Figs.  70.1 and 70.2). In Table 70.1  MRI findings of spinal hematomas according to Braun et al. Stage Hyperacute

Timing < 24 h

Acute

1–3 days

Early subacute Late subacute Chronic

3–7 days

T1-weighted image T2-weighted image Isointense Slightly hyperintense Slightly Hypointense hypointense Hyperintense Hypointense

7– Hyperintense 14 days > 14 days Slightly hypointense

Hyperintense Hypointense

a

addition, the extradural fat tissue is conserved in subdural hematoma and there is no interior displacement of the dura. When needed, MR angiography, computed tomography scan angiography, or digital subtraction spinal angiography will be performed for identifying latent vascular malformations and for assessment of the hemorrhagic source. However, these angiographic explorations should not waste the time needed for the timely surgical evacuation of the hematoma. On spinal imaging, some spinal subdural hematomas may be confused with a wide spectrum of other subdural lumbosacral pathologies whether they are tumoral, traumatic, infectious, vascular, iatrogenic, inflammatory, granulomatous, or malformative (Table 70.2). Furthermore, patients should be assessed by appropriate biological and imaging studies to look for potential underlying disorders or concomitant lesions.

b

c

Fig. 70.1  “Inverted Mercedes-Benz sign” of lumbar subdural hematoma (a-c). Due to the presence of two lateral denticulate ligaments and the midline dorsal (posterior) septum, the subdural space is subdivided

into three compartments with an anterior collection (arrow) and two posterolateral collections (b) compared to the normal appearance in the axial section (a)

Further Reading

781

Fig. 70.2  Posterior lumbar subdural hematoma compressing the cauda equina nerve roots as seen in the sagittal section

Table 70.2  Different subdural and intradural lumbosacral lesions mimicking spinal subdural hematomas Vascular Hematoma Tumor

Cavernoma, vascular malformations Spontaneous (anticoagulation), post-traumatic Nerve sheath tumors (namely meningioma, schwannoma, and neurofibroma) and intradural metastases Granulomatous Tuberculoma, sarcoidosis Infection Bacterial empyema/abscess, fungal, viral, parasitic collections (e.g., schistosomiasis, cysticercosis, hydatidosis) Inflammation Arachnoiditis, Guillain-Barré syndrome Dysembryogenetic Lipoma, epidermoid cyst, dermoid cyst, teratoma, neurenteric cyst Arachnoid cysts Leptomeningeal cysts Degenerative Intradural lumbar disc herniation Iatrogenic Foreign bodies

70.4 Treatment Options and Prognosis A lumbosacral subdural hematoma can be managed conservatively, surgically, or via percutaneous drainage. However, in most occasions, surgical evacuation should be given increased concern to prevent potential permanent neurologic damage induced by this disease. Surgical procedures typically comprise decompressive laminectomy, dura incision (durotomy), and hematoma evacuation. Any active bleeding should be stopped and controlled. Then, the dura will be closed in a hermetic manner to

avoid a postoperative cerebrospinal fluid fistula, pseudomeningocele, and potential meningitis. Percutaneous drainage, with or without neuroimaging guidance, may be considered in cases where the hematoma is situated dorsally and without coagulopathy. However, the hematoma should be well-liquefied. Conservative management may be considered if no or mild deficits are present, the blood collection is small, or neurological symptoms are improving. The hematoma will decrease or resolve spontaneously. However and despite the conservative therapy, it is necessary to have attentive clinical monitoring. In patients presenting with rapid or severe neurological deterioration, urgent surgical evacuation is indicated. Treatment success varies depending on a number of factors such as the patient’s conditions, the severity of preoperative symptoms, the presence or absence of coagulopathies, underlying etiologies of bleeding, associated lesions, and timing of surgical intervention. It seems that idiopathic cases, subdural hematomas located in the lumbosacral region, and those without coexisting subarachnoid bleeding are expected to have a more positive result.

Further Reading Akhaddar A.  Review of Craniospinal acute, subacute, and chronic subdural hematomas. In: Turgut M, Akhaddar A, Hall WA, Turgut AT, editors. Subdural Hematoma. Switzerland, Cham:

782 Springer International Publishing; 2021. p.  1–24. https://doi. org/10.1007/978-­3-­030-­79371-­5_1. Braun P, Kazmi K, Nogués-Meléndez P, Mas-Estellés F, Aparici-­ Robles F.  MRI findings in spinal subdural and epidural hematomas. Eur J Radiol. 2007;64:119–25. https://doi.org/10.1016/j. ejrad.2007.02.014. Hsieh JK, Colby S, Nichols D, Kondylis E, Liu JKC. Delayed development of spinal subdural hematoma following cranial trauma: a case report and review of the literature. World Neurosurg. 2020;141:44– 51. https://doi.org/10.1016/j.wneu.2020.05.158. Kobayashi K, Imagama S, Ando K, Nishida Y, Ishiguro N.  Acute non-traumatic idiopathic spinal subdural hematoma: radiographic findings and surgical results with a literature review. Eur Spine J. 2017;26:2739–43. https://doi.org/10.1007/s00586-­017-­5013-­y. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev. 2003;26:1– 49. https://doi.org/10.1007/s10143-­002-­0224-­y. Krishnan P, Banerjee TK. Classical imaging findings in spinal subdural hematoma - “Mercedes-Benz” and “cap” signs. Br J Neurosurg. 2016;30:99–100. https://doi.org/10.3109/02688697.2015.1071319. Matsumoto H, Matsumoto S, Yoshida Y.  Concomitant intracranial chronic subdural hematoma and spinal subdural hematoma: a case report and literature review. World Neurosurg. 2016;90:706.e1–9. https://doi.org/10.1016/j.wneu.2016.03.020.

70  Spinal Subdural Hematomas Pierce JL, Donahue JH, Nacey NC, Quirk CR, Perry MT, Faulconer N, et  al. Spinal hematomas: what a radiologist needs to know. Radiographics. 2018;38:1516–35. https://doi.org/10.1148/ rg.2018180099. Porter ZR, Johnson MD, Horn PS, Ngwenya LB.  Traumatic spinal subdural hematoma: an illustrative case and series review. Interdisciplinary Neurosurgery. 2020;19:100570. https://doi. org/10.1016/j.inat.2019.100570. Su D, Chong Z, Ran R, Peng X, Hou L, Zong Q, et  al. Spinal subdural hematoma in a patient with immune thrombocytopenic purpura following microvascular decompression: a rare case report. J Int Med Res. 2023;51(4):3000605221121952. https://doi. org/10.1177/03000605221121952. Vastani A, Mirza AB, Lavrador JP, Boardman TM, Khan MF, Malik I, Barazi S, et  al. Risk factor analysis and surgical outcomes of acute spontaneous spinal subdural hematoma. An institutional experience of four cases and literature review. World Neurosurg. 2021;146:e384–97. https://doi.org/10.1016/j.wneu.2020.10.096. Wurm G, Pogady P, Lungenschmid K, Fischer J.  Subdural hemorrhage of the cauda equina. A rare complication of cerebrospinal fluid shunt. Case report. Neurosurg Rev. 1996;19:113–7. https://doi. org/10.1007/BF00418081.

Spinal Subarachnoid Hematomas

71.1 Generalities and Relevance A spinal subarachnoid hematoma is a collection of blood in the intraspinal subarachnoid space that lies between the pia mater and the arachnoid and is filled with cerebrospinal fluid (CSF) that envelops the brain, the spinal cord, and the spinal nerve roots. While most intraspinal hematomas occurred at the level of thoraco-lumbar and cervico-thoracic regions, subarachnoid hematomas can cover the whole length of the spinal subarachnoid space because the CSF can flow freely cranio-spinally. In the lower lumbar and sacral levels, this uncommon bleeding has the potential to cause secondary neurologic damage by compressing or irritating the cauda equina nerve roots. There are many etiological factors in patients with subarachnoid hematomas. The most common etiologies are, in decreasing order of frequency, as follows: • Intraspinal tumors (e.g., ependymoma, neuroma, neurofibroma, glioma, and hemangioblastoma) • Intraspinal vascular malformations (e.g., arteriovenous malformation or aneurysm) • Coagulation abnormality • Lumbar puncture for diagnostic or spinal anesthetic procedures • Unknown etiology (recognized as “idiopathic”) Other causes are various and similar to those of the entire group of spinal hematomas such as hematologic disease, anticoagulation therapy, spinal surgery, or traumatic injury. Additionally, these factors may be present separately or variously combined. Traumatic intracranial hemorrhage and cerebral artery aneurysm with rearrangement of blood products by CSF flow should also be considered.

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Spinal subarachnoid hematomas are an uncommon clinical entity less frequent than those occurring in the epidural space but more usual than spinal subdural hematomas. In a literature review of 613 intraspinal hematomas, only 15.7% were sited in the subarachnoid space.

71.2 Clinical Presentations Clinical signs and symptoms of spinal subarachnoid hematoma are similar to those of other intraspinal hematomas. Usually, patients will present with spontaneous acute onset of back pain and varying degrees of radicular pain with or without sciatica. Then, rapidly progressive neurologic deficits developed. Chronic clinical forms are rare and more subtle. Unlike acute forms, chronic spinal subdural hematomas usually show mild radicular pain and mild or no motor deficit. However, the subarachnoid form additionally presents with intracranial symptoms comparable to those of cerebral subarachnoid hemorrhage (e.g., meningitis symptoms, nausea, vomiting, etc.) in about one-third of patients. Sometimes, diagnosis may be more difficult because some cases may present unspecific symptoms (such as personality change, disturbance of consciousness, papillary edema, nystagmus, diplopia, and epileptic seizures) pointing to a potential cerebral lesion. Most patients are aged between 50 and 70  years old. However, those with spinal malformations are younger often under 20 years of life. Of all patients with spinal subarachnoid hematoma, about 60% are men. In the lumbosacral spine, many patients will present with partial or complete cauda equina syndrome due to nerve root compression. Progression of neurologic symptoms tends to be slower in patients with spinal subarachnoid hemorrhage than in those with epidural or subdural hematomas.

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71.3 Imaging Features

71.4 Treatment Options and Prognosis

Like other intraspinal hematomas, magnetic resonance imaging is considered the gold standard in the diagnosis of spinal subarachnoid hematoma. Magnetic resonance (MR) imaging can visualize both the subarachnoid hematoma, and its exact location, and may help identify the potential underlying lesions such as vascular malformations or tumors. The appearance of the hematoma itself has a variable T1 and T2 signal depending on the chronicity of the bleeding (Table 71.1). The axial MR images are particularly important for separating subdural and subarachnoid hematomas. Pure subarachnoid bleeding is localized within the thecal sac without an “inverted Mercedes Benz sign“which is a typical finding in subdural hematoma. Additionally, diagnosis of ­subarachnoid hematoma may be possible when MR imaging detects the CSF surrounding the hematoma and separates the blood collection from the dura matter. In both types of hematomas, the extradural fat tissue is conserved without interior displacement of the dura. Sometimes, it is difficult to differentiate between a subarachnoid and subdural hematoma on neuroimaging. In this last situation, only surgical exploration will confirm the exact localization of the hematoma. MR angiography and/or digital subtraction spinal angiography will be used for identifying any vascular malformation or not and for the assessment of other potential hemorrhagic etiologies. Furthermore, patients should be assessed by appropriate biological and imaging studies to look for potential underlying disorders or concomitant lesions.

Lumbosacral subarachnoid hematoma can be managed conservatively or surgically to avoid permanent neurologic damage induced by the compression and to prevent recurrent bleeding. Surgical procedures typically comprise decompressive laminectomy, dura incision (durotomy), and hematoma evacuation. The dura should be closed under saline irrigation and in a hermetic manner to avoid both secondary arachnoiditis and a postoperative CSF fistula. Conservative management may be an option for some selected patients with mild paralysis or those with cerebral symptoms secondary to subarachnoid bleeding. Although the treatment is conservative, it is necessary to have attentive clinical monitoring. Patients presenting with rapid or severe neurological deterioration require urgent surgical decompression and hematoma removal. Underlying causes should be controlled such as intraspinal tumors or vascular malformations. Traumatic cases may be treated conservatively. Patients with tumors or vascular malformations should need more aggressive treatment such as surgery or endovascular procedures to prevent recurrent hemorrhage. Surgical treatment of idiopathic spinal subarachnoid bleeding may be done if there are signs of spinal compression due to organized blood clots or arachnoid adhesions. As with other spinal hematomas, the results of treatment vary depending on a number of factors such as the patient’s conditions, the severity of preoperative symptoms, presence or absence of coagulopathies, underlying etiologies of bleeding, associated lesions, the position of the hematoma, and timing of surgical intervention.

Table 71.1  MR imaging findings of spinal hematomas according to Braun et al. Stage Hyperacute

Timing 14 days

Hypointense

Slightly hypointense

Further Reading Artner J, Leucht F, Schulz C, Cakir B. Sciatica and incomplete paraplegia after spontaneous haematoma of the spinal cord due to a cumarine  - induced coagulopathy: case report. Open Orthop J. 2012;6:189–93. https://doi.org/10.2174/1874325001206010189. Domenicucci M, Ramieri A, Paolini S, Russo N, Occhiogrosso G, Di Biasi C, et al. Spinal subarachnoid hematomas: our experience and literature review. Acta Neurochir. 2005;147:741–50; discussion 750. https://doi.org/10.1007/s00701-­004-­0458-­2.

Further Reading Ghedira K, Matar N, Bouali S, Zehani A, Jemel H.  Acute paraplegia revealing a hemorrhagic cauda Equina Paragangliomas. Asian J Neurosurg. 2019;14:245–8. https://doi.org/10.4103/ajns. AJNS_206_17. Kashefiolasl S, Brawanski N, Platz J, Bruder M, Senft C, Marquardt G, et  al. MRI-detection rate and incidence of lumbar bleeding sources in 190 patients with non-aneurysmal SAH.  PLoS One. 2017;12:e0174734. https://doi.org/10.1371/journal.pone.0174734. Kim JS, Lee SH.  Spontaneous spinal subarachnoid hemorrhage with spontaneous resolution. J Korean Neurosurg Soc. 2009;45:253–5. https://doi.org/10.3340/jkns.2009.45.4.253. Kim YH, Cho KT, Chung CK, Kim HJ. Idiopathic spontaneous spinal subarachnoid hemorrhage. Spinal Cord. 2004;42:545–7. https://doi. org/10.1038/sj.sc.3101620. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev. 2003;26:1– 49. https://doi.org/10.1007/s10143-­002-­0224-­y.

785 Lee SH.  Spinal subarachnoid hematoma with hyperextension lumbar fracture in diffuse idiopathic skeletal hyperostosis: a case report. Spine (Phila Pa 1976). 2009;34:E673–6. https://doi.org/10.1097/ BRS.0b013e3181b0b3ac. Park JH, Kim JY. Iatrogenic spinal subarachnoid hematoma after diagnostic lumbar puncture. Korean J Spine. 2017;14:158–61. https:// doi.org/10.14245/kjs.2017.14.4.158. Pierce JL, Donahue JH, Nacey NC, Quirk CR, Perry MT, Faulconer N, et  al. Spinal hematomas: what a radiologist needs to know. Radiographics. 2018;38:1516–35. https://doi.org/10.1148/ rg.2018180099. Plotkin R, Ronthal M, Froman C.  Spontaneous spinal subarachnoid haemorrhage. Report of 3 cases. J Neurosurg. 1966;25:443–6. https://doi.org/10.3171/jns.1966.25.4.0443. Sather MD, Gibson MD, Treves JS.  Spinal subarachnoid hematoma resulting from lumbar myelography. AJNR Am J Neuroradiol. 2007;28:220–1.

Lumbar Epidural Varices

72.1 Generalities and Relevance Lumbar epidural varices (LEVs) are an unusual pathological entity, mainly acquired, that results from dilation of the internal vertebral venous plexus. The varices (AKA varicoses) are enlarged, engorged, and tortuous veins in the epidural spaces often in the intervertebral foramen. These abnormal veins can cause irritation or compression of the dural sac and particularly nerve roots leading to various degrees of lumbosacral radiculopathy. The normal epidural venous system in the lumbar spine is a network of valveless (avalvular) veins that surround the vertebral bodies and communicate with adjacent vertebral levels (Fig. 72.1). Radiculopathy is often attributable to the

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anterior internal vertebral veins and/or the supra-pediculate radicular veins. Pathogenesis of LEV is not well known but seems to be related to epidural vein compression and outflow blood disturbance. Many etiologies have been then suspected in the involvement of this condition as summarized in Table 72.1. This condition develops solely or in combination with some degenerative lesions such as lumbar spinal stenosis and lumbar disc herniation. The first description of symptomatic LEV was reported by Cohen in 1941. Since then, many cases have been reported in the literature, especially in the last few decades with the development of modern neuroimaging explorations. The true incidence of LEV is unknown; however, this rate is about

Fig. 72.1  Epidural venous system of the lumbar spine as seen in a transverse section

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_72

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788 Table 72.1  Main etiologies of lumbar epidural varices reported in the literature •  Intervertebral foraminal stenosis •  Large central disc herniation •  Epidural lipomatosis • Dysraphism •  Inferior vena cava obstruction or occlusion •  Iliac vein stenosis • Increased intra-abdominal pressure (e.g., obesity, pregnancy, bladder distention) •  Portal venous hypertension •  Budd-Chiari syndrome •  Intracranial hypotension •  Previous discectomy • Idiopathic

4.4% in patients operated on for degenerative lumbar disease. The majority of patients are diagnosed between their fourth and sixth decades with a mean age of 40 years. Until now, many symptomatic LEVs are regularly misdiagnosed and sometimes detected only during surgery. Morphologically, the epidural varices are somewhat similar to varicose veins found throughout the body. Most LEV involves the anterior longitudinal veins, retrocorporeal veins, and sometimes intervertebral veins. Regarding intervertebral vein engorgement, the lesion is usually situated adjacent to the axillary region of the lumbosacral nerve root. According to Slin’ko and co-authors, there are three varieties of LEV: (a) Segmentary varices, caused by dilation of the intervertebral veins. (b) Local varices, caused by limited dilation of anterior and, less often, posterior longitudinal veins, or the intervertebral veins at one or two levels. (c) Extensive varices, associated with widespread epidural venous enlargement of the anterior, and, less often, posterior longitudinal veins (usually affecting the whole epidural vertebral venous system, secondary to inferior vena cava system involvement). Some additional causative factors have been reported such as Behcet’s disease, oral contraceptives, protein C deficiency, coagulopathy, Factor V Leiden mutation, and abdominal malignancy. Clinical manifestations of epidural varices may be caused by two mechanisms: (a) Compression of the dural sac and the nerve roots by the dilated veins or irritation of the roots by the dilated veins. (b) High pressure in the epidural veins that is transmitted to the perimedullary veins draining the spinal cord and the nerve roots.

When LEVs are concomitant to lumbar spinal stenosis, lumbar herniated disc, or spondyloarthropathies, it is difficult to assign the exact cause of the symptoms whether to the engorged epidural veins or the underlying spinal lesion(s).

72.2 Clinical Presentations Signs and symptoms of LEV do not differ from those related to traditional lumbar discogenic or spinal lumbar stenosis. However, most patients with segmentary and local LEV have unilateral or bilateral sciatic pain, respectively. However, cases with extensive LEV present with symptoms of classic spinal lumbar stenosis. More clinical forms are chronic and developed progressively with mild or no sensitive-motor deficit. The straight leg raising test result is often positive with associated lumbosacral spinal root stretching. Cauda equina syndrome is rare but previously reported. In the majority of cases, the general condition remains preserved. However, potential underlying diseases and some predisposing factors should constantly be taken into consideration in clinical presentations. Whatever the clinical expression be, the diagnosis of distended epidural veins is always unsuspected before a neuroimaging evaluation. Some cases will only be diagnosed intraoperatively.

72.3 Imaging Features Like other intraspinal vascular lesions, magnetic resonance imaging (MRI) is the method of choice for imaging spinal LEV. Axial and sagittal T2-weighted sequences and particularly, spin echo T1 weight with fat saturation post intravenous gadolinium, generally showed enlargements, and tortuosity of epidural venous plexus between T12-S1 and mainly occurred between L4 and S1 level. MRI can visualize the location of the dilated venous lesion, the nerve root compression, and other concomitant lesions. Additionally, MRI should explore the paravertebral area including the region of the inferior vena cava. However, venography has become an excellent complement to MRI for establishing the type of LEV and the venous blood flow patterns. Indeed, using radiological, anatomical, and physiological data, Hanley et  al. categorized epidural varices into three types based on MRI results (Table 72.2). When needed, MRI angiography, computed tomography scan angiography, or digital subtraction spinal angiography will be used for identifying other potential vascular abnormalities.

Further Reading Table 72.2  Main types of lumbar epidural varices according to Hanley et al. Type Type I Type II Type III

Description Thrombosed dilated epidural vein (mainly the anterior longitudinal vein and occasionally the intervertebral vein) Dilated epidural vein without thrombosis (post-thrombotic dilation of the vein resulting from its repermeabilization) Epidural contained hematoma formed by bleeding from the varicose veins

Sometimes, unfortunately, the true diagnosis is made only during surgery. Because epidural varices may resemble typical cystic or even cystic-like epidural lesions on MRI, differential diagnoses include: • • • • • • • • •

Herniated disc (mainly sequestrated disc fragment) Epidural abscess Tumor Hematoma Vascular malformations (e.g., arteriovenous fistulization) Facet synovial cyst Ligamentum flavum cyst Posterior longitudinal ligament cyst Tarlov cyst (perineural cyst)

72.4 Treatment Options and Prognosis Lumbosacral epidural varices can be managed conservatively or surgically. However, in most diagnosed cases, surgical decompression and/or removal are performed. When a symptomatic LEV does not respond to conservative treatment or leads to neurological deficits, surgery is the preferred approach to relieve symptoms and prevent more complications. Various surgical procedures are reported in the literature, including decompressive laminectomy, coagulation of the distended veins, careful hematoma aspiration, cutting of the epidural varices, and varix compression with a resorbable gelatin sponge. However, the surgeon should avoid rupture of the engorged veins during surgery because significant active venous hemorrhage may occur and any hemostasis will be then difficult to obtain. If appropriate, the treatment of associated degenerative spinal lesions will be done during the same surgical procedure. Additionally, any underlying cause of LEV should be managed appropriately in order to avoid any potential recurrence. Some authors recommend an immediate postoperative MRI to confirm adequate obliteration of the LEV. For others, control MRI is not necessary because clinical symptoms do

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not correlate with postoperative morphological or radiological changes in many patients. In the majority of cases, the surgical treatment led to a positive clinical result, with improvement or complete resolution of the neurological symptoms. However, cases with extensive LEV and those with inferior vena cava hypertension are expected to have a less effective result. In a few reported cases, there was a favorable clinical outcome without surgery, especially in pregnant women.

Further Reading Alexander LM, Philip VJ.  A rare presentation of a nondiscogenic cause of acute lumbar radiculopathy. Ann Indian Acad Neurol. 2017;20:416–7. https://doi.org/10.4103/aian.AIAN_245_17. Aoyama T, Hida K, Akino M, Yano S, Saito H, Iwasaki Y. Radiculopathy caused by lumbar epidural venous varix: case report. Neurol Med Chir (Tokyo). 2008;48:367–71. https://doi.org/10.2176/nmc.48.367. Bursalı A, Akyoldas G, Guvenal AB, Yaman O. Lumbar Epidural Varix Mimicking Disc Herniation. J Korean Neurosurg Soc. 2016;59:410– 3. https://doi.org/10.3340/jkns.2016.59.4.410. Celik H, Erdem Y, Karatay M, Yorubulut M, Gursoy T, Sertbas I, et  al. Lumbar epidural varicose vein: early neurological improvement and late radiological full recovery with surgery; the importance of magnetic resonance imaging in follow-up. Turk Neurosurg. 2015;25:824–7. https://doi.org/10.5137/1019-­5149. JTN.11226-­14.0. Cohen I. Extradural varix simulating herniated nucleus proposes. J Mt Sinai Hosp. 1941;8:136–8. Dabasia H, Rahim N, Marshall R.  Neurogenic claudication without spinal stenosis arising as a result of lumbar epidural varices. J Bone Joint Surg (Br). 2012;94:1292–4. https://doi. org/10.1302/0301-­620X.94B9.29322. Endres S.  Epidural varicosis as a possible cause of radicular pain: a case report. J Med Case Rep. 2011;5:537. https://doi. org/10.1186/1752-­1947-­5-­537. Epstein BS. Low back pain associated with varices of the epidural veins simulating herniation of the nucleus pulposa. Am J Roentgenol Radium Ther. 1947;57:736–40. Fredrickson VL, Patel A, Pham MH, Strickland BA, Ohiorhenuan I, Chen T. Spine surgery complicated by an engorged lumbar epidural venous plexus from cerebrospinal fluid overshunting: a case report and review of the literature. World Neurosurg. 2018;111:68–72. https://doi.org/10.1016/j.wneu.2017.12.027. Genevay S, Palazzo E, Huten D, Fossati P, Meyer O. Lumboradiculopathy due to epidural varices: two case reports and a review of the literature. Joint Bone Spine. 2002;69:214–7. https://doi.org/10.1016/ s1297-­319x(02)00376-­7. Gümbel U, Pia HW, Vogelsang H. Lumbosacral vascular anomalies as the cause of ischialgia. Acta Neurochir. 1969;20:131–51. https:// doi.org/10.1007/BF01401958. Hammer A, Knight I, Agarwal A.  Localized venous plexi in the spine simulating prolapse of an intervertebral disc: a report of six cases. Spine (Phila Pa 1976). 2003;28:E5–E12. https://doi. org/10.1097/00007632-­200,301,010-­00025. Hanley EN Jr, Howard BH, Brigham CD, Chapman TM, Guilford WB, Coumas JM.  Lumbar epidural varix as a cause of radiculopathy. Spine (Phila Pa 1976). 1994;19:2122–6. https://doi. org/10.1097/00007632-­199,409,150-­00022.

790 Hassan O, Lewis CS, Aradhyula L, Hirshman BR, Pham MH. Engorged venous plexus mimicking adjacent segment disease: case report and review of the literature. Surg Neurol Int. 2020;11:104. https://doi. org/10.25259/SNI_166_2020. Im IK, Son ES, Kim DH. Lumbar epidural varix causing radicular pain: a case report and differential diagnosis of lumbar cystic lesions. PM R. 2018;10:1283–7. https://doi.org/10.1016/j.pmrj.2018.04.002. Jeong HJ, Sim WS, Park HJ, Lee SH, Oh MS, Cho MK, et al. Severe lumbar radiculopathy with epidural venous plexus engorgement in a morbidly obese pediatric patient: A case report. Medicine (Baltimore). 2019;98:e16842. https://doi.org/10.1097/ MD.0000000000016842. Ju JH, Ha HG, Jung CK, Kim HW, Lee CY, Kim JH. Patterns of epidural venous varicosity in lumbar stenosis. Korean J Spine. 2012;9:244– 9. https://doi.org/10.14245/kjs.2012.9.3.244. Kramer KM. Massive epidural varix mimicking lumbar disc herniation: case report and literature review. Conn Med. 2014;78:525–7. Paksoy Y, Gormus N. Epidural venous plexus enlargements presenting with radiculopathy and back pain in patients with inferior vena cava obstruction or occlusion. Spine (Phila Pa 1976). 2004;29:2419–24. https://doi.org/10.1097/01.brs.0000144354.36449.2f. Pennekamp PH, Gemünd M, Kraft CN, von Engelhardt LV, Lüring C, Schmitz A.  Epidural varicosis as a rare cause of acute radiculopathy with complete foot paresis--case report and literature review. Z Orthop Ihre Grenzgeb. 2007;145:55–60. https://doi. org/10.1055/s-­2007-­960,503. Pusat S, Kural C, Aslanoglu A, Kurt B, Izci Y. Lumbar epidural varix mimicking perineural cyst. Asian Spine J. 2013;7:136–8. https:// doi.org/10.4184/asj.2013.7.2.136. Ramieri A, Domenicucci M, Seferi A, Paolini S, Petrozza V, Delfini R.  Lumbar hemorrhagic synovial cysts: diagnosis, pathogenesis,

72  Lumbar Epidural Varices and treatment. Report of 3 cases. Surg Neurol. 2006;65:385–90. https://doi.org/10.1016/j.surneu.2005.07.073. Siam L, Rohde V.  Varicosis of the venous epidural plexus caused by portocaval hypertension mimicking symptomatic lumbar disc herniation: case report and review of the literature. Cent Eur Neurosurg. 2011;72:155–8. https://doi.org/10.1055/s-­0029-­1,246,131. Slin’ko EI, Al-Qashqish II. Surgical treatment of lumbar epidural varices. J Neurosurg Spine. 2006;5:414–23. https://doi.org/10.3171/ spi.2006.5.5.414. Subbiah M, Yegumuthu K. Lumbar epidural varices: An unusual cause of lumbar claudication. Indian J Orthop. 2016;50:440–3. https://doi. org/10.4103/0019-­5413.185613. Tofuku K, Koga H, Yone K, Komiya S.  Spontaneous regression of symptomatic lumbar epidural varix: a case report. Spine (Phila Pa 1976). 2007;32:E147–9. https://doi.org/10.1097/01. brs.0000255811.64922.47. Wiltse LL, Fonseca AS, Amster J, Dimartino P, Ravessoud FA.  Relationship of the dura, Hofmann’s ligaments, Batson’s plexus, and a fibrovascular membrane lying on the posterior surface of the vertebral bodies and attaching to the deep layer of the posterior longitudinal ligament. An anatomical, radiologic, and clinical study. Spine (Phila Pa 1976). 1993;18:1030–43. https://doi. org/10.1097/00007632-­199,306,150-­00013. Wong CH, Thng PL, Thoo FL, Low CO. Symptomatic spinal epidural varices presenting with nerve impingement: report of two cases and review of the literature. Spine (Phila Pa 1976). 2003;28:E347–50. https://doi.org/10.1097/01.BRS.0000090500.10184.7A. Zimmerman GA, Weingarten K, Lavyne MH.  Symptomatic lumbar epidural varices. Report of two cases. J Neurosurg. 1994;80:914–8. https://doi.org/10.3171/jns.1994.80.5.0914.

Ligamentum Flavum Hematomas

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73.1 Generalities and Relevance

73.2 Clinical Presentations

Hematomas of the ligamentum flavum are benign bleeding collections developed within the layers of the ligamentum flavum (yellow ligament). Most cases occur in the anterolateral spinal epidural space and may compress the neural elements and result in a neurological disturbance in many patients. In the lumbar region, a significant number of cases will manifest as unilateral or bilateral sciatica. These hematomas should be distinguished from those associated with other diseases such as ligamentum flavum cysts, synovial cysts, and ganglion cysts. This rare entity was first described in the English literature by Sweasey et al. in 1992. Since then, less than 70 cases have been reported, preferentially located in the spinal lumbar region (about 85%), and less frequently in the cervical and thoracic spine. Most cases developed at a single level. There is one case report of lumbar double contiguous hematomas in the ligamentum flavum. In the histopathology study, except for a common myxoid degeneration and some capillary proliferation around the hematoma, there were no specific lesions. The exact pathogenesis and etiology of ligamentum flavum hematoma are not well explained, but it has supposed to be related to minor back trauma or sustained physical effort. Overall, the context of degenerative spinal changes is often considered. Indeed, most ligamentum flavum hematomas are reported in patients older than 65 years, especially in the male gender (about 60%). Also, there were some patients with essential hypertension (factor of precipitating bleeding?) and spondylotic spine with hypertrophic ligamentum flavum. Interestingly, most cases of yellow intraligamentary bleeding occur in the Asian population.

The clinical presentations depend on the volume of the hematoma, its exact site, and its relationship to the surrounding bony and neural structures. In the lumbar spine, ligamentum flavum hematoma may induce various degrees of progressive or acute neurological deterioration by compressing one or multiple cauda equina nerve roots. However, the majority of patients had a chronic symptom progress that was longer than that for typical spontaneous epidural hematoma. Acute clinical presentations with sudden onset are more unusual. A history of low-back pain may precede the radicular symptoms. Asymmetric compression may present with unilateral radicular pain and mimic typical lumbar disc herniation or foraminal stenosis. The central situation of the hematoma into the lumbar spinal canal may manifest as symptoms of lumbar canal stenosis with classic neurogenic claudication. However, knowing that some patients can have concomitant lumbar spondylosis. Although rare, severe cases can present with more serious neurologic conditions such as partial or complete cauda equina syndrome due to a large intraligamentous hematoma compression or coexistence of lumbar spinal stenosis. Whatever its clinical expression be, the diagnosis of ligamentum flavum hematoma is often unpredicted before a neuroimaging evaluation.

73.3 Imaging Features Magnetic resonance imaging (MRI) is considered the gold standard for suspected spinal epidural hematoma. MRI can visualize both the epidural collection, its exact location and

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Fig. 73.1  Magnetic resonance imaging (MRI), T2-weighted axial view and appearance of resected ligamentum flavum. MRI revealed the masses were located in the intraspinal extradural space, and the signal intensity of masses was mixed, high and low. Each resected ligamentum flavum was found to contain a brownish mass (arrowhead). Hematoma

and hemorrhage were found within each extirpated ligamentum flavum (arrows). (Reproduced from Takahashi M, Satomi K, Hasegawa A, Hasegawa M, Taki N, Ichimura S.  Ligamentum flavum hematoma in the lumbar spine. J Orthop Sci. 2012;17:308–12. doi: 10.1007/s00776-­ 011-­0083-x.; with permission)

extension, and both thecal sac and nerve root compression (Fig.  73.1). The appearance of the hematoma itself has a variable T1 and T2 signal depending on the temporal changes of the bleeding. Inconstant Gadolinium enhancement has been reported with ligamentum flavum hematoma. Most cases had only a slight to moderate enhancement in the border of the bleeding collection. Computed tomography (CT) scan is often inconclusive. It can show an iso or high-density extradural lesion adjacent to or within the ligamentum flavum. Degenerative spinal joint features may also be seen. A bony CT scan may be useful for identifying possible secondary chronic bone changes. Imaging appearances are atypical and may be confused with other possible epidural lesions in the lumbosacral region such as:

73.4 Treatment Options and Prognosis

–– Bleeding within ligamentum flavum cyst or juxta-­articular cyst –– Spontaneous epidural hematoma –– Epidural primitive neoplasm or metastasis –– Epidural abscess

Conservative management may be considered if no or mild deficits are present, the blood collection is small, or neurological symptoms are improving. However, no case of spontaneous resorption has been reported and conservative therapy was known to be unsuccessful in patients with lumbar ligamentum flavum hematomas. The aim of surgery is to remove completely the hematoma along with the ligamentum flavum (flavectomy) and decompress the neural roots with preservation of the facet joint. Most cases will be operated on via an interlaminar approach. If needed, a more extensive approach will be used such as a hemilaminectomy or even complete laminectomy (lumbar spinal stenosis). Care should be taken to minimize nerve root damage and the possibility of cerebrospinal fluid leaks. Recently, endoscopic resection of a ligamentum flavum hematoma through a percutaneous endoscopic translaminar approach was performed in five patients with good results. Rarely, a spinal fusion with posterolateral instrumentation may be required if there is a supposed instability secondary to an extensive facetectomy.

Further Reading

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Kim K, Isu T, Miyamoto M, Matsumoto R, Isobe M, Takahashi T.  Haemorrhage into the ligamentum flavum of the lumbar spine: case report and review of the literature. Br J Neurosurg. 2005;19:511–2. https://doi.org/10.1080/02688690500495380. Kono H, Nakamura H, Seki M, Motoda T. Foot drop of sudden onset caused by acute hematoma in the lumbar ligamentum flavum: a case report and review of the literature. Spine (Phila Pa 1976). 2008;33:E573–5. https://doi.org/10.1097/BRS.0b013e31817c6cb5. Kotil K, Bilge T.  A ligamentum flavum hematoma presenting as an Further Reading L5 radiculopathy. J Clin Neurosci. 2007;14:994–7. https://doi. org/10.1016/j.jocn.2006.05.015. Lee YS, Yi JS, Kim HJ, Kim JO, Choi ES.  Epidural block-induced Ak H, Vural S. Simultaneous presence of juxtafacet cyst and ligamenligamentum flavum hematoma mimicking epidural hematoma in tum flavum hematoma. Asian J Neurosurg. 2020;15:184–6. https:// the lumbar spine: a case report. Spine J. 2011;11:e23–7. https://doi. doi.org/10.4103/ajns.AJNS_271_19. org/10.1016/j.spinee.2010.12.014. Albanese A, Braconi A, Anile C, Mannino S, Sabatino G, Mangiola Liu HP, Chen CL, Chen NF, Liao CY, Ou CY. Ligamentum flavum hemaA. Spontaneous haematoma of ligamentum flavum. Case report and toma due to stretching exercise. Am J Emerg Med. 2016;34:2058. literature review. J Neurosurg Sci. 2006;50:59–61. e3–6. https://doi.org/10.1016/j.ajem.2016.03.042. Braun P, Kazmi K, Nogués-Meléndez P, Mas-Estellés F, Aparici-­ Robles F.  MRI findings in spinal subdural and epidural hema- Miyakoshi N, Kasukawa Y, Ando S, Shimada Y. Two-level ligamentum flavum hematoma in the lumbar spine. Case report Neurol Med Chir tomas. Eur J Radiol. 2007;64:119–25. https://doi.org/10.1016/j. (Tokyo). 2008;48:179–82. https://doi.org/10.2176/nmc.48.179. ejrad.2007.02.014. Ozdemir B, Kanat A, Batcik OE, Gucer H, Yolas C.  Ligamentum Cruz-Conde R, Berjano P, Buitron Z.  Ligamentum flavum hemaflavum hematomas: Why does it mostly occur in old Asian toma presenting as progressive root compression in the lummales? Interesting point of reported cases: Review and case bar spine. Spine (Phila Pa 1976). 1995;20:1506–9. https://doi. report. J Craniovertebr Junction Spine. 2016;7:7–12. https://doi. org/10.1097/00007632-­199,507,000-­00012. org/10.4103/0974-­8237.176605. Gazzeri R, Canova A, Fiore C, Galarza M, Neroni M, Giordano M. Acute hemorrhagic cyst of the ligamentum flavum. J Spinal Disord Tech. Salehpour F, Mirzaei F, Rezakhah A, Aeinfar K, Kazemzadeh M, Alavi SAN.  Ligamentum Flavum Hematoma Presented with Low Back 2007;20:536–8. https://doi.org/10.1097/BSD.0b013e31804b4605. Pain: A Case Report and Review of the Literature. Int J Spine Surg. Ghent F, Ye X, Yan M, Mobbs RJ. A contrast-enhancing lumbar ligamen2018;12:337–41. https://doi.org/10.14444/5039. tum flavum haematoma. BMJ Case Rep. 2014;2014:bcr2013202521. Sweasey TA, Coester HC, Rawal H, Blaivas M, McGillicuddy https://doi.org/10.1136/bcr-­2013-­202,521. JE. Ligamentum flavum hematoma. Report of two cases. J Neurosurg. Hisamitsu Y, Uchikado H, Makizono T, Miyagi T, Miyahara T.  Case 1992;76:534–7. https://doi.org/10.3171/jns.1992.76.3.0534. of lumbar ligamentum flavum hematoma with epidural hemaTakahashi M, Satomi K, Hasegawa A, Hasegawa M, Taki N, Ichimura toma resulting in cauda equina compression. Surg Neurol Int. S. Ligamentum flavum hematoma in the lumbar spine. J Orthop Sci. 2022;13:550. https://doi.org/10.25259/SNI_967_2022. 2012;17:308–12. https://doi.org/10.1007/s00776-­011-­0083-­x. Ishimoto Y, Kawakami M, Curtis E, Cooper C, Moriguchi N, Nakagawa Y.  A succession of mri scans supports the diagnosis of lumbar Takeno K, Kobayashi S, Miyazaki T, Yayama T, Baba H. Microsurgical excision of hematoma of the lumbar ligamentum flavum. ligamentum flavum hematoma: a case report and review of the Joint Bone Spine. 2010;77:351–4. https://doi.org/10.1016/j. literature. Case Rep Orthop. 2018;2018:2860621. https://doi. jbspin.2010.01.018. org/10.1155/2018/2860621. Kaneko T, Oshima Y, Inoue H, Iwai H, Takano Y, Inanami H, Koga Yu D, Lee W, Chang MC. Ligamentum flavum hematoma following a traffic accident: A case report. World J Clin Cases. 2021;9:6125–9. H.  Successful treatment of lumbar ligamentum flavum hematoma https://doi.org/10.12998/wjcc.v9.i21.6125. using a spinal full-endoscopic system. J Spine Surg. 2018;4:744–9. https://doi.org/10.21037/jss.2018.09.09.

Generally, postoperative complications are mild and rare. The majority of patients showed good clinical results after full surgical aspiration of the hematoma and the affected yellow ligament. To our knowledge, no recurrence has been reported.

Spinal Cavernous Angioma (Cavernoma)

74.1 Generalities and Relevance Among the intraspinal causes of sciatic pain, vascular lesions are sometimes developing diagnostic confusion with the traditional degenerative etiologies. However, lumbosacral radicular symptoms are frequently poorly defined and rarely isolated. These vascular lesions are variable and can be intradural or extradural. Depending on their origin (arterial, venous, arteriovenous, or cavernous), the most frequent spinal vascular etiologies that contribute to sciatic pain are as follows: • • • • • •

Cavernous angioma (cavernoma) Epidural varices Arteriovenous malformation Arteriovenous fistula Capillary angioma Venous angioma

Pathologic, structural, and hemodynamic changes may lead to the following: (a) (b) (c) (d)

Compression and mass effect on neural structures Irritation of neural elements Local destruction of underlying nerves Ischemia secondary to vasa vasorum compression and/ or due to vascular ‘steal’

The basic mechanism of vascular lesions-related sciatica may be multifactorial depending on their origin, localization, size, and progression (acute, subacute, or chronic). Most vascular lesions develop progressively, finally leading to the development of neurologic symptoms and complications with time. However, vascular rupture and sudden hemorrhage may result in an acute presentation in some patients. Cavernous angioma and epidural varices represent the main causes of intraspinal vascular lesions inducing sciatic pain. In this chapter, we will focus on cavernous angiomas

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(AKA cavernous hemangioma or cavernoma). Please refer to Chap. 72 about “Lumbar Epidural Varices.” Like in the brain parenchyma, cavernous angioma consists of a vascular spongy well defined but unencapsulated mass less than 2 diameter. Intraoperatively, it can appear as a space-occupying or hemorrhagic lesion. Cavernoma is classically composed of abnormal, dilated, and packed vascular sinusoidal channels separated by a modest connective tissue stroma. Most spinal cavernous angiomas (SpCA) are sporadic (occur as single lesions) but some cases are multiples, being both intraspinal and intracranial. Pathogenesis of SpCA is not known with certainty but seems to be congenital as a hamartomatous malformation. SpCA can grow in time, either as a result of repeated intralesional bleeding or as a consequence of an intrinsic capacity for endothelial proliferation and/or neoangiogenesis. Indeed, for some authors, cavernous angioma is a true vascular neoplasm. Less than 40 cases of pure intraspinal lumbosacral cavernous angiomas have been previously reported in the literature, mainly in the intradural space (known as cauda equina cavernomas). Extradural forms are even rarer because less than 10 cases were described. The rest of the lumbosacral intraspinal vascular lesions are exceptional or rarely cause sciatic pain. Cauda equina cavernomas are rarely seen in children and are often diagnosed in middle age or the elderly without gender predominance.

74.2 Clinical Presentations Lumbar SpCA may present with mono radicular sciatic or pluriradicular pain, low-back pain, neurological deficit (weakness and/or sensory loss in the lower limbs), cauda equina syndrome (CES) or, more rarely with subarachnoid hemorrhage (headache, nuchal rigidity, and vomiting) or hydrocephalus (symptoms of intracranial hypertension).

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There are no symptomatic or signs of difference between patients with epidural SpCA and those with intradural forms. Most spinal cavernomas develop progressively, finally leading to the development of symptoms and complications with time. However, sudden mass extension, secondary to intralesional hemorrhage or cases with extralesional bleeding may result in an acute clinical presentation with a total or subtotal CES as well as symptoms of spinal subarachnoid bleeding. In the majority of cases, the general condition remains preserved. Whatever the clinical expression be, the diagnosis of SpCA is always non-suspected prior to a neuroimaging evaluation. Some cases will only be diagnosed intraoperatively. Treating clinicians should look for intracranial neurologic symptoms and vascular cutaneous disorders.

–– –– –– ––

74.3 Paraclinic Features Cavernomas are angiographically occult vascular lesions undetected on traditional spinal angiography. Computed tomography scan is also inconclusive although some rare cases are calcified (Fig. 74.1).

a

However, magnetic resonance imaging (MRI) remains the gold standard for the diagnosis of this intraspinal vascular entity given the characteristic appearance of a heterogeneous well-defined iso to low-intensity lesion on both T1- and T2-weighted images with a hypointense ring of hemosiderin in T2-WI with no or little gadolinium enhancement (Figs. 74.2 and 74.3). This heterogeneous aspect is related to the presence of mixed subacute and chronic hemorrhage. The majority of cauda equina cavernoma is located around the L2 vertebral body. Subarachnoid hemorrhage due to secondary bleeding from this malformation occurs in about one-quarter of cases. MRI features of SpCA may be confused with other differential diagnoses such as:

b

Lumbar disc fragment Neurinoma and meningioma Ependymoma and paraganglioma Other intraspinal vascular lesions (e.g., capillary angioma and arteriovenous malformation

Sometimes, epidural cavernomas may grow into the intervertebral foramen mimicking a schwannoma.

c

Fig. 74.1  A 37-year-old woman with foraminal L5-S1 cavernous angioma (arrows) as seen on axial CT scan (a–c). This lesion may mimic a lumbar disc herniation or a schwannoma

74.3  Paraclinic Features

a

797

b

c

Fig. 74.2  Foraminal L5-S1 epidural cavernous angioma as seen on sagittal T1-weighted MRI before (a) and after gadolinium injection (b) as well as on T2-weighted MRI (c). Note the little gadolinium enhancement of the vascular lesion (b)

a

c

b

d

e

Fig. 74.3  Axial T1-weighted MRI (a, b) and with fat saturation (FS) sequences (c, d) as well as on sagittal FS sequences (e) showing the L5-S1 epidural cavernous angioma (stars)

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74.4 Treatment Options and Prognosis

74  Spinal Cavernous Angioma (Cavernoma)

Esene IN, Ashour AM, Marvin E, Nosseir M, Fayed ZY, Seoud K, et al. Pure spinal epidural cavernous hemangioma: A case series of seven cases. J Craniovertebr Junction Spine. 2016;7:176–83. https://doi. Surgical excision is the treatment of choice for SpCA. Because org/10.4103/0974-­8237.188419. of the excessive vascularity of the cavernoma, en bloc resec- Falavigna A, Righesso Neto O, dos Santos JA, Ferraz FA.  Cavernous angioma of the cauda equina: case report. tion was encouraged and biopsy should be avoided to preArq Neuropsiquiatr. 2004;62:531–4. https://doi.org/10.1590/ vent unnecessary bleeding. Surgery is classically performed s0004-­282x2004000300029. through a posterior approach via a limited laminectomy. Harrington JF Jr, Khan A, Grunnet M.  Spinal epidural cavernous angioma presenting as a lumbar radiculopaSome authors recommend the intraoperative use of intraopthy with analysis of magnetic resonance imaging erative monitoring for intradural forms. characteristics: case report. Neurosurgery. 1995;36:581–4. https:// Total cavernoma resection saving the affected nerve root doi.org/10.1227/00006123-­199,503,000-­00018. is usually possible under microscopic magnification. Khalatbari MR, Hamidi M, Moharamzad Y, Taheri B.  Cauda equina cavernous angioma presenting as acute low back pain and sciSometimes the spinal nerve root would be sacrificed, espeatica. A report of two cases and literature review. Neuroradiol J. cially when the cavernous angioma is purely intraneural. 2011;24:636–42. https://doi.org/10.1177/197140091102400421. Most spinal epidural cavernomas showed a well-­ Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature surdemarcated dissection plane without dural adhesion facilitatvey with meta-analysis of 613 patients. Neurosurg Rev. 2003;26:1– 49. https://doi.org/10.1007/s10143-­002-­0224-­y. ing complete surgical removal. In the majority of cases, the surgical treatment led to a Krings T, Mull M, Gilsbach JM, Thron A.  Spinal vascular malformations. Eur Radiol. 2005;15:267–78. https://doi.org/10.1007/ positive clinical result, with improvement or complete s00330-­004-­2510-­2. ­resolution of the neurological symptoms. However, cases Kumar V, Nair R, Kongwad LI, Menon RG.  Cavernous haemangioma of the cauda region: case report and review of literature. Br presenting cauda equina syndrome are expected to have a J Neurosurg. 2017;31:614–65. https://doi.org/10.1080/02688697.2 less effective result. No case of recurrence has been reported. 016.1199784. Potential residual radicular pain may be treated medically Miyake S, Uchihashi Y, Takaishi Y, Sakagami Y, Kohmura E. Multiple accordingly. cavernous angiomas of the cauda equina. Case report Neurol Med Chir (Tokyo). 2007;47:178–81. https://doi.org/10.2176/nmc.47.178. Nie QB, Chen Z, Jian FZ, Wu H, Ling F.  Cavernous angioma of the cauda equina: a case report and systematic review of Further Reading the literature. J Int Med Res. 2012;40:2001–8. https://doi. org/10.1177/030006051204000542. Apostolakis S, Mitropoulos A, Diamantopoulou K, Vlachos Popescu M, Titus Grigorean V, Julieta Sinescu C, Dumitru Lupascu C, K.  Cavernoma of the cauda equina. Surg Neurol Int. 2018;9:174. Popescu G, Mihaela Sandu A, et al. Cauda equina intradural extrahttps://doi.org/10.4103/sni.sni_212_18. medullary cavernous haemangioma: case report and review of the Caroli E, Acqui M, Trasimeni G, Di Stefano D, Ferrante L.  A case literature. Neurol Med Chir (Tokyo). 2013;53:890–5. https://doi. of intraroot cauda equina cavernous angioma: clinical considerorg/10.2176/nmc.cr2012-­0309. ations. Spinal Cord. 2007;45:318–21. https://doi.org/10.1038/ Ramos F Jr, de Toffol B, Aesch B, Jan M. Hydrocephalus and caversj.sc.3101964. noma of the cauda equina. Neurosurgery. 1990;27:139–42. https:// Caruso G, Galarza M, Borghesi I, Pozzati E, Vitale M.  Acute predoi.org/10.1097/00006123-­199,007,000-­00023. sentation of spinal epidural cavernous angiomas: case report. Takeshima Y, Marutani A, Tamura K, Park YS, Nakase H.  A case of Neurosurgery. 2007;60:E575–6. https://doi.org/10.1227/01. cauda equina cavernous angioma coexisting with multiple cerebral NEU.0000255345.48829.0B. cavernous angiomas. Br J Neurosurg. 2014;28:544–6. https://doi. Cecchi PC, Rizzo P, Faccioli F, Bontempini L, Schwarz A, Bricolo org/10.3109/02688697.2013.841856. A.  Intraneural cavernous malformation of the cauda equina. Ueda S, Saito A, Inomori S, Kim I.  Cavernous angioma of the J Clin Neurosci. 2007;14:984–6. https://doi.org/10.1016/j. cauda equina producing subarachnoid hemorrhage. Case jocn.2006.06.015. report. J Neurosurg. 1987;66:134–6. https://doi.org/10.3171/ Chun SW, Kim SJ, Lee TH, Koo HS.  Intra-root cavernous angioma jns.1987.66.1.0134. of the cauda equina: a case report and review of the literature. J Van Gompel JJ, Griessenauer CJ, Scheithauer BW, Amrami KK, Korean Neurosurg Soc. 2010;47:291–4. https://doi.org/10.3340/ Spinner RJ.  Vascular malformations, rare causes of sciatic neujkns.2010.47.4.291. ropathy: a case series. Neurosurgery. 2010;67:1133–42. https://doi. Da Ros V, Picchi E, Ferrazzoli V, Schirinzi T, Sabuzi F, Grillo P, et al. org/10.1227/NEU.0b013e3181ecc84e. Spinal vascular lesions: anatomy, imaging techniques and treat- Yang T, Wang F, Niu C.  Clinical characteristics and surgical outment. Eur J Radiol Open. 2021;8:100369. https://doi.org/10.1016/j. comes of solitary spinal epidural cavernous angiomas. Oncol Lett. ejro.2021.100369. 2018;15:6036–42. https://doi.org/10.3892/ol.2018.8024. Demeulenaere A, Spelle L, Lafitte F, Brunet E, Chiras J.  Vertebro-­ Yang T, Wu L, Yang C, Deng X, Xu Y.  Cavernous angiomas of the epidural lumbosacral vascular malformations. An unusual cause of cauda equina: clinical characteristics and surgical outcomes. Neurol lumbo-sciatic pain. J Neuroradiol. 1999;26:225–35. Med Chir (Tokyo). 2014;54:914–23. https://doi.org/10.2176/nmc. Drazin D, Kappel A, Withrow S, Perry T, Chu R, Phuphanich S. Post-­ oa.2014-­0115. irradiation lumbosacral radiculopathy associated with multiple Zhang L, Qiao G, Shang A, Yu X.  Clinical features and long-term cavernous malformations of the cauda equina: Case report and surgical outcomes of pure spinal epidural cavernous hemangioma-­ review of the literature. Surg Neurol Int. 2017;8:26. https://doi. report of 23 cases. Acta Neurochir. 2020;162:2915–21. https://doi. org/10.4103/2152-­7806.200574. org/10.1007/s00701-­020-­04358-­x. Duke BJ, Levy AS, Lillehei KO.  Cavernous angiomas of the cauda equina: case report and review of the literature. Surg Neurol. 1998;50:442–5. https://doi.org/10.1016/s0090-­3019(97)00354-­6.

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Spinal Hygromas

75.1 Generalities End Relevance

75.3 Imaging Features

A spinal subdural hygroma is a collection of cerebrospinal fluid (CSF) trapped in the subdural space between the spinal arachnoid mater and the spinal dura mater. Some spinal hygromas can be extradural, but this is a very rare condition. Spinal hygromas are encountered in all age groups from children to aging adults. In the lumbosacral spinal canal, this rare condition has the potential to cause secondary neurologic damage by compressing nerve roots. Sciatica related to spinal hygromas is mainly due to compression of the lumbosacral roots. A spinal subdural hygroma is typically seen in patients with a history of recent blunt trauma or following a spinal/ cranial surgery. However, other underlying causes or associated pathologies may exist such as:

On neuroimaging, most spinal hygromas have a crescent or spindle-shaped form and can normally extend over more than a few spinal levels, from the cervical to the lumbosacral spinal region. On computed tomography (CT) scan without intrathecal contrast injection, it is not possible to differentiate subdural hygroma from other intraspinal cystic lesions. However, both CT myelography and T2-weighted magnetic resonance imaging (MRI) are good primary choices for the diagnosis and can additionally identify the potential dural tear or CSF leak. Other imaging procedures may be useful such as MRI myelography with intrathecal gadolinium or radionuclide cisternography. In the axial plane, intraspinal hygromas can have a tri-­ radiate pattern so-called an “inverted Mercedes Benz sign” in the lumbar area due to the position of the cauda equina spinal nerve roots. Some large spinal hygromas can show MRI features of craniospinal hypotension such as engorgement of the venous sinuses, enhancement of the pachymeninges, pituitary hyperemia, and a reduced pontomesencephalic angle. Signal cystic contents are like those of CSF on all MRI sequences. However, in some cases, especially following trauma or surgery, there is a heterogeneous signal on MRI especially, hyperintensity on the fluid-attenuated inversion recovery (FLAIR) sequence correlated to a combination of CSF and blood.

• Iatrogenic procedure (e.g., lumbar puncture, epidural anesthesia, or intrathecal chemotherapy). • Spontaneous intracranial hypotension. • Following bacterial meningitis, especially in children. Intraspinal hygroma differs from other intraspinal cystic lesions in many aspects such as the content of the subdural fluid collection, neuroimaging appearance, and clinical manifestations.

75.2 Clinical Presentations Most patients with spinal hygroma are pauci or asymptomatic. Clinical symptoms are various and nonspecific and consist of back pain with or without sciatica, postural headaches, nausea/vomiting, blurred vision, vestibulocochlear manifestations, diplopia, or symptoms related to cauda equina or spinal cord compression. Overall, severe symptomatology and neurologic deficit are uncommon. Other symptoms may be linked to the primary etiology of the disease.

75.4 Treatment Options and Prognosis Patients with no or mild symptomatology and those with a small collection or without radicular mass effect can be treated conservatively. The spinal hygroma will often decrease or resolve spontaneously. Whenever possible, the underlying cause should be determined and treated. For example, treatment of spontaneous

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intracranial hypotension or post-lumbar puncture headache with autologous epidural blood patching and treatment of bacterial meningitis with appropriate antibiotic therapy as soon as possible. Surgical procedures typically comprise decompressive laminectomy, dura incision (durotomy), and cystic evacuation. Sometimes, the surgical procedure will be directed to closing the underlying leak of hygroma. Considering the wide communicating cystic cavity, the spinal subdural hygroma can potentially be treated surgically with only a limited durotomy and then a wide arachnoid fenestration. Finally, the dura should be closed hermetically to avoid a postoperative CSF fistula, pseudomeningocele, and potential meningitis. Overall, surgical decompression is a reasonable option in patients with sciatica accompanied by motor deficits, especially cauda equina syndrome, or in those who have failed conservative management. Most of the patients operated on are doing well.

Further Reading Akhaddar A. Differential diagnosis of Intraspinal arachnoid cysts. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: state-of-the-art concepts. Switzerland, Cham: Springer International Publishing; 2022. https://doi.org/10.1007/978-­3-­031-­22701-­1_23. Burtis MT, Ulmer JL, Miller GA, Barboli AC, Koss SA, Brown WD.  Intradural spinal vein enlargement in craniospinal hypotension. AJNR Am J Neuroradiol. 2005;26:34–8.

75  Spinal Hygromas Darwish HA, Oldfield EH. Lumbar subdural cerebrospinal fluid collection with acute cauda equina syndrome after posterior fossa decompression for Chiari malformation type I: case report. J Neurosurg Spine. 2016;25:328–31. Elder BD, Ishida W, Goodwin RC, Bydon A.  Iatrogenic spinal subdural extra-arachnoid Hygroma following uncomplicated lumbar decompression. Cureus. 2017;9:e1171. https://doi.org/10.7759/ cureus.1171. Eswaradass P, Dhasakeerthi T, Ansari S, Salhab MM. Spinal epidural Hygroma in a young adult: a rare complication of lumbar puncture. Can J Neurol Sci. 2021;48:725–6. https://doi.org/10.1017/ cjn.2020.266. Kranz PG, Luetmer PH, Diehn FE, Amrhein TJ, Tanpitukpongse TP, Gray L.  Myelographic techniques for the detection of spinal CSF leaks in spontaneous intracranial hypotension. AJR Am J Roentgenol. 2016;206:8–19. https://doi.org/10.2214/AJR.15.14884. Mack J, Squier W, Eastman JT.  Anatomy and development of the meninges: implications for subdural collections and CSF circulation. Pediatr Radiol. 2009;39:200–10. https://doi.org/10.1007/ s00247-­008-­1084-­6. Sneyers B, Ramboer K. Spinal subdural hygroma. Acta Neurol Belg. 2021;121:311–9. https://doi.org/10.1007/s13760-­020-­01558-­1. Thompson D, Robinson T, Singleton W, Patel N, Wigfield C, Malcolm G. Post-operative tension spinal subdural extra-arachnoid hygroma of the lumbar spine: case series, literature review, and recommendations for clinical management. Br J Neurosurg. 2022;21:1–6. https://doi.org/10.1080/02688697.2022.2154748. Weindling SM, Kotsenas AL.  Spontaneous craniospinal hypotension. J Magn Reson Imaging. 2005;22:804–9. https://doi.org/10.1002/ jmri.20441. Yi CK, Biega TJ, Burgos RM.  Spontaneous resolution of idiopathic lumbar subdural hygroma on CT myelography and lumbar spine MRI. BMJ Case Rep. 2014;2014:bcr2014206223.

Postoperative Spinal Etiologies of Sciatica

76.1 Generalities and Relevance Following lumbosacral surgery, some patients may present with postoperative sciatica. This sciatic pain may appear after surgery, or the surgery may exacerbate or insufficiently ameliorate existing pain. This postoperative difficult condition is often frustrating for both patients and surgeons. As a part of failed back surgery syndrome, the key management of postoperative sciatic pain is firstly to identify the etiology of the sciatic radicular pain. Postoperative sciatica is reported to affect between 5 and 30% of patients following a spinal surgical procedure. However, the true incidence of this condition is difficult to establish due to the wide range of its definition and its various/heterogeneous etiologies and predictive factors. Epidural fibrosis, neural scarring, recurrent disc herniation, persistent herniated disc material, iatrogenic spinal

76

instability, the wrong level of operation, discitis and/or osteomyelitis, nerve root injury, secondary spinal stenosis, and inadequate surgical techniques represent the most frequently reported etiologies. However, various predictive factors are associated with postoperative sciatic pain and are classically distributed into preoperative, intraoperative, and postoperative factors (Table  76.1). Sometimes, the exact cause is unknown in about 5% of operated patients and the postoperative sciatica is then considered “idiopathic”. Some studies suggest that some socio-demographic factors such as female gender, smoking, increased age, obesity, low socioeconomic status, and low education level may be correlated with poor outcomes following LDH surgery. Also, the presence of certain co-morbidities, pre-existing chronic pain disorders, or psychological conditions may all prevent a successful postoperative outcome.

Table 76.1  Various etiologies and predictive factors associated with sciatic pain secondary to spinal surgery Preoperative factors:  •  Patient psychosocial factors, secondary gains, and psychiatric comorbidities  •  Litigation or worker’s compensation claims  •  Other causes of sciatica (spinal or extraspinal)  •  Double Crush syndrome involving different sites  •  Some anatomic variations (e.g., conjoined nerve roots, lumbarization, sacralization, spina bifida)  •  Other symptoms mimicking sciatic radicular pain (differential diagnosis)  •  Inadequate preoperative spinal imaging  •  Inappropriate lesion on spinal imaging (sciatica attributed to a non-attributable pathology)  •  Inappropriate surgical candidate  •  Inappropriate surgical approach  •  Patients who have undergone multiple prior lumbosacral surgical procedures Intraoperative factors:  •  Wrong vertebral level surgery (Figs. 76.1, 76.2, and 76.3)  •  Improper surgical technique  •  Insufficient radicular decompression  •  Missing disc fragment(s)  •  Iatrogenic damages +++ (c.f. Chap. 13 about Surgical Complications of Discogenic Sciatica)  •  Unwanted bone cement leaks (extravasation) during vertebroplasty or kyphoplasty (continued)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_76

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Table 76.1 (continued) Postoperative complications:  •  Epidural or peridural fibrosis (including granulomas) (Figs. 76.4, 76.5, 76.6, 76.7, and 76.8)  •  Adhesive arachnoiditis (Figs. 76.9, 76.10, and 76.11)  •  Pseudomeningocele (Figs. 76.12, 76.13, and 76.14)  •  Nerve roots herniations/entrapments (Figs. 76.13, 76.14, and 76.15)  •  Recurrent LDH (Figs. 76.16, 76.17, and 76.18)  •  Lumbar spinal stenosis (especially lateral stenosis of the foramina)  •  Spinal instability (lateral rotational instability, spondylolisthesis, scoliosis, or pseudarthrosis)  •  Incorrect patient positioning during surgery  •  LDH at other adjacent levels (mainly due to redistribution of load to adjacent disc)  •  Infections (e.g., discitis, spondylodiscitis, epidural abscess) (Figs. 76.18, 76.19, 76.20, 76.21, and 76.22)  •  Epidural hematoma  •  Free epidural fat grafting  •  Extradural Fibrous Entrapment of Lumbosacral Nerve Roots (Figs. 76.6 and 76.7)  •  Screw and implant misplacements or migrations (Figs. 76.23 and 76.24)  •  Synovial cyst  •  Discal cyst/pseudocyst (Fig. 76.25)  •  Epidural gas (Fig. 76.26)  •  Psychosocial issues and secondary gain  •  Depressions

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Fig. 76.1  Case 1. This 47-year-old patient was operated on in another hospital for a giant L4-L5 disc herniation (arrows) as seen on sagittal T1(a), T2-weighted MRI (b), and STIR sequence (c) as well as on axial T2-weighted images (d, e)

76.1  Generalities and Relevance

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Fig. 76.2  Case 1. Since the patient was not improved, a postoperative MRI was done showing a wrong vertebral level surgery at L3-L4 (arrows) instead of L4-L5. Sagittal T1- (a) and T2-weighted images (b), as well as on axial T2-weighted images (c, d)

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Fig. 76.3  Case 2. Wrong L1-L2 laminectomy (bracket) instead of L3-L4 (arrows) in a 58-year-old woman operated on at another hospital for lumbar spinal stenosis without improvement. Sagittal T1- (a) and T2-weighted images (b), as well as on axial T2-weighted images (c, d)

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.4  Case 3. Postoperative epidural and peridural fibrosis at L5-S1 disc level in a patient operated on 4 months before for a lumbar disc herniation (arrows). Axial post-gadolinium T1- (a, b) and T2-weighted MRI (c, d)

76.1  Generalities and Relevance

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Fig. 76.5  Case 4. Extradural fibrous entrapment of S1 nerve root (roots) in a 25-year-old man operated on 20 months earlier for an L5-S1 disc herniation on the left side. Sagittal T1- (a) and T2-weighted images (b), as well as on axial T2-weighted images (c, d)

Fig. 76.6  Case 5. Large S1 swollen root (arrows) in a patient operated on 1 year earlier for an L5-S1 disc herniation on the right side. Axial T2-weighted MRI (a, b)

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.7  Case 6. Intracanalar retained foreign body granuloma (gossypiboma—retained surgical cottonoid) (stars) diagnosed 10  months following L4-L5 disc surgery performed in another hospital. Axial CT

scan (a) and T2-weighted MR imaging (b) as well as sagittal T1-(c) and T2-weighted MR imaging (d). This compressive epidural granuloma (arrows) can be confused with a re-herniation or an epidural abscess

Successful treatment, whether it is medical and/or surgical, is usually predicated on the triad of clinical symptoms, physical findings, and imaging correlation. It is important to differentiate treatable from untreatable causes.

Fig. 76.8  Case 6. Microscopic image showing a foreign body granuloma containing foamy macrophages and multinucleated giant cells around foreign body fibers (arrows) (Hematoxylin and eosin, original magnification ×100)

76.1  Generalities and Relevance Fig. 76.9  Case 7. Postoperative arachnoiditis occurred 6 months following the initial unilateral L4-L5 herniectomy/discectomy. Sagittal (a) and axial (b) T2-weighted MR imaging. There is a retraction of the thecal sac and the nerve roots are adherent to the parietal arachnoid peripherally (arrows)

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.10  Case 8. This 38-year-old man was operated on for a right paramedian L5-S1 disc herniation (arrows) (a, b). Two years later, he reported a contralateral postoperative sciatica due to contralateral nerve

root traction or stretching (arrowheads) (c, d). This phenomenon is known as a Bowstring disease (c.f. Chap. 5 about Pathophysiological Mechanisms of Sciatica)

76.1  Generalities and Relevance

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Fig. 76.11  Case 9. Postoperative arachnoiditis: the lumbosacral nerve roots are adherent to the parietal arachnoid peripherally as seen on lumbar sagittal (a) and axial T2-weighted MRI (b, c). This patient was previously operated on for an L4-L5 disc herniation

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.12  Case 10. Large compressive pseudomeningocele (stars) in a patient operated on 6 months earlier in another neurosurgical center for an L5 lumbar central spinal stenosis. Sagittal T1- (a) and T2-weighted images (b), as well as on axial T2-weighted images (c, d)

76.1  Generalities and Relevance

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Fig. 76.13  Case 11. Postoperative small pseudomeningocele (arrows) with nerve entrapment/herniation (arrowhead) in a patient operated on for an L5-S1 herniated disc on the left side. Lumbosacral sagittal (a, b) and axial (c) T2-weighted MR imaging

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.14  Case 12. Postoperative pseudomeningocele (arrowheads) associated with transdural nerve root herniation (arrow) outside the thecal sac in a patient operated on in another department for lumbar spinal

stenosis. Lumbosacral sagittal (a) and axial (b) T2-weighted MR imaging. Posterior operative view (c)

76.1  Generalities and Relevance Fig. 76.15  Case 13. Postoperative L5-S1 intradiscal nerve root entrapment (arrowheads). Lumbosacral sagittal (a) and axial (b) T2-weighted MR imaging

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Fig. 76.16  Case 14. Recurrent giant L4-L5 disc herniation (yellow arrows) in a 56-year-old man operated via a left-sided L4-L5 interlaminar approach (black arrows) 2 years earlier. Lumbosacral sagittal (a, b) and axial (c, d) T2-weighted MR imaging

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.17  Case 15. Recurrent L5-S1 disc herniation (yellow arrows) in a 47-year-old man operated 10 years earlier via a left-sided L5-S1 interlaminar approach (black arrows). Lumbosacral sagittal (a) and axial (b, c) T2-weighted MR imaging

76.1  Generalities and Relevance

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Fig. 76.18  Case 16. Recurrent L5-S1 disc herniation (arrows) with surgical site abscess (stars) in a 40-year-old man operated on 2 months earlier for a lumbar disc herniation with a lumbar central spinal steno-

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sis. Sagittal reconstruction CT scan (a), post-gadolinium T1- (b), and T2-weighted MR imaging (c)

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.19  Case 16. Postoperative surgical site infection (epidural abscess) (stars) with recurrent L5-S1 disc herniation (arrows). Axial CT scan (a), post-gadolinium T1- (b), and T2-weighted MR imaging (c)

76.1  Generalities and Relevance

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Fig. 76.20  Case 17. This 45-year-old man was operated on 2 months earlier for an L4-L5 disc herniation as seen on sagittal T2-weighted MRI (arrow) (a). There is a postoperative epidural abscess with a spon-

dylodiscitis (surgical site infection) (arrows) on sagittal T1-weighted MRI before (b) and after (c) gadolinium injection. The spondylodiscitis is also seen on sagittal (d) and axial T2-weighted MRI (e, f) (stars)

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76  Postoperative Spinal Etiologies of Sciatica

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Fig. 76.21  Case 18. L5-S1 spondylodiscitis (arrows) following herniectomy and discectomy at an outside institution for a lumbar disc herniation. Lumbosacral sagittal T1- (a) and T2-weighted MRI (b). Axial post-gadolinium T1-weighted MRI (c)

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Fig. 76.22  Case 18. Postoperative L5-S1 spondylodiscitis (arrows). Lumbosacral sagittal reconstruction (a, b) and axial (c, d) CT scan

76.1  Generalities and Relevance

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Fig. 76.23  Case 19. Postoperative sciatica in a woman operated on for an L3-L5 spondylolisthesis at an outside hospital. There is a right-sided L5 screw misplacement (circle) as seen on axial (a), coronal (b), and sagittal (c) reconstructions CT scan

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76  Postoperative Spinal Etiologies of Sciatica

Fig. 76.24  Case 20. L5 pedicle screw misplacement (star) in an 18-year-old man operated on for a traumatic lumbar spine injury as seen on axial CT scan

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Fig. 76.25  Case 21. A postoperative discal cyst (arrows) occurring after L4-L5 herniectomy and discectomy for disc herniation as seen on sagittal (a, b) and axial (c) T2-weighted MR imaging. (Courtesy of Pr. Abad Cherif El Asri)

76.2  Clinical Presentations

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Fig. 76.26  Case 22. Recurrent L4-L5 disc herniation with compressive gaz pseudocysts (arrows) in a 56-year-old patient operated on 1 year earlier for an L4-L5 disc herniation with central spinal stenosis. Lumbosacral sagittal reconstruction (a, b) and axial (c, d) CT scan

76.2 Clinical Presentations As with other presentations of sciatic pain, the initial evaluation should include a sufficient and detailed history as well as a neurologic, spinal, and somatic examination. There was no uniform clinical presentation in the patients. Nevertheless, most cases develop progressive spinal and neurologic radicular symptoms over several weeks or months. Sciatic severity also varies considerably. It seems that patients with extensive fibrosis were 3.2 times more likely to experience radicular symptoms than those with recurrent LDH. The characteristics, intensity, neuropathic or nociceptive components, mode of onset, precise location, and timing of the patient’s sciatic pain should be identified and compared to pre-surgical pain. The positive Straight Leg Raise test is a sensitive test for lumbosacral nerve root compression. Lack of immediate release of sciatic pain may suspect operation at

the wrong disc level whereas instant new-onset sciatic pain may indicate surgically induced nerve damage. Epidural hematoma should also be excluded over the hours following the operation. Timing is also an important factor. For example, approximately 50% of all recurrent LDH occur within the first year following the surgical procedure. An early recurrence of LDH within 30 days of discharge after a primary discectomy is more related to persistent herniated disc material than a true LDH. In patients treated by spinal fusion, delayed consolidation, pseudoarthrosis, instability, or higher vertebral level abnormalities should be considered. Secondary spinal instability should be suspected in the case of recurrence with a longer pain-free interval and in those with multiple previous spinal surgical procedures. Physicians should assess and appropriately recognize the gravity of neurologic symptoms especially severe neurologic

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deficit in the lower extremities and cauda equina syndrome. Other symptoms may be correlated to other underlying etiologies of the disease such as fever and chills suggesting postoperative infection (e.g., discitis). Neurogenic intermittent claudication indicates the likelihood of the coexistence of lumbar spinal stenosis. Sometimes, the symptoms are more painful and severe than those presented before the first decompression surgery. Neuropathic manifestations are more common with postoperative sciatic pain than those found preoperatively. Besides sciatic pain, most patients report a variety of signs and symptoms related to musculoskeletal abnormalities such as low back pain, in addition to those related to facet joint arthropathies, sacroiliac joint disorders, or myofascial etiologies. Some authors recommend a psychiatric evaluation due to the high comorbidity of anxiety/depression and other ­psychiatric disorders in patients with postoperative sciatica and those with failed back surgery syndrome. Electromyogram (EMG) and/or nerve conduction velocity (NCV) tests may be used to assess the lower limb nerve damage and sometimes to evaluate clinico-imaging concordance. Sometimes, the severity of sciatic pain and neurologic symptoms did not have a strong correlation with the lesion seen on postoperative spinal imaging.

76.3 Paraclinic Evaluations Plain radiography is the first imaging evaluation for suspected postoperative sciatic pain. Plain lumbosacral X-rays are useful for detecting vertebral defects, spondylosis, spinal misalignment (including spondylolisthesis), and instability (dynamic X-rays). Adjacent segment degeneration and loss of lordosis are common anomalies seen on plain radiography. Computed tomography (CT) scan using reconstruction is helpful to detect spinal stenosis, intervertebral discs (enhancing with possible rim enhancement), epidural scarring (enhancing), or fibrosis following post-contrast injection (Figs. 76.7, 76.18, 76.19, 76.22, 76.23, 76.24, and 76.26). In patients with ferromagnetic implants, a CT saccoradiculogram (myelogram) is used to avoid implant artifacts found on magnetic resonance imaging (MRI). MRI with and without gadolinium injection remains the most effective imaging technique for distinguishing the cause of sciatica following spinal surgery due to its excellent ability to detect soft tissue abnormalities (Figs.  76.1, 76.2, 76.3, 76.4, 76.5, 76.6, 76.7, 76.10, 76.11, 76.12, 76.13, 76.14, 76.15, 76.16, 76.17, 76.18, 76.19, 76.20, 76.21, and 76.25). The postoperative appearance of the intervertebral disc, neural roots, and epidural space largely depends on the time of

76  Postoperative Spinal Etiologies of Sciatica

spinal imaging since the surgical procedure. The immediate postoperative MRI usually reveals highly heterogeneous content within the epidural space, consisting of air, debris, blood, and potential residual discal tissue. Unless an important quantity of residual disc material is present, differentiating residual disc herniation from other tissue types is habitually very difficult on early postoperative MRI.  Later, MRI helps find the cause of postoperative sciatic pain in more than 90% of cases. However, the first challenge of neuroimaging is to distinguish recurrent LDH from epidural fibrosis (c.f. Chap. 28 about Recurrent Lumbar Disc Herniations). The differential diagnosis of enlarged and asymmetric nerve root must include intervertebral disc fragment, conjoined nerve roots (normal variant), dilated root sleeve, perineural cysts, nerve root tumors, iatrogenic radicular neuroma, and even scar tissue formation or fibrosis following surgical decompression. Sometimes, other tests may be used to elucidate the etiology of postoperative sciatic pain such as Erythrocyte sedimentation rate and C-reactive protein (possible infection) and transforaminal epidural nerve blocks (foraminal ­stenosis). When combined with steroids, nerve block procedures can also offer therapeutic relief. When postoperative discitis is suspected, blood cultures should be done and completed by culture results of samples taken from the affected disc using a percutaneous CT-guided procedure.

76.4 Treatment Options Therapies for the management of postoperative sciatica are generally divided into conservative and aggressive (surgical) treatment. Except in patients with indications for emergency surgery (motor weakness, bowel/bladder impairment, and cauda equina syndrome), conservative management should always be the first option before invasive techniques. In addition, the majority of patients with epidural fibrosis or adhesive arachnoiditis require only symptomatic treatment. Treatment of cases with a predominant neuropathic part is based on the use of analgesics, especially antiepileptics (GABA analogs), antidepressants, or transcutaneous electrical stimulation. Muscle relaxants are a helpful treatment option for patients with concomitant paravertebral skeletal muscle spasms. Epidural spinal infiltration should be considered as second-line treatment in view of the risk of some neurological and infectious complications. After the failure of these previous conservative measures, many authors recommend spinal cord stimulation before considering chronic opiate therapy. The most important reason to perform surgical revision is for patients with clearly identified compressive pathologies

Further Reading

that may be relieved with surgery. Surgical technique is highly dependent on the sub-etiology detected on spinal imaging. A detailed description of each surgical treatment for the various causes of postoperative sciatica is beyond the scope of this chapter (c.f. different relevant chapters of this book). Infection should be treated with broad-spectrum antibiotics that can be modified based on antimicrobial susceptibility. Sequestrectomy, purulent drainage, and discectomy with or without fusion may be needed after unsuccessful medical therapy. Potential spinal instability can require spinal reconstruction and surgical implants (c.f. Chap. 52 about Spondylodiscitis). Some selective patients who present chronic intractable sciatic pain can be managed using some specific technics such as implanted spinal fluid pumps, nerve, and spinal cord stimulation, or ablative procedures.

76.5 Outcome and Prognosis Adequate decompressive surgery offers a favorable outcome when the organic cause of the recurrent sciatica is obvious. However, the success rate of the surgery decreases with every reoperation. Removal of fibrosis and scar tissue may lead to a poor result but the removal of recurrent or residual herniated discs often leads to a good outcome (c.f. Chap. 28 about Recurrent Lumbar Disc Herniations). In addition to intractable sciatic pain, patients often suffer from associated disorders especially psychiatric comorbidities (e.g., depression). Some patients may also present complications from their pain treatment. Long use of non-steroidal anti-inflammatory drugs has significant adverse effects on gastrointestinal and renal function. Opioids also have the potential risk of dependence and addiction. Any patients with cognitive or behavioral disorders require appropriate psychologic or psychiatric support in combination with a functional rehabilitation program. Unfortunately, some patients are unable to return to work for health reasons pending medicolegal or workers’ compensation benefits.

Further Reading Akhaddar A, Baallal H, Elktaibi A.  Abscess due to textiloma (gossypiboma: retained surgical cottonoid). Surg Neurol Int. 2018;9:70. https://doi.org/10.4103/sni.sni_64_18. Akhaddar A, Atmane el M.  Pedicle screw malposition following spinal lumbar injury. Pan Afr Med J. 2014;17:266. https://doi. org/10.11604/pamj.2014.17.266.4120. Akhaddar A, Oukabli M, Albouzidi A, Boucetta M.  Recurrent lumbosciatica because of cotton granuloma after surgery for lumbar

823 disc herniation. Spine J. 2011;11:363–4. https://doi.org/10.1016/j. spinee.2011.03.002. Aljawadi A, Sethi G, Islam A, Elmajee M, Pillai A. Sciatica presentations and predictors of poor outcomes following surgical decompression of herniated lumbar discs: a review article. Cureus. 2020;12:e11605. https://doi.org/10.7759/cureus.11605. Arts MP, Kols NI, Onderwater SM, Peul WC. Clinical outcome of instrumented fusion for the treatment of failed back surgery syndrome: a case series of 100 patients. Acta Neurochir. 2012;154:1213–7. https://doi.org/10.1007/s00701-­012-­1380-­7. Baba H, Chen Q, Kamitani K, Imura S, Tomita K.  Revision surgery for lumbar disc herniation. An analysis of 45 patients. Int Orthop. 1995;19:98–102. https://doi.org/10.1007/BF00179969. Baber Z, Erdek MA. Failed back surgery syndrome: current perspectives. J Pain Res. 2016;9:979–87. https://doi.org/10.2147/JPR. S92776. BenDebba M, Augustus van Alphen H, Long DM. Association between peridural scar and activity-related pain after lumbar discectomy. Neurol Res. 1999;21(Suppl 1):S37–42. https://doi.org/10.1080/016 16412.1999.11741025. Chaljub G, Sullivan RD, Patterson JT. The triad of nerve root enhancement, thickening, and displacement in patients with sciatica and recurrent disk herniation in the postoperative lumbar spine may prompt further surgical treatment in patients with failed-back surgical syndrome. AJNR Am J Neuroradiol. 2009;30:1068–9. https:// doi.org/10.3174/ajnr.A1552. Clancy C, Quinn A, Wilson F. The aetiologies of failed Back surgery syndrome: a systematic review. J Back Musculoskelet Rehabil. 2017;30:395–402. https://doi.org/10.3233/BMR-­150318. Cobanoğlu S, Imer M, Ozylmaz F, Memiş M. Complication of epidural fat graft in lumbar spine disc surgery: case report. Surg Neurol. 1995;44:479–81. https://doi.org/10.1016/0090-­3019(95)00222-­7. Davis RA.  A long-term outcome analysis of 984 surgically treated herniated lumbar discs. J Neurosurg. 1994;80:415–21. https://doi. org/10.3171/jns.1994.80.3.0415. Durand G, Girodon J, Debiais F. Medical management of failed back surgery syndrome in Europe: evaluation modalities and treatment proposals. Neurochirurgie. 2015;61(Suppl 1):S57–65. https://doi. org/10.1016/j.neuchi.2015.01.001. Erbayraktar S, Acar F, Tekinsoy B, Acar U, Güner EM.  Outcome analysis of reoperations after lumbar discectomies: a report of 22 patients. Kobe J Med Sci. 2002;48:33–41. Erman T, Tuna M, Göçer AI, Idan F, Akgül E, Zorludemir S. Postoperative radicular neuroma. Case report. Neurosurg Focus. 2001;11:ecp. https://doi.org/10.3171/foc.2001.11.5.9. Fritsch EW, Heisel J, Rupp S.  The failed back surgery syndrome: reasons, intraoperative findings, and long-term results: a report of 182 operative treatments. Spine (Phila Pa 1976). 1996;21:626–33. https://doi.org/10.1097/00007632-­199603010-­00017. Fu CF, Tian ZS, Yao LY, Yao JH, Jin YZ, Liu Y, et  al. Postoperative discal pseudocyst and its similarities to discal cyst: a case report. World J Clin Cases. 2021;9:1439–45. https://doi.org/10.12998/ wjcc.v9.i6.1439. Geisler FH.  Prevention of peridural fibrosis: current methodologies. Neurol Res. 1999;21(Suppl 1):S9–22. https://doi.org/10.1080/0161 6412.1999.11741021. Kim KD, Wang JC, Robertson DP, Brodke DS, BenDebba M, Block KM, et al. Reduction of leg pain and lower-extremity weakness for 1  year with Oxiplex/SP gel following laminectomy, laminotomy, and discectomy. Neurosurg Focus. 2004;17:ECP1. https://doi. org/10.3171/foc.2004.17.1.8. Kim SB, Lee KW, Lee JH, Kim MA, An BW. The effect of hyaluronidase in interlaminar lumbar epidural injection for failed back surgery syndrome. Ann Rehabil Med. 2012;36:466–73. https://doi. org/10.5535/arm.2012.36.4.466.

824 Lequin MB, Verbaan D, Bouma GJ. Posterior lumbar interbody fusion with stand-alone trabecular metal cages for repeatedly recurrent lumbar disc herniation and back pain. J Neurosurg Spine. 2014;20:617–22. https://doi.org/10.3171/2014.2.SPINE13548. Long DM, BenDebba M, Torgerson WS, Boyd RJ, Dawson EG, Hardy RW, et  al. Persistent back pain and sciatica in the United States: patient characteristics. J Spinal Disord. 1996;9:40–58. Machado GC, Witzleb AJ, Fritsch C, Maher CG, Ferreira PH, Ferreira ML. Patients with sciatica still experience pain and disability 5 years after surgery: a systematic review with meta-analysis of cohort studies. Eur J Pain. 2016;20:1700–9. https://doi.org/10.1002/ejp.893. Mastronardi L, Pappagallo M, Tatta C, Roperto R, Elsawaf A, Ferrante L.  Prevention of postoperative pain and of epidural fibrosis after lumbar microdiscectomy: pilot study in a series of forty cases treated with epidural vaseline-sterile-oil-morphine compound. Spine (Phila Pa 1976). 2008;33:1562–6. https://doi.org/10.1097/ BRS.0b013e3181788744. Meadeb J, Rozenberg S, Duquesnoy B, Kuntz JL, Le Loët X, Sebert JL, et  al. Forceful sacrococcygeal injections in the treatment of ­postdiscectomy sciatica. A controlled study versus glucocorticoid injections. Joint Bone Spine. 2001;68:43–9. https://doi.org/10.1016/ s1297-­319x(00)00234-­7. Partheni M, Kalogheropoulou C, Karageorgos N, Panagiotopoulos V, Voulgaris S, Tzortzidis F.  Radiculopathy after lumbar discectomy due to intraspinal retained Surgicel: clinical and magnetic resonance imaging evaluation. Spine J. 2006;6:455–8. https://doi. org/10.1016/j.spinee.2005.12.006. Pereira P, Severo M, Monteiro P, Silva PA, Rebelo V, Castro-Lopes JM, et al. Results of lumbar endoscopic Adhesiolysis using a radiofre-

76  Postoperative Spinal Etiologies of Sciatica quency catheter in patients with postoperative fibrosis and persistent or recurrent symptoms after discectomy. Pain Pract. 2016;16:67–79. https://doi.org/10.1111/papr.12266. Rogerson A, Aidlen J, Jenis LG.  Persistent radiculopathy after surgical treatment for lumbar disc herniation: causes and treatment options. Int Orthop. 2019;43:969–73. https://doi.org/10.1007/ s00264-­018-­4246-­7. Ross JS. MR imaging of the postoperative lumbar spine. Magn Reson Imaging Clin N Am. 1999;7:513–24. viii Sasani M, Ozer AF, Oktenoglu T, Cosar M, Karaarslan E, Sarioglu AC.  Recurrent radiculopathy caused by epidural gas after spinal surgery: report of four cases and literature review. Spine (Phila Pa 1976). 2007;32:E320–5. https://doi.org/10.1097/01. brs.0000261565.76537.ea. Sebaaly A, Lahoud MJ, Rizkallah M, Kreichati G, Kharrat K. Etiology, evaluation, and treatment of failed back surgery syndrome. Asian Spine J. 2018;12:574–85. https://doi.org/10.4184/asj.2018.12.3.574. Turgut M, Akhaddar A, Turgut AT. Retention of nonabsorbable hemostatic materials (retained surgical sponge, gossypiboma, textiloma, gauzoma, muslinoma) after spinal surgery: a systematic review of cases reported during the last half-century. World Neurosurg. 2018;116:255–67. https://doi.org/10.1016/j.wneu.2018.05.119. Wilson CA, Roffey DM, Chow D, Alkherayf F, Wai EK. A systematic review of preoperative predictors for postoperative clinical outcomes following lumbar discectomy. Spine J. 2016;16:1413–22. https://doi.org/10.1016/j.spinee.2016.08.003.

Extradural Fibrous Entrapment of Lumbosacral Nerve Roots

77.1 Generalities and Relevance Nerve roots extradural fibrous entrapment is a rare pathologic entity defined by circumferential fibrous adhesion of intraspinal extradural nerve roots with subsequent constriction and entrapment but without remarkable neuroimaging findings. The lesion is typically limited to the spinal lumbosacral region. It should be distinguished from other classic etiologies of nerve root entrapment and mechanical compression secondary to degenerative changes (e.g., intervertebral disc herniation or spinal canal stenosis), inflammation, infections, tumors, traumatic injuries, or post-surgical procedures. First published in 2001 by the Japanese orthopedic surgeons Kazuhiro Ido and Hiroko Urushidani, lumbosacral nerve roots extradural fibrous entrapment is a rare disease with fewer than ten cases reported to date. In fact, this entity is surely unrecognized and therefore undiagnosed. Fibrous adhesive entrapment of lumbosacral nerve roots is an important condition because it may induce various degrees of unexplained sciatic pain due to negative neuroimaging results. The pathogenesis remains unclear. It may be secondary to unknown mechanical compression and/or chemical inflammation of both the nerve roots and posterior longitudinal ligament. The majority of cases are described as females (62%) in their fifth decade of life (mean age of 43 years).

77.2 Clinical Presentations Clinical symptoms are nonspecific and are similar to those associated with other more common spinal conditions including low back pain and unilateral lower limb radiculopathy (particularly L5 and S1) without neurologic deficit or sphincter dysfunction.

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There was no uniform clinical presentation in the patients. However, most cases develop progressive spinal and radicular symptoms over several months (mean of 7 months). On physical examination, the majority of patients had a positive straight leg raising (Lasègue test) on the ipsilateral side of sciatic pain. Electromyogram (EMG) or nerve conduction velocity (NCV) tests may be used to study the lower limb nerve damage.

77.3 Imaging Features All neuroimaging examinations including myelography, computed tomography (CT) scan, and magnetic resonance imaging (MRI) showed no compressive lesion. However, post-gadolinium-enhanced MRI has not been systematically done for screening of nerve root fibrous adhesion. Interestingly, all previously reported patients have made a nerve root block using lidocaine with complete relief of sciatica and low back pain. The diagnostic of fibrous adhesion is confirmed intraoperatively.

77.4 Treatment Options and Prognosis The aim of surgery is to decompress the affected nerve root and release the fibrous adhesion. All the reported patients were treated surgically. Seven cases underwent a laminotomy followed by unroofing of the nerve root involved (mainly L5 or S1). Only one patient was treated under a full endoscopic interlaminar approach. All the patients experienced complete relief from sciatic pain and low back pain immediately after the surgical procedure without neurologic pain recurrence. However, some patients have presented mild residual low back pain.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_77

825

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Further Reading da Cunha RM. Lumbar nerve root entrapment treated under full endoscopic interlaminar approach. J Neurol Neurophysiol. 2018;9:50. https://doi.org/10.4172/2155-­9562-­C7-­079. Ido K, Urushidani H.  Fibrous adhesive entrapment of lumbosacral nerve roots as a cause of sciatica. Spinal Cord. 2001;39:269–73. https://doi.org/10.1038/sj.sc.3101157. Jayson MI.  Vascular damage, fibrosis, and chronic inflammation in mechanical back pain problems. Semin Arthritis Rheum. 1989;18:73–6. https://doi.org/10.1016/0049-­0172(89)90020-­6.

77  Extradural Fibrous Entrapment of Lumbosacral Nerve Roots Jayson MI. The role of vascular damage and fibrosis in the pathogenesis of nerve root damage. Clin Orthop Relat Res. 1992;279:40–8. Rydevik BL, Myers RR, Powell HC. Pressure increase in the dorsal root ganglion following mechanical compression. Closed compartment syndrome in nerve roots. Spine (Phila Pa 1976). 1989;14:574–6. https://doi.org/10.1097/00007632-­198906000-­00004. Schmid AB, Fundaun J, Tampin B.  Entrapment neuropathies: a contemporary approach to pathophysiology, clinical assessment, and management. Pain Rep. 2020;5:e829. https://doi.org/10.1097/ PR9.0000000000000829.

Nerve Roots Herniation and Entrapment

78.1 Generalities and Relevance A dural tear or “unintended incidental durotomy” is a common and well-known complication following spinal surgery. It occurs in up to 16.7% of spinal operations especially when associated with previous or revised spinal surgery, increasing age, and severe spinal stenosis. Persistent cerebrospinal fluid (CSF) leakage and/or fistulas may result in pseudomeningoceles which are defined as extradural collections of CSF with no dural covering. Postoperative pseudomeningoceles occur in less than 2% of spinal surgery. Small pseudomeningoceles are generally asymptomatic and require no special treatment. However, larger ones may be the source of low back pain and headaches, which may be reproduced by direct pressure of the cystic lesion through its cutaneous structures (Fig. 78.1). Pseudomeningoceles can have further consequences such as infection (wound, meningitis, or epidural abscess), intracranial hypotension (postural headache), and herniation of the nerve roots outside the thecal sac. This last entity may cause lumbosacral radicular symptoms secondary to two mechanisms:

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(a) Direct entrapment or incarceration or compression of one or multiple nerve roots (cauda equina) at the site of dura defect (the neck of the meningocele) (b) Irritation of the rootlet herniation during body movements Sometimes, nerve entrapment can cause irreversible damage through strangulation and nerve ischemia leading to permanent neurological deficit. In the majority of cases, transdural nerve root entrapment is due to the presence of a dural tear that arises from the posterior (Fig.  78.2) or posterolateral aspect of the thecal sac (Fig. 78.3). However, in some cases, nerve root entrapment may be found in the intervertebral disc space anteriorly through a ventral dural tear (Fig. 78.4). More rarely, the herniated nerve root is located in the adjacent facet joint when the durotomy is lateral. Approximately 30 cases of iatrogenic transdural nerve root entrapment have been previously reported in the literature. Most cases were encountered following lumbosacral spinal surgical procedures. However, some other causative factors were previously published (Table 78.1).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_78

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828

78  Nerve Roots Herniation and Entrapment

a

c

b

d

Fig. 78.1  Postoperative pseudomeningocele (extradural collections of CSF with no dural covering) (stars). Lumbosacral sagittal (a) and axial (b) T1-weighted MR imaging as well as sagittal (c) and axial (d) T2-weighted MR imaging

78.1  Generalities and Relevance

a

829

b

c

Fig. 78.2  Case 1. L4-L5 posterior pseudomeningocele (arrowheads) in an elderly previously operated on for lumbar spinal stenosis at another hospital. Sagittal (a) and axial (b) T2-weighted MRI. Note that

the nerve root entrapment is hardly observed on MRI (arrows) and is often diagnosed intraoperatively (nerve incarceration through the dural defect) (c)

830

78  Nerve Roots Herniation and Entrapment

a

b

c

d

Fig. 78.3  Case 2. L5-S1 posterolateral pseudomeningocele (arrows) in a patient previously operated on for a lumbar disc herniation at another institution. Sagittal (a, b) and axial (c, d) T2-weighted MRI. The nerve root is entrapped within the thecal sac (arrowheads) Fig. 78.4  Case 3. A postoperative nerve root entrapment is found in the intervertebral disc space through a ventral dural tear (ventral opening) (arrowheads) as seen on sagittal (a) and axial (b) T2-weighted MRI

a

b

831

78.4  Treatment Options and Prognosis Table 78.1  The main cause of transdural nerve root entrapment inducing sciatic pain as reported in the literature Iatrogenic

Non-­ iatrogenic

Surgery for spinal degenerative diseases Surgery for spinal intradural tumor Lumbar puncture Post-traumatic Calcified lumbar disc herniation

Lumbar disc herniation, spinal stenosis, spondylolisthesis L3-L4 intradural schwannoma For myelography Lumbar burst fracture and/or laminar fracture Sharp-edged disc had eroded the dura

78.2 Clinical Presentations Clinical symptoms are various and sometimes nonspecific similar to those associated with other more common spinal conditions including low back pain, lower limb radiculopathy, spinal claudication with or without paresthesia, or even partial or complete cauda equina syndrome (mostly lower limb weakness with bowel/bladder dysfunction). Clinical presentations are attributed to the compressive pseudomeningocele and/or to the nerve root(s) entrapment. More specifically, patients with lumbosacral pseudomeningocele may present with postural headache (intracranial hypotension) and progressively enlarging swelling under the skin of the operated area. A palpable liquid collection may be encountered if the pseudomeningocele extends posteriorly through the lumbosacral fascia. Symptoms and signs may occur several weeks, months, or even years after the initial spinal lumbar surgery. Acute forms are possible but unusual. Some patients with postoperative pseudomeningocele may be asymptomatic (incidental imaging findings). Other symptoms may be related to other primary etiologies of the disease. Neurophysiologic evaluation (electromyogram and nerve conduction velocity) may be performed to determine the severity of sciatic nerve damage (axonal loss, demyelination, or both) and to evaluate recovery.

78.3 Imaging Features On magnetic resonance imaging, pseudomeningocele typically appears as a homogenous para-spinal CSF collection hypointense on T1-weighted images and hyperintense on T2-weighted images without post-gadolinium enhancement. The collection is usually adjacent to the dural sac, had a tendency to be irregular, well-limited, lobulated, or oblong. However, nerve root(s) entrapment is hardly observed on MRI and is often undiagnosed (Fig.  78.2). Many reported cases are only found during revision surgery. The typical

appearance of root entrapment is a “beak-like appearance” in the sagittal view. In the axial view, the entrapped roots are located posteriorly, anteriorly, or laterally depending on the location of the dural opening (Figs.  78.2 and 78.3). On T2-weighted images, CSF leakage may be extended into the involved disc space (ventral opening) (Fig. 78.4) or the posterior joint space (lateral opening). Sometimes, computerized tomography (CT) scan can help in visualizing calcification/ossification of chronic pseudomeningoceles and even adjacent spinal osseous erosion. Furthermore, before any surgical exploration, it is important to obtain osseous reconstruction images to assess the bone structures. CT myelography and CISS (constructive interference in steady state) MRI sequence may be an interesting technique to detect the CSF fistula and nerve root(s) herniation. Sometimes imaging appearances of pseudomeningocele are atypical and may be confused with other potential postoperative complications encountered in the lumbosacral region such as: –– Epidural abscess –– Epidural hematoma –– Retained foreign body hemostatic materials (textiloma, gossypiboma)

78.4 Treatment Options and Prognosis Management of pseudomeningocele depends on the size of the collection, clinical symptoms, associated complications, and the causative disease. Overall, small asymptomatic isolated pseudomeningocele may need to be monitored because most of them progressively resolve naturally. In large pseudomeningoceles, some authors had attempted conservative treatments including bed rest, focal compression, appropriate positioning, and even closed subarachnoid drainage. If conservative measures failed, operative revision should be considered and the entire sac removed. CSF drainage would be effective but was associated with some risk of meningitis. Surgical revision is recommended and performed under microscopic techniques, as soon as possible, when a symptomatic nerve root(s) herniation is suspected to avoid additional neurological worsening. Under microscopic magnification, herniated root(s) should be carefully replaced intradural and the dura watertight closed. Various dural reparation techniques are used including direct primary suture, fibrin glue, hydrogel or cyanoacrylate, bioabsorbable staples, and different types of grafting and patching. Among all these procedures, a direct primary suture using a simple interrupted suture with an autologous myofascial graft is considered the gold standard for achieving microsurgical closure (Figs. 78.2 and 78.5).

832

a

78  Nerve Roots Herniation and Entrapment

b

Fig. 78.5  Case 1. Intraoperative view of the posterior pseudomeningocele before (a) and after microsurgical closure using autologous myofascial graft (b). Note the “neck” of the pseudomeningocele (dotted circle) following careful replacement of the nerve root in the dural sac

Both Gelfoam or myofascial graft alone positioned over the dural defect are unsuccessful in stopping the CSF leak. Unlike posterior dural tears, anterior ones are more challenging to be restored due to the smaller and deeper operative field. This is why a dorsal durotomy should be performed first, then nerve root(s) reduction on the intradural side, and lastly closure of the ventral dural defect and the dorsal durotomy. All reported cases with transdural entrapped nerve root(s) were operated on or re-operated, with total or subtotal recovery in many cases. However, some patients remained in a permanent neurological deficit. Some preventive measures are important to be remembered. If a dural opening with or without CSF leakage is suspected during surgery, a Valsalva maneuver should be performed before wound closure. It is important to emphasize that treatment with gelfoam and/or fibrin glue alone may not prevent CSF leakage. Rapid identification and careful closure of the dural tear during the original surgery leads to a good result and a favorable outcome. Iatrogenic-related forms can result in medico-legal claims.

Further Reading Akhaddar A, Boulahroud O, Boucetta M.  Nerve root herniation into a calcified pseudomeningocele after lumbar laminectomy. Spine J. 2012;12:273. https://doi.org/10.1016/j.spinee.2012.02.008. Alshameeri ZAF, El-Mubarak A, Kim E, Jasani V. A systematic review and meta-analysis on the management of accidental dural tears in spinal surgery: drowning in information but thirsty for a clear message. Eur Spine J. 2020;29:1671–85. https://doi.org/10.1007/ s00586-­020-­06401-­y. Asha MJ, George KJ, Choksey M. Pseudomeningocele presenting with cauda equina syndrome: is a ‘ball-valve’ theory the answer? Br J Neurosurg. 2011;25:766–8. https://doi.org/10.3109/02688697.201 1.578768.

Bostelmann R, Eicker S, Steiger HJ, Cornelius JF. Spontaneous disruption of dura mater and fascicular continuity of the L5 nerve root by a calcified disc herniation. Acta Neurochir. 2011;153:1447–8. https:// doi.org/10.1007/s00701-­011-­1027-­0. Choi JH, Kim JS, Jang JS, Lee DY.  Transdural nerve rootlet entrapment in the intervertebral disc space through minimal dural tear: report of 4 cases. J Korean Neurosurg Soc. 2013;53:52–6. https:// doi.org/10.3340/jkns.2013.53.1.52. Denis F, Burkus JK. Diagnosis and treatment of cauda equina entrapment in the vertical lamina fracture of lumbar burst fractures. Spine (Phila Pa 1976). 1991;16:S433–9. Hasegawa K, Yamamoto N.  Nerve root herniation secondary to lumbar puncture in the patient with lumbar canal stenosis. A case report. Spine (Phila Pa 1976). 1999;24:915–7. https://doi. org/10.1097/00007632-­199905010-­00015. Hyndman OR, Gerber WF.  Spinal extradural cysts, congenital and acquired; report of cases. J Neurosurg. 1946;3:474–86. https://doi. org/10.3171/jns.1946.3.6.0474. Iida J, Miyakoshi N, Hongo M, Sasaki H, Ito H, Kubota H, et  al. Herniation of the cauda equina into the facet joint through a pseudomeningocele: a case report and literature review. Surg Neurol Int. 2021;12:30. https://doi.org/10.25259/SNI_893_2020. Kamali R, Naderi Beni Z, Naderi Beni A, Forouzandeh M.  Postlaminectomy lumbar pseudomeningocele with nerve root entrapment: a case report with review of literature. Eur J Orthop Surg Traumatol. 2012;22(Suppl 1):57–61. https://doi.org/10.1007/ s00590-­011-­0934-­3. Kim YJ. Incarceration of spinal nerve root through incidental durotomy as a cause of sciatica. Korean J Spine. 2017;14:103–5. https://doi. org/10.14245/kjs.2017.14.3.103. Kothbauer KF, Seiler RW.  Transdural cauda equina incarceration after microsurgical lumbar discectomy: case report. Neurosurgery. 2000;47:1449–51. Matsumoto T, Okuda S, Haku T, Maeda K, Maeno T, Yamashita T, et al. Neurogenic shock immediately following posterior lumbar interbody fusion: report of two cases. Global Spine J. 2015;5:e13–6. https://doi.org/10.1055/s-­0034-­1395422. Nishi S, Hashimoto N, Takagi Y, Tsukahara T. Herniation and entrapment of a nerve root secondary to an unrepaired small dural laceration at lumbar hemilaminectomies. Spine (Phila Pa 1976). 1995;20:2576– 9. https://doi.org/10.1097/00007632-­199512000-­00020. O’Connor D, Maskery N, Griffiths WE.  Pseudomeningocele nerve root entrapment after lumbar discectomy. Spine (Phila Pa 1976). 1998;23:1501–2. https://doi. org/10.1097/00007632-­199807010-­00014.

Further Reading Odate S, Shikata J.  Spinal nerve root herniation into a pseudomeningocele associated with lumbar spondylolysis: a case report. J Orthop Surg (Hong Kong). 2010;18:367–9. https://doi. org/10.1177/230949901001800323. Oterdoom DL, Groen RJ, Coppes MH.  Cauda equina entrapment in a pseudomeningocele after lumbar schwannoma extirpation. Eur Spine J. 2010;19(Suppl 2):S158–61. https://doi.org/10.1007/ s00586-­009-­1219-­y. Pavlou G, Bucur SD, van Hille PT.  Entrapped spinal nerve roots in a pseudomeningocoele as a complication of previous spinal surgery. Acta Neurochir. 2006;148:215–9. https://doi.org/10.1007/ s00701-­005-­0696-­y. Popadic B, Scheichel F, Themesl M, Decristoforo I, Sherif C, Marhold F.  Nerve root herniation with entrapment in the facet joint gap after lumbar decompression surgery: a case presentation. BMC Musculoskelet Disord. 2021;22:736. https://doi.org/10.1186/ s12891-­021-­04601-­1. Rahyussalim AJ, Djaja YP, Saleh I, Safri AY, Kurniawati T. Preservation and tissue handling technique on iatrogenic dural tear with

833 herniated nerve root at cauda equina level. Case Rep Orthop. 2016;2016:4903143. https://doi.org/10.1155/2016/4903143. Shu W, Wang H, Zhu H, Li Y, Zhang J, Lu G, Ni B. Nerve root entrapment with pseudomeningocele after percutaneous endoscopic lumbar discectomy: a case report. J Spinal Cord Med. 2020;43:552–5. https://doi.org/10.1080/10790268.2018.1507802. Tewari VK, Gupta HK. Reposing the herniated spinal nerves following accidental iatrogenic dural tear in spine surgery-the “no touch hip flexion technique”. J Neurosci Rural Pract. 2014;5:S106–7. https:// doi.org/10.4103/0976-­3147.145245. Töppich HG, Feldmann H, Sandvoss G, Meyer F.  Intervertebral space nerve root entrapment after lumbar disc surgery. Two cases. Spine (Phila Pa 1976). 1994;19:249–50. https://doi. org/10.1097/00007632-­199401001-­00021. Yan L, Liu Y, He B, Liu J, Luo Z, Hao D. Clinical case-series report of traumatic cauda equina herniation: a pathological phenomena occurring with thoracolumbar and lumbar burst fractures. Medicine (Baltimore). 2017;96:e6446. https://doi.org/10.1097/ MD.0000000000006446.

Synovial Cysts of the Facet Joints

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79.1 Generalities and Relevance Spinal synovial cysts are benign cystic lesions attached to the facet joint (also named zygapophyseal joint) and containing clear/straw color fluid lined by a cuboid/pseudostratified membrane (Figs.  79.1 and 79.2). In the spine, these cysts are found ventral to the ligamentum flavum and they are also described in the literature as “ganglion cysts” or mostly “juxtafacet cysts”. Although the first case was described during an autopsy in 1880, the first clinical case was diagnosed by Kao et al. in 1968 in the United States. Sometimes, the cyst walls are calcified or the cyst fluid may contain gas or blood. Most intraspinal synovial cysts occur in the lower lumbar column, especially around L4-L5 vertebral level which is the most mobile lumbar segment. The etiology of synovial cysts is supposed to be related to hypermobility or trauma of the

Fig. 79.2  Microscopic image of a lumbar spinal synovial cyst. There is a cystic structure with papillary projections lined by a layer of flat and elongated synovial cells (arrows) (hematoxylin & eosin, ×100). (Courtesy of Pr. Mohamed Amine Azami)

Fig. 79.1  Microscopic image showing a cystic structure lined by a pseudostratified membrane with synovial cells (arrows), compatible with a synovial cyst (hematoxylin-eosin stain, ×60). (Courtesy of Pr. Mohamed Amine Azami)

facet joints. These cysts are also correlated to the degenerative phenomenon. Indeed, most of them are classically associated with adjacent facet joint arthropathy or spondylosis. Some cases may be accompanied by spinal instability such as spondylolisthesis. In six cases, the lumbar synovial cysts are caused by calcium pyrophosphate dihydrate crystal deposition [c.f. Chap. 50 about Lumbar Spinal Gout and Pseudogout]. Due to the widespread use of MRI in spinal diagnostics, lumbar synovial cysts are nowadays considered relatively common especially in the adult population over the age of 60  years with a small female predominance. Unilateral or

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_79

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bilateral, most cases develop in the anterolateral epidural space and may result in sciatic pain in a large number of patients.

79.2 Clinical Presentations Clinical presentations depend on the volume of the cyst, its site, and its relationship to the surrounding bony and neural structures. Most patients with a lumbar facet joint syndrome show a positive Kemp sign (AKA quadrant test or extension-­rotation test), which is attributable to a facet joint pathology (i.e., degenerative or inflammatory). This provocative test combines forced dorsolateral extension and rotation of the lower back. The Kemp test is considered positive when the patient reports pain, numbness, or tingling in the affected region. However, this test can also be positive for any nerve root compression or narrowing in the extraforaminal area. Most of the symptomatic patients present with radicular pain especially sciatica and neurological deficits. A history of low-back pain may precede the radicular pain as well as a facet joint syndrome which is a clinical condition in which the facet joints become a source of pain. Concomitant low back pain is aggravated by lumbar spine extension. The most frequently occurring symptom is unilateral or bilateral painful radiculopathy followed by neurogenic claudication. Neurological deficits are less frequent and include sensory and/or motor deficits with or without reflex abnormalities. Although rare, severe cases can present with more serious neurologic conditions such as partial or complete cauda equina syndrome due to large cyst compression or coexistence of lumbar spinal stenosis. A sudden exacerbation in pain may be due to acute bleeding within the cyst contents or a rapidly enlarging cyst. However, many cases will remain asymptomatic and the cyst will be found only incidentally on MRI.

79  Synovial Cysts of the Facet Joints

79.3 Imaging Features On computed tomography (CT) scan, the synovial cyst appears as a benign low-density extradural cystic lesion adjacent to a facet joint. Degenerative spinal joint disease may also be seen (Fig. 79.3). Some cyst walls are calcified and certain cysts may contain gas or hemorrhage (Fig. 79.4). A bony CT scan may be useful for identifying possible secondary bone changes such as erosion of the bony lamina or the posterior vertebral body (scalloping). On MRI, there are typically well-defined thin-walled juxtafacet lesions and the contents display the signal intensity of water on all sequences (Figs.  79.5, 79.6, 79.7, 79.8, 79.9, 79.10, and 79.11). Mural enhancement may be seen following contrast injection. However, gadolinium administration is rarely required. Very rarely secondary acute bleeding or inflammation may occur within the cyst, changing its signal characteristics, and it may present with a high signal on T1 and a heterogeneous low signal on T2-weighted images. Intracystic contrast injection can be useful in differentiating between synovial cysts and other epidural degenerative cysts. Occasionally, imaging appearances are atypical and may be confused with other possible cystic lesions in the lumbosacral region such as: • • • • • • •

Tarlov or arachnoid cysts Ligamentum flavum cyst Meningocele Nerve sheath tumor Epidural abscess Hematoma Hydatidosis

79.3  Imaging Features

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Fig. 79.3  Case 1. Degenerative zygapophyseal joint changes (arrows) at Right-sided L4-L5 in a patient with adjacent synovial cyst. Axial (a, b) and sagittal reconstruction (c) CT scan of the lumbosacral spine

Fig. 79.4  Case 2. Calcified synovial cyst at right L5-S1 facet joint (arrows) as seen on axial CT scan on parenchymal (a) and bone (b) windows. (Courtesy of Pr. Redouane Roukhsi)

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79  Synovial Cysts of the Facet Joints

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Fig. 79.5  Case 1. Giant synovial cyst arising from right L4-L5 facet joint (arrows) as seen on axial T2-weighted MRI (a, b) and CISS sequences (c, d). Note the communication between the synovial cyst and the facet joint (arrowheads)

79.3  Imaging Features Fig. 79.6  L4-L5 synovial cyst (arrows) as seen on axial (a) and sagittal (b) T2-weighted MRI. Note compression of the homolateral L5 nerve root

Fig. 79.7  Left-sided L3-L4 synovial cyst (arrows) as seen on axial (a) and sagittal (b) T2-weighted MRI

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79  Synovial Cysts of the Facet Joints

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Fig. 79.8  L4-L5 synovial cyst (arrows) with severe central spinal stenosis as seen on sagittal T1- (a) and T2-weighted MRI (b) as well as on axial T2-weighted MRI (c, d)

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Fig. 79.9  Synovial cyst (arrows) at L4-L5 vertebral level as seen on sagittal T1- (a), T2- (b), and STIR sequences (c)

79.3  Imaging Features

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Fig. 79.10  Case 2. Calcified synovial cyst at right L5-S1 facet joint (arrows) as seen on sagittal T1- (a) and T2- weighted MRI (b) as well as on axial T2-weighted MRI (c)

Fig. 79.11  Extraforaminal L3-L5 synovial cyst (arrow) as seen on axial T2-weighted MRI

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79.4 Treatment Options and Prognosis Lumbar synovial cysts can be managed conservatively or surgically. Conservative therapy includes pain control medications, physiotherapy, and other physical modalities resulting in more or less control of the patient’s pain. Surgical treatment is largely recommended in all cases of intractable pain such as sciatica or neurological deficit. Surgical procedures comprise radicular decompression which offers neurologic and painful relief for many cases. The cyst may be adherent to the dura or to the nerve root. Most typical cases will be operated on via small flavectomy followed by complete cyst excision. If needed, a more extensive approach will be used such as hemilaminectomy or full decompressive bilateral laminectomy, especially in patients with associated stenotic spinal canal or those with a voluminous synovial cyst (Fig. 79.12). Care should be taken to minimize joint damage and the possibility of cerebrospinal leaks.

79  Synovial Cysts of the Facet Joints

Rarely, a spinal fusion, with or without instrumentation, may be suggested if there is a supposed instability, particularly in patients with associated lumbar spondylolisthesis. A percutaneous approach was used under CT scan-guided access into the inferior articular recess using a spinal needle. When the intra-articular site is recognized via contrast injection, and communication with the synovial cyst is established, rupture of the cyst is tried using a steroid/anesthetic mixture with acceptable long-term results. Some physicians promote only cyst aspiration; however, most cysts recur after a few months. Postoperatively, the outcomes are excellent or good in nearly all of the patients; however, cyst recurrence is not rare. Some rare cysts may resolve spontaneously.

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Fig. 79.12  Case 1. Intraoperative views of the synovial cyst before (a, b) and after the resection (c, d). Note the cyst content after opening (d)

Further Reading

Further Reading Akhaddar A, Qamouss O, Belhachmi A, Elasri A, Okacha N, Boucetta M. Cervico-thoracic juxtafacet cyst causing spinal foraminal widening. Joint Bone Spine. 2008;75:747–9. https://doi.org/10.1016/j. jbspin.2008.04.009. Amoretti N, Huwart L, Foti P, Boileau P, Amoretti ME, Pellegrin A, et  al. Symptomatic lumbar facet joint cysts treated by CT-guided intracystic and intra-articular steroid injections. Eur Radiol. 2012;22:2836–40. https://doi.org/10.1007/s00330-­012-­2533-­z. Arthur B, Lewkonia P, Quon JA, Street J, Bishop PB. Acute sciatica and progressive neurological deficit secondary to facet synovial cysts: a report of two cases. J Can Chiropr Assoc. 2012;56:173–8. Bandiera S, Campanacci L, De Iure F, Bertoni F, Picci P, Boriani S. Hemorrhagic synovial lumbar cyst: a case report and review of the literature. Chir Organi Mov. 1999;84:197–203. Boody BS, Savage JW. Evaluation and treatment of lumbar facet cysts. J Am Acad Orthop Surg. 2016;24:829–42. https://doi.org/10.5435/ JAAOS-­D-­14-­00461. Boviatsis EJ, Stavrinou LC, Kouyialis AT, Gavra MM, Stavrinou PC, Themistokleous M, et  al. Spinal synovial cysts: pathogenesis, ­diagnosis and surgical treatment in a series of seven cases and literature review. Eur Spine J. 2008;17:831–7. https://doi.org/10.1007/ s00586-­007-­0563-­z. Bruder M, Cattani A, Gessler F, Droste C, Setzer M, Seifert V, et al. Synovial cysts of the spine: long-term follow-up after surgical treatment of 141 cases in a single-center series and comprehensive literature review of 2900 degenerative spinal cysts. J Neurosurg Spine. 2017;27:256–67. https://doi.org/10.3171/2016.12.SPINE16756. Campbell RJ, Mobbs RJ, Rao PJ, Phan K.  Interventions for lumbar synovial facet joint cysts: a comparison of percutaneous, surgical decompression and fusion approaches. World Neurosurg. 2017;98:492–502. https://doi.org/10.1016/j.wneu.2016.11.044. Epstein NE.  Lumbar synovial cysts: a review of diagnosis, surgical management, and outcome assessment. J Spinal Disord Tech. 2004;17:321–5. https://doi.org/10.1097/01.bsd.0000096267.75190. eb. Epstein NE, Baisden J.  The diagnosis and management of synovial cysts: efficacy of surgery versus cyst aspiration. Surg Neurol Int. 2012;3:S157–66. https://doi.org/10.4103/2152-­7806.98576. Ewald C, Kalff R.  Resolution of a synovial cyst of the lumbar spine without surgical therapy—a case report. Zentralbl Neurochir. 2005;66:147–51. https://doi.org/10.1055/s-­2005-­836475. Gadgil AA, Eisenstein SM, Darby A, Cassar Pullicino V.  Bilateral symptomatic synovial cysts of the lumbar spine caused by calcium pyrophosphate deposition disease: a case report. Spine (Phila Pa 1976). 2002;27:E428–31. https://doi. org/10.1097/00007632-­200210010-­00024. Garg K, Kasliwal MK.  Outcomes and complications following minimally invasive excision of synovial cysts of the lumbar spine: a systematic review and meta-analysis. Clin Neurol Neurosurg. 2021;206:106667. https://doi.org/10.1016/j.clineuro.2021.106667. Hadhri K, Salah MB, Bellil M.  Lumbar synovial cyst causing cauda Equina syndrome. Neurol India. 2022;70:1684. https://doi. org/10.4103/0028-­3886.355166.

843 Haider SJ, Na NR, Eskey CJ, Fried JG, Ring NY, Bao MH, et  al. Symptomatic lumbar facet synovial cysts: clinical outcomes following percutaneous CT-guided cyst rupture with intra-articular steroid injection. J Vasc Interv Radiol. 2017;28:1083–9. https://doi. org/10.1016/j.jvir.2017.04.021. Ikeda O, Minami N, Yamazaki M, Koda M, Morinaga T. Hemorrhagic lumbar facet cysts accompanying a spinal subdural hematoma at the same level. J Spinal Cord Med. 2015;38:239–44. https://doi.org/10. 1179/2045772314Y.0000000216. Khan AM, Girardi F.  Spinal lumbar synovial cysts. Diagnosis and management challenge. Eur Spine J. 2006;15:1176–82. https://doi. org/10.1007/s00586-­005-­0009-­4. Kao CC, Uihlein A, Bickel WH, Soule EH. Lumbar intraspinal extradural ganglion cyst. J Neurosurg. 1968;29:168–72. https://doi. org/10.3171/jns.1968.29.2.0168. Mahmud T, Basu D, Dyson PH. Crystal arthropathy of the lumbar spine: a series of six cases and a review of the literature. J Bone Joint Surg Br. 2005;87:513–7. https://doi.org/10.1302/0301-­620X.87B4.15555. Namazie MR, Fosbender MR.  Calcium pyrophosphate dihydrate crystal deposition of multiple lumbar facet joints: a case report. J Orthop Surg (Hong Kong). 2012;20:254–6. https://doi. org/10.1177/230949901202000225. Perolat R, Kastler A, Nicot B, Pellat JM, Tahon F, Attye A, et  al. Facet joint syndrome: from diagnosis to interventional management. Insights Imaging. 2018;9:773–89. https://doi.org/10.1007/ s13244-­018-­0638-­x. Reddy P, Satyanarayana S, Nanda A.  Synovial cyst of lumbar spine presenting as disc disease: a case report and review of literature. J La State Med Soc. 2000;152:563–6. Ramieri A, Domenicucci M, Seferi A, Paolini S, Petrozza V, Delfini R.  Lumbar hemorrhagic synovial cysts: diagnosis, pathogenesis, and treatment. Report of 3 cases. Surg Neurol. 2006;65:385–90. https://doi.org/10.1016/j.surneu.2005.07.073. Scholz C, Hubbe U, Kogias E, Klingler JH.  Incomplete resection of lumbar synovial cysts—evaluating the risk of recurrence. Clin Neurol Neurosurg. 2015;136:29–32. https://doi.org/10.1016/j. clineuro.2015.05.028. Shtaya A, Sadek AR, Walker M, Nader-Sepahi A. Ventral lumbar synovial cyst causing cauda equina compression: case report and literature review. World Neurosurg. 2017;106:1055.e1–3. https://doi. org/10.1016/j.wneu.2017.07.068. Sinha P, Panbehchi S, Lee MT, Parekh T, Pal D.  Spontaneous resolution of symptomatic lumbar synovial cyst. J Surg Case Rep. 2016;2016:rjw166. https://doi.org/10.1093/jscr/rjw166. Suo S, Chen Y, Mao X, Chen S, Fu Z. Percutaneous endoscopic surgery for lumbar discal cyst: two case reports. J Med Cases. 2020;11:178– 81. https://doi.org/10.14740/jmc3474. van Kleef M, Vanelderen P, Cohen SP, Lataster A, Van Zundert J, Mekhail N. 12. Pain originating from the lumbar facet joints. Pain Pract. 2010;10:459–69. https://doi. org/10.1111/j.1533-­2500.2010.00393.x.

Ligamentum Flavum Cystic Lesions

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80.1 Generalities and Relevance

80.2 Clinical Presentations

Cysts of the ligamentum flavum, also known as “flaval cysts”, are benign fluid collections developed within the layers of the ligamentum flavum (yellow ligament). Most cases grow into the anterolateral spinal epidural space and may compress the neural elements and result in a neurological disturbance in many patients. In the lumbar region, a considerable number of cases will manifest as unilateral or bilateral sciatica. However, some cases remain asymptomatic. This rare entity was first described in the English literature by Moil et al. in 1967. Since then, a hundred cases have been reported, preferentially located in the spinal lumbar region (90%), and less frequently in the cervical spine (10%). The L4-L5 level was, by far, the favored site. Classically, this cystic lesion had no connection with the dural sac, nerve roots, facet joints, or other spinal ligaments. However, many reported cases have been confused with synovial or ganglion cysts. In histopathology study, the cysts contain clear serous or mucous fluid with a collagenous fibrous wall. Myxoid degeneration may also be seen as well as infiltration of inflammatory cells and areas of calcification. Unlike synovial cysts, there is no epithelial or synovial lining. However, the cyst fluid may contain air or blood. One case developed a tubercular ligamentum flavum cyst. The exact pathogenesis of flaval cyst is not well clarified, but it has supposed to be related to hypermobility, persistent micro-instability, and concomitant repetitive microtrauma of the affected spinal segment. Overall, the context of degenerative spinal changes is often considered. Indeed, most ligamentum flavum cysts are reported in the middle-aged and elderly without sex predilection.

Clinical presentations depend on the volume of the cyst, its site, and its relationship to the surrounding bony and neural structures. In the lumbar spine, cysts of the ligamentum flavum may induce various degrees of progressive or acute neurological deterioration by compressing one or multiple cauda equina nerve roots. Asymmetric compression may present with unilateral radicular pain and mimic typical lumbar disc herniation or foraminal stenosis. The central situation of the cyst into the lumbar spinal canal may manifest as symptoms of lumbar canal stenosis with classic neurogenic claudication. The most common presenting feature is lumbosacral radicular pain (about 97%) [mainly unilateral and a single nerve root] followed by sensory changes (55%), motor deficits (39%), a positive Lasègue sign (33%), and osteotendinous reflex abnormalities (18%). Although rare, severe cases can present with more serious neurologic conditions such as partial or complete cauda equina syndrome due to large cyst compression or coexistence of lumbar spinal stenosis. A sudden exacerbation in radicular pain may be due to acute bleeding within the cyst contents. With the increasing usage of neuroimaging techniques, many incidental asymptomatic cysts are being discovered on computed tomography (CT) scan and/or magnetic resonance imaging (MRI).

80.3 Imaging Features On CT scan, the flaval cyst appears as a benign low or isodense extradural cystic lesion attached to the ligamentum flavum medially or laterally (Fig. 80.1). Concomitant degen-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_80

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846 Fig. 80.1  A ligamentum flavum cyst on axial (a) and coronal reconstruction (b) CT scan. The cyst looks as a benign hypodense extradural cystic lesion attached to the ligamentum flavum laterally on L3-L4 (arrows)

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80  Ligamentum Flavum Cystic Lesions

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Fig. 80.2  Sagittal T1- (a) and T2-weighted MRI (b) as well as axial T2-weighted MRI (c, d) showing a typical well-defined cystic lesion involving a thickened ligamentum flavum on L4-L5 (arrows)

erative discal and/or spinal joint lesions may also be seen. Wall calcifications are rare but certain cysts may contain gas or hemorrhage. Generally, there is a typical well-defined cystic lesion involving a thickened ligamentum flavum on MRI. There was no communication with the intervertebral disc or the

zygapophyseal joints. The contents display the signal intensity of water on all sequences (Figs. 80.2, 80.3, and 80.4). Mural enhancement may be seen following contrast injection. However, gadolinium administration is rarely required. Very rarely secondary acute bleeding or inflammation may occur within the cyst, changing its signal char-

80.3  Imaging Features

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Fig. 80.3  Axial (a, b) and sagittal (c) T2-weighted MRI showing a well-defined cystic lesion of the ligamentum flavum on L3-L4 (arrows)

acteristics, and it may present with an iso-high signal on T1 and a heterogeneous low signal on T2-weighted images. Intracystic contrast injection can be useful in differentiating between flaval cysts and synovial cysts but this is rarely used. Sometimes imaging appearances are atypical and may be confused with other possible cystic lesions in the lumbosacral region such as:

–– –– –– –– –– –– –– ––

Juxta-articular cysts (ganglion and synovial cyst) Discal cyst Tarlov or Arachnoid cysts Meningocele Cystic nerve sheath tumors Dermoid or epidermoid cysts Epidural abscess or Hematoma Rheumatoid arthritis pannus

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80  Ligamentum Flavum Cystic Lesions

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Fig. 80.4  An L3-L4 ligamentum flavum cyst (arrows) with concomitant lumbar spinal stenosis on axial (a, b) and sagittal (c) T2-weighted MRI

80.4 Treatment Options and Prognosis Ligamentum flavum cysts can be managed conservatively or surgically. Conservative therapy includes pain control medications, physiotherapy, and other physical modalities resulting in more or less control of the patient’s pain. Conservative treatment associated with a percutaneous approach under a CT scan (aspiration with or without steroid injection) can achieve a varying degree of success. However, it seems that flaval cysts are less controllable with conservative therapy, and surgical treatment may often be considered as the initial management.

The aim of surgery is to remove completely the cyst along with the ligamentum flavum and decompress the neural roots with preservation of the facet joint. The cyst may be adherent to the dura mater or to the nerve root, an especially large cyst. Most cases will be operated on via an interlaminar approach. If needed, a more extensive approach will be used such as a hemilaminectomy. Care should be taken to minimize nerve root damage and the possibility of CSF leaks. Dura matter adhesions are known to be the main reason for incomplete cystic excision.

Further Reading

Recently, endoscopic resection of a ligamentum flavum cyst through the interlaminar approach was reported in two patients with good results. Generally, postoperative complications are mild and rare. The majority of patients showed good clinical results after full surgical excision of the cyst and the affected yellow ligament. Recurrence of a ligamentum flavum cyst is rare (6%) and occurs especially in patients following incomplete surgical resection.

Further Reading Gazzeri R, Canova A, Fiore C, Galarza M, Neroni M, Giordano M. Acute hemorrhagic cyst of the ligamentum flavum. J Spinal Disord Tech. 2007;20:536–8. https://doi.org/10.1097/BSD.0b013e31804b4605. Kalidindi KKV, Bhat MR, Gupta M, Mannem A, Chhabra HS.  Ligamentum flavum cyst with acute onset motor deficit: a ­literature review and case series. Int J Spine Surg. 2020;14:544–51. https://doi.org/10.14444/7072. Kim HS, Singh R, Adsul NM, Oh SW, Noh JH, Kim PY, et  al. Symptomatic tuberculous ligamentum Flavum cyst treated by full endoscopic resection: review with technical notes. World Neurosurg. 2019;122:112–5. https://doi.org/10.1016/j.wneu.2018.10.141. Mahallati H, Wallace CJ, Hunter KM, Bilbao JM, Clark AW.  MR imaging of a hemorrhagic and granulomatous cyst of the ligamentum flavum with pathologic correlation. AJNR Am J Neuroradiol. 1999;20:1166–8.

849 Moiel RH, Ehni G, Anderson MS. Nodule of the ligamentum flavum as a cause of nerve root compression. Case report. J Neurosurg. 1967;27:456–8. https://doi.org/10.3171/jns.1967.27.5.0456. Seo DH, Park HR, Oh JS, Doh JW. Ligamentum flavum cyst of lumbar spine: a case report and literature review. Korean J Spine. 2014;11:18–21. https://doi.org/10.14245/kjs.2014.11.1.18. Shah K, Segui D, Gonzalez-Arias S. Midline ligamentum Flavum cyst of lumbar spine. World Neurosurg. 2018;110:284–7. https://doi. org/10.1016/j.wneu.2017.11.075. Sharma SB, Lin GX, Kim JS. Full-endoscopic resection of ligamentum flavum cyst in lumbar spine. World Neurosurg. 2019;130:427–31. https://doi.org/10.1016/j.wneu.2019.07.120. Singh V, Rustagi T, Mahajan R, Priyadarshini M, Das K. Ligamentum ­ flavum cyst: rare presentation report and literature review. Neurol India. 2020;68:1207–10. https://doi. org/10.4103/0028-­3886.299172. Taha H, Bareksei Y, Albanna W, Schirmer M.  Ligamentum flavum cyst in the lumbar spine: a case report and review of the literature. J Orthop Traumatol. 2010;11:117–22. https://doi.org/10.1007/ s10195-­010-­0094-­y. Vernet O, Fankhauser H, Schnyder P, Déruaz JP. Cyst of the ligamentum flavum: report of six cases. Neurosurgery. 1991;29:277–83. https://doi.org/10.1097/00006123-­199108000-­00021. Watanabe K, Mitsui K, Sasaki J, Kumaki D. Subacute hemorrhagic cyst of the ligamentum flavum occurred in the lumbosacral transitional vertebra presenting as progressive lumbar nerve root compression: a case report. J Spine Surg. 2021;7:238–43. https://doi.org/10.21037/ jss-­20-­683. Wildi LM, Kurrer MO, Benini A, Weishaupt D, Michel BA, Brühlmann P. Pseudocystic degeneration of the lumbar ligamentum flavum: a little known entity. J Spinal Disord Tech. 2004;17:395–400. https:// doi.org/10.1097/01.bsd.0000109837.59382.0e.

Ligamentum Flavum Ossifications

81.1 Generalities and Relevance Ligamentum flavum ossification (LFO) or “ossified yellow ligament” is an uncommon pathologic entity characterized by heterotopic endochondral ossification of the ligamentum flavum. It may induce spinal canal stenosis with subsequent development of myelopathy and/or radiculopathy due to direct neurologic compression, ischemia, or stretching. However, some cases remain asymptomatic. Sometimes, LFO may be confused with calcification of juxtafacet cysts, hypertrophic facet joint degeneration, or calcification of ligamentum flavum cysts. In histopathology study, there is a mixture of fibrosis, calcification, and ossification within the yellow ligament. The adjacent dura matter can also be involved. The ossification can be localized to only one or two vertebral segments; however, several segments can be involved in about 20% of cases. Sato et  al. in 1998 classified LFO according to its development on lateral, extended, enlarged, fused, or tuberous types. Since first described by Polgar in 1920, the disease most commonly affects the lower thoracic spine, upper/middle thoracic spine, and less frequently in the cervical spinal region. The frequency of lumbar LFO is much lower than that of the other spinal sites. Indeed, the first cases of lumbar LFO were not published in the English literature until the 1970s. Concomitant ossification of other spinal ligaments may be seen in the same or different spinal segments such as anterior or posterior spinal ligaments. In addition, co-­existing lumbar disc herniation or spinal degenerative lesions are not rare. The cause of LFO is not well determined, but there is an increasing incidence of diffuse idiopathic skeletal hyperostosis (also known as ankylosing hyperostosis), ankylosing spondylitis, Paget’s disease, fluorosis, disorders in calcium metabolism, obesity, and diabetes mellitus. Other multifactorial conditions like genetic, environmental, or lifestyle fac-

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tors seem to play a role. Also, spinal hypermobility and mechanical stress are often considered. The prevalence of symptomatic LFO increases with age, especially among patients over 50 years of age with a male predominance. Once considered a disease limited to patients from Asian ethnic groups (particularly the Japanese), it is now encountered in other populations outside Asia. Rarely, some LFOs may involve the thoraco-lumbar junction and induce lumbosacral radicular pain (c.f. Chap. 43 about Conus Medullaris Lesions).

81.2 Clinical Presentations In the lumbar spine, LFO can cause varying degrees of neurological symptoms depending on the size of the ossifications, their exact site and extension, their relationship to the surrounding neural structures, and coexisting lumbar disc herniation or other ossified spinal ligaments. An asymmetric extension may lead to unilateral radicular pain and mimic typical lumbar disc herniation or foraminal stenosis. Overall, symptoms are similar to those recognized in cases of degenerative central lumbar spinal stenosis such as lumbar intermittent claudication and/or bilateral lumbosacral radiculopathies. However, because of the insidious progression of the ossifications, lumbosacral nerve damages are more severe than those encountered in other causes of lumbar stenosis particularly lower limb motor weakness and urinary disturbances. Most of the symptomatic patients present with progressive neurologic symptoms evolving for several months before diagnosis. A history of low-back pain may precede the radicular pain. Acute presentations are rare. You should know that many patients with LFO will remain asymptomatic and the ossification will be found only incidentally on computed tomography (CT) scan or magnetic resonance imaging (MRI).

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81.3 Imaging Features Plain radiography often fails to show the LFO.  Without a post-myelography CT scan, which is an invasive imaging technic, a combination of CT scan and MRI is a complementary tool for the diagnosis of an ossified yellow ligament in addition to planning surgical intervention. On MRI, there is a thickened area within the ligamentum flavum which is hypointense on both T1- and T2-weighted images. The ossification was seen to compress the thecal sac postero-laterally and the nerve roots laterally (Fig. 81.1). Sagittal images are particularly useful in evaluating neural structures. There is no enhancement following gadolinium injection. However, bone marrow may be seen within the area of ossification in thicker lesions. Interestingly, complete spine T2-weighted sagittal images should be achieved in all patients with LFO because of the risk of co-existing multiple-level ossification as well as combined degenerative pathologies.

Fig. 81.1  L3-L4 bony density mass attached to the adjacent spinal laminae on the left side causing adjacent foraminal stenosis (arrows) as seen on sagittal reconstruction (a) and axial (b) CT scan as well as on axial T2-weighted MR imaging (c). Note that the bone marrow is seen within this ossified lesion (arrow) (c)

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On CT scan, LFO appears as a bony density mass attached to the adjacent spinal laminae. The ossification may be ­unilateral or bilateral and developed on the postero-lateral epidural space. Reconstruction CT scan on bone windows is important for determining the thickness, the form of the ossification, its extension, and the degree of spinal canal stenosis (Figs. 81.1, 81.2, 81.3, and 81.4). Electromyographic procedures help identify nerve root lesions of the cauda equina but are rarely required. The differential diagnosis of LFO includes other calcified or ossified epidural lesions encountered in the lumbosacral region such as: • • • • • • •

Calcified lumbar disc herniation Calcified juxtafacet or ligamentum flavum cysts Calcified or ossified posterior longitudinal ligament Posterior ring apophysis separation Hypertrophic facet joints degeneration Hypertrophic ligamentum flavum Calcified tumors especially meningioma or schwannoma

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81.3  Imaging Features

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Fig. 81.2  L4-L5 ossified yellow ligament on the left side (arrows) as seen on axial CT scan (a–c). This lesion causes posterolateral spinal canal stenosis at these vertebral levels

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Fig. 81.3  Bilateral ossification of the yellow ligaments at L4-L5 vertebral level (arrows) as seen on axial CT scan on parenchymal (a–c) and bone (d–f) windows. These lesions are responsible for a lumbar central spinal stenosis

854 Fig. 81.4  Co-existence of a posterior longitudinal ligament ossification (a) and a bilateral ossified yellow ligaments (b) in the same patient (arrows) as seen on axial CT scan (a, b)

81  Ligamentum Flavum Ossifications

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81.4 Treatment Options and Prognosis Lumbar ossified ligamentum flavum can be managed conservatively or surgically. Conservative treatment modalities include bed rest, pain control medications, anti-inflammatory medications, and physiotherapy resulting in more or less control of the patient’s pain. For patients with tolerable pain or without neurologic deficits, the literature suggests initially conservative measures. The aim of surgery is to decompress the neural roots with resection of the ossified ligament as much as possible. No standard surgical procedure exists for the treatment of lumbar LFO.  There are various surgical techniques for nerve decompression using a posterior approach. However, most cases were operated on via a partial or complete laminectomy with partial medial facetectomy. Laminotomy, laminoplasty, or interlaminar fenestration have also been suggested. High-speed burrs may be helpful for the excision of the ossification. If needed, a unilateral or bilateral lateral recess decompression can be performed. Also, an additional herniated disc will be removed at the time of surgery. Care should be taken to minimize nerve root damage and the possibility of incidental durotomy and CSF leak (up to 30%). If needed, posterior lumbar fusion with or without posterior instrumentations can be performed. An additional herniated disc will be removed at the time of surgery. Recently, microendoscopic posterior decompression with resection of ossified ligamentum flavum through the interlaminal or translaminal approaches were performed in some patients with good results. Postoperative complications are not rare and more frequent with dural ossification. Surgeons should be aware of about the possibility of adhesions between LFO and dura matter or nerve roots, particularly large and extensive ossifications.

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Long-standing motor deficits and urinary incontinence did not recover completely. Early diagnosis and early decompression are the most important factors for obtaining better outcomes. Overall, the result is better than that of patients with cervical or thoracic LFO. Recurrences are possible but rare.

Further Reading Ahn DK, Lee S, Moon SH, Boo KH, Chang BK, Lee JI. Ossification of the ligamentum flavum. Asian Spine J. 2014;8:89–96. https://doi. org/10.4184/asj.2014.8.1.89. Akhaddar A, Mansouri A, Zrara I, Gazzaz M, Maftah M, Benomar S, et  al. Thoracic spinal cord compression by ligamentum flavum ossifications. Joint Bone Spine. 2002;69:319–23. https://doi. org/10.1016/s1297-­319x(02)00400-­1. Akhaddar A, Boucetta M.  Letter to the editor regarding “ossification of the ligamentum flavum at the thoracic and lumbar region in an achondroplastic patient”. World Neurosurg. 2020;143:585–6. https://doi.org/10.1016/j.wneu.2020.07.023. Al-Jarallah K, Al-Saeed O, Shehab D, Dashti K, Sheikh M.  Ossification of ligamentum flavum in Middle East Arabs: a hospital-based study. Med Princ Pract. 2012;21:529–33. https://doi. org/10.1159/000339120. Iwai H, Inanami H, Koga H.  Full-endoscopic spine surgery for the treatment of lumbar ossification of the ligamentum flavum: technical report. World Neurosurg. 2020;142:487–94.e1. https://doi. org/10.1016/j.wneu.2020.06.132. Jaffan I, Abu-Serieh B, Duprez T, Cosnard G, Raftopoulos C. Unusual CT/MR features of putative ligamentum flavum ossification in a north African woman. Br J Radiol. 2006;79:e67–70. https://doi. org/10.1259/bjr/15381140. Kato K, Yabuki S, Otani K, Nikaido T, Otoshi KI, Watanabe K, et al. Ossification of the ligamentum flavum in the thoracic spine mimicking sciatica in a young baseball pitcher: a case report. Fukushima J Med Sci. 2021;67:33–7. https://doi.org/10.5387/fms.2020-­26. Pantazis G, Tsitsopoulos P, Bibis A, Mihas C, Chatzistamou I, Kouzelis C. Symptomatic ossification of the ligamentum flavum at the lumbar spine: a retrospective study. Spine (Phila Pa 1976). 2008;33:306–11. https://doi.org/10.1097/BRS.0b013e3181624535. Perna F, Geraci G, Mazzotti A, Stefanini N, Panciera A, Faldini C.  Acute presentation of lumbar spinal stenosis due to ossified ligamentum Flavum: the possible role of spondylolisthesis: a case

Further Reading report. JBJS Case Connect. 2019;9:e0039. https://doi.org/10.2106/ JBJS.CC.18.00039. Polgar F.  Uber interakuelle wirbelverkalkung. Fort Geb Rant Nukle Ergan. 1920;40:292–8. Sidronio T, Kumar S.  Ossification of the ligamentum flavum of the lumbar spine. Cureus. 2021;13:e19023. https://doi.org/10.7759/ cureus.19023. Tamai K, Kaneda K, Iwamae M, Terai H, Katsuda H, Shimada N, et al. The short-term outcomes of minimally invasive decompression sur-

855 gery in patients with lumbar ossification or calcification of the ligamentum flavum. J Neurosurg Spine. 2020:1–8. https://doi.org/10.31 71/2020.6.SPINE20946. Weiss MH, Spencer GE. Ossification of a lumbar interspinous ligament with compression of the cauda equina. A case report. J Bone Joint Surg Am. 1970;52:165–7. Yoshii S, Ikeda K, Murakami H. Myxomatous degeneration of the ligamentum flavum of the lumbar spine. Spinal Cord. 2001;39:488–91. https://doi.org/10.1038/sj.sc.3101195.

Posterior Longitudinal Ligament Cysts

82.1 Generalities and Relevance Cysts of the posterior longitudinal ligament (PLL) are benign small fluid collections developed within the layers of the spinal PLL.  They were previously described as degenerative “ganglion cysts” but they are unrelated to posterior nerve root ganglions. This appearing-cystic lesion grows into the anterolateral spinal epidural space and may compress the neural elements and result in a neurological disturbance in many patients. In the lumbar region, a considerable number of cases will manifest as unilateral or bilateral sciatica. This rare entity was first described in the English literature in the early 1990s. Since then, fewer than 20 cases have been reported; all of them restricted to the lumbar spine. Classically, the cyst had no connection with the dural sac, facet joints, or nerve roots. PLL cysts must be distinguished from discal cysts because they do not communicate with the adjacent intervertebral disc. In histopathology study, the cysts contain clear serous or mucous fluid with a collagenous fibrous wall. Myxoid degeneration may also be seen. Unlike synovial cysts, there are no epithelial or synovial layers. However, the cyst fluid may contain sometimes gas or blood.

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The etiology of synovial cysts is supposed to be related to repetitive trauma and hypermobility that may induce a chronic process of cystic degeneration of the ligament. All cases are described in young men between 17 and 40 years old, principally in athletes.

82.2 Clinical Presentations Clinical presentations depend on the volume of the cyst, its site, and its relationship to the surrounding bony, joints, and neural structures. Most of the symptomatic patients with PLL cysts present with progressive unilateral lumbosacral radicular pain related to nerve root compression but without serious neurological deficits or sphincter disturbances. A history of low-back pain may precede the radicular pain. Only one case presented with footdrop and sciatica; however, no case of cauda equina syndrome has been previously reported. Certainly, many patients with posterior longitudinal ligament cysts will remain asymptomatic and the cystic lesion will be found only incidentally on magnetic resonance imaging (MRI) as shown in Fig. 82.1.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_82

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858 Fig. 82.1 Posterior longitudinal ligament cyst (arrows) as seen on lumbar sagittal T1-weighted-MRI (a) and sagittal (b), axial (c), and coronal (d) T2-weighted MRI. Note that the cyst content is hypointense on T1-weighted sequence and hyperintense on T2-weighted sequence. (Courtesy of Pr. Salah Bellasri)

82  Posterior Longitudinal Ligament Cysts

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82.3 Imaging Features On the computed tomography (CT) scan, the intraspinal cyst appears as a low-density extradural benign round cystic lesion attached to the posterior longitudinal ligament between L3 and S1 vertebral body levels. Degenerative discal or zygapophyseal joint lesions may also be seen despite the patients’ young age. There is no enhancement following contrast injection. Some cyst walls may be calcified and certain cysts may contain gas or hemorrhage. On MRI, there is a well-defined thin-walled anterolateral cystic lesion, about 1 cm in size, within the PLL and the content is hypointense on T1-weighted sequence and hyperintense on T2-weighted sequence (Fig.  82.1). The cyst was seen to compress the dura posteromedially and the nerve root laterally. Mural enhancement may be present following intravenous gadolinium administration; however, there is no communication with the adjacent ana-

tomic structures. Intracystic contrast injection could be useful in differentiating between ganglion cysts and other epidural spinal degenerative cysts but this procedure has never been performed. Mainly because of its rarity, a PLL cyst can be confused with a number of other cystic lumbosacral intraspinal lesions like: • • • • • • • • • •

Discal cyst/pseudocyst Tarlov or arachnoid cysts Synovial cyst Ligamentum flavum cyst Meningocele Nerve sheath cystic tumor Enteric or dermoid cysts Epidural abscess Hematoma Hydatidosis

Further Reading

82.4 Treatment Options and Prognosis Initially, and outside any emergency, the lumbosacral radicular pain may be managed conservatively. Conservative therapy includes bed rest, pain control medications, physiotherapy, and other physical modalities resulting in more or less control of the patient’s pain. Surgical treatment is largely recommended in all cases of intractable radicular pain or neurological deficit. Surgical procedures comprise cyst excision and radicular ­decompression without entering the adjacent disc space. The cyst may be adherent to the dura mater or to the nerve root, especially the voluminous cyst. Most cases will be operated on via interlaminar approach and unilateral flavectomy followed by complete cyst excision. If needed, a more extensive approach will be used such as hemilaminectomy. Care should be taken to minimize nerve root damage and the possibility of cerebrospinal fluid leaks. All cases reported in the literature were operated on with total resection of the cyst walls. No postoperative complications have been reported. A complete cure was established after surgery. No recurrence was noted in the literature except in one patient. Three months after the first surgery, this patient presented with recurrent unilateral sciatica. The new cystic lesion was fully resected using a full-endoscopic approach with a good result.

Further Reading Akhaddar A.  Differential diagnosis of Intraspinal arachnoid cysts. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: state-of-the-art concepts. Switzerland: Springer International Publishing; 2022. p.  311–26. https://doi. org/10.1007/978-­3-­030-­79371-­5_26.

859 Baba H, Furusawa N, Maezawa Y, Uchida K, Kokubo Y, Imura S, et al. Ganglion cyst of the posterior longitudinal ligament causing lumbar radiculopathy: case report. Spinal Cord. 1997;35:632–5. https://doi. org/10.1038/sj.sc.3100442. Barea D, Teschner D, Chouc P, Jeandel P, Briant JF. Cyst of the lumbar posterior longitudinal ligament. An unusual cause of non-discal sciatica. J Radiol. 1996;77:579–81. Biji B, Moorthy RK, Rajshekhar V.  Posterior longitudinal ligament cyst as a rare cause of lumbosacral radiculopathy with positive straight leg raising test. Neurol India. 2008;56:96–7. https://doi. org/10.4103/0028-­3886.39330. Cho SM, Rhee WT, Lee SY, Lee SB. Ganglion cyst of the posterior longitudinal ligament causing lumbar radiculopathy. J Korean Neurosurg Soc. 2010;47:298–301. https://doi.org/10.3340/jkns.2010.47.4.298. Jadhav N, Sivakumar L, Talibi SS, Momoh P, Rasul F, Hussain R, et  al. Lumbar discal cyst and post-operative discal pseudocyst: a case series. J Surg Case Rep. 2022;2022:rjac239. https://doi. org/10.1093/jscr/rjac239. Le Breton C, Garreau de Luobresse C, Awky J, Khalil A, Sibony M, et  al. L5 radicular pain related to a cystic lesion of the posterior longitudinal ligament. Eur Radiol. 2000;10:1812–4. https://doi. org/10.1007/s003300000445. Lin RM, Wey KL, Tzeng CC.  Gas-containing “ganglion” cyst of lumbar posterior longitudinal ligament at L3. Case report. Spine (Phila Pa 1976). 1993;18:2528–32. https://doi. org/10.1097/00007632-­199312000-­00026. Marshman LA, Benjamin JC, David KM, King A, Chawda SJ. “Disc cysts” and “posterior longitudinal ligament ganglion cysts”: synonymous entities? Report of three cases and literature review. Neurosurgery. 2005;57:E818. https://doi.org/10.1093/ neurosurgery/57.4.e818. Mizutamari M, Sei A, Fujimoto T, Taniwaki T, Mizuta H. L5 radiculopathy caused by a ganglion cyst of the posterior longitudinal ligament in a teenager. Spine J. 2009;9:e11–4. https://doi.org/10.1016/j. spinee.2008.05.013. Park JH, Im SB, Kim HK, Hwang SC, Shin DS, Shin WH, et  al. Histopathological findings of hemorrhagic ganglion cyst causing acute radicular pain: a case report. Korean J Spine. 2013;10:242–5. https://doi.org/10.14245/kjs.2013.10.4.242. Simonin A, Philippe J, Fournier JY.  Full-endoscopic resection of a recurrent posterior longitudinal ligament cyst: technical note. World Neurosurg. 2021;153:2–5. https://doi.org/10.1016/j. wneu.2021.05.104.

Posterior Longitudinal Ligament Ossifications

83.1 Generalities and Relevance Ossification of the posterior longitudinal ligament (OPLL) is an uncommon pathologic entity characterized by heterotopic ossification of the posterior longitudinal ligament, as the appellation suggests. It may induce spinal canal stenosis with subsequent development of myelopathy and/or radiculopathy due to direct neurologic compression, ischemia, or stretching. Sometimes, OPLL may be confused with spinal osteophytes, posterior ring apophysis separation (PRAS) of the vertebral body, and calcification of the intervertebral disc. In histopathology study, there is a mixture of fibrosis, calcification, and ossification within the posterior longitudinal ligament. The adjacent dura matter can also be involved. In the spine, the ossification can be: • Segmental (several segments are affected, and ossification is disrupted because it does not cross the intervertebral disc) • Continuous (ossification of several vertebral body segments covering the intervertebral disc) • Mixed (both of the above) • Localized (circumscribed, only one or two segments) The disease is specially located in the cervical spine (70– 75%), and less frequently in the thoracic spinal region (15– 20%). The frequency of lumbar OPLL (10%) is much lower than that of the other spinal sites. Additional cervical, thoracic, and/or lumbar OPLL may be seen with various combinations. Also, concomitant ossification of other spinal ligaments may be seen in the same or different spinal segments such as ligament flavum and anterior longitudinal ligament ossifications. In addition, co-existing lumbar disc herniation is not rare [up to 40% of cases in the lumbar spine]. The etiology of OPLL is unknown, but there is an increasing incidence of ankylosing hyperostosis (AKA diffuse idiopathic skeletal hyperostosis or Forestier’s disease) and

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ankylosing spondylitis. Genetic, environmental, or lifestyle factors seem to play a role. The prevalence of OPLL increases with age with a mean of 53 years and a slight male predominance. Once considered a disease limited to patients from the Asian population (particularly the Japanese), it is now encountered in all ethnic groups.

83.2 Clinical Presentations The OPLL can cause varying degrees of neurological symptoms depending on the size of the ossifications, their exact site and extension, their relationship to the surrounding neural structures, and coexisting lumbar disc herniation or ossified ligamentum flavum. On the lumbar spine, many patients with OPLL will remain asymptomatic and the ossification will be found only incidentally on computed tomography (CT) scan or magnetic resonance imaging (MRI). While others have evidence of lumbar claudication and/or lumbosacral radiculopathies with or without lower leg weakness. It seems that OPLL in the upper lumbar spine is associated with lumbar intermittent claudication and those in the lower lumbar spine either with uni or bilateral radicular symptoms. Most of the symptomatic patients present with progressive neurologic symptoms evolving for more than 12  months before diagnosis. A history of low-back pain may precede the radicular pain. A partial or complete cauda equina syndrome has been previously reported but recognized as rare.

83.3 Imaging Features Plain radiography often fails to show the OPLL (Fig. 83.1). In the absence of a post-myelography CT scan, which is an invasive imaging technic, a combination of CT scan and

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MRI is a complementary tool for the diagnosis of the ossified posterior longitudinal ligament as well as for planning surgical intervention. On CT scan, OPLL appears as an ossifying mass (bony density lesion) posterior to the vertebral bodies and intervertebral discs. Reconstruction of CT scan on bone windows is important for determining the thickness, the form of the ossification, its extension, and the degree of spinal canal stenosis (Figs. 83.1 and 83.2). On MRI, there is a thickened area along the posterior longitudinal ligament which is hypointense on both T1- and T2-weighted images (Figs. 83.3, 83.4, and 83.5). The ossification was seen to compress the thecal sac antero-medially and the nerve roots laterally. Sagittal images are particularly

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Fig. 83.1  Case 1. Ossification of the posterior longitudinal ligament (arrows) as seen on lateral plain radiography (a) and sagittal reconstructions CT scan (b, c). The involved ligament appears as an ossifying

useful in evaluating neural structures. There is no enhancement following gadolinium injection. However, bone marrow may be seen within the area of ossification in thicker lesions. Electromyographic procedures help identify radicular lesions of the cauda equina but are rarely used. The differential diagnosis of OPLL includes other anterior epidural masses or plaque-like lesions in the lumbosacral region such as: –– –– –– ––

Calcified lumbar disc herniation Posterior ring apophysis separation Giant osteophyte (Spurs) Calcified tumors especially meningioma or neurinoma

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mass (bony density lesion) posterior to the vertebral bodies and intervertebral discs. This lesion induces a concomitant spinal canal stenosis

83.3  Imaging Features Fig. 83.2  Case 1. Ossified ligament appearance on axial CT scan (a–d) (arrows)

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83  Posterior Longitudinal Ligament Ossifications

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Fig. 83.3  Ossification of the posterior longitudinal ligament (arrows) shown on lumbar MRI and CT scan (arrows). Sagittal T2-weighted MRI (a), sagittal reconstruction (b), and axial (c, d) CT scan. There is a concomitant disc herniation on L4-L5 (arrowhead) (a)

83.3  Imaging Features

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Fig. 83.4  Case 2. Sagittal T1- (a) and T2-weighted MRI (b), and sagittal reconstruction CT scan (c) showing ossification of the posterior longitudinal ligament on L4-L5 and L5-S1 (arrows). The ossification was seen to compress the thecal sac anteriorly

866 Fig. 83.5  Case 2. Axial T2-weighted MRI (a) and axial CT scan on parenchymal (b) and bone windows (c, d) showing the ossified ligament (arrows) and the thecal sac compression medially and laterally, especially on the right side (d)

83  Posterior Longitudinal Ligament Ossifications

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83.4 Treatment Options and Prognosis

elderly. Most cases were operated on via a posterior approach. The decision regarding the resection of OPLL is not clearly The ossified posterior longitudinal ligament in the lumbar established. For some authors, posterior decompression alone may be sufficient except if the OPLL directly comspine can be managed conservatively or surgically. Conservative treatment modalities include bed rest, pain pressed unilateral nerve roots. In this last situation, OPLL control medications, anti-inflammatory medications, and resection is mandatory. Care should be taken to minimize physiotherapy resulting in more or less control of the nerve root damage and the high possibility of cerebrospinal patient’s pain. For patients with tolerable pain or without fluid leaks. If needed, posterior lumbar fusion with or withneurologic deficits, the literature suggests initially non-­ out posterior instrumentations can be performed. An additional herniated disc will be removed at the time of surgery. operative measures. Postoperative complications are mild and unusual. The aim of surgery is to decompress the neural roots with or without resection of the ossified ligament. No standard Surgeons should be aware of the possibility of adhesions surgical procedure exists for the treatment of lumbar between OPLL and dura matter or nerve roots, particularly OPLL.  There are various surgical techniques for nerve large and extensive ossifications. The majority of patients decompression. Lumbar spinal approaches include anterior, showed satisfactory clinical results after surgery. Overall, the outcome is better than that of patients with cervical or thoposterior, or a combination of both. The anterior approach may provide direct vision and racic OPLL. Recently, transforaminal endoscopic decompression complete excision of ossified lesions but this approach is relatively invasive. The posterior approach (e.g., laminec- using the posterolateral approach was performed in one tomy or laminoplasty) seems to be better tolerated in the patient with good results.

Further Reading

Further Reading Barrios-Anderson A, Wang EJ, Sastry R, Fridley JS.  Ossification of the posterior longitudinal ligament in the cervical, thoracic, and lumbar spine. Cureus. 2021;13:e14041. https://doi.org/10.7759/ cureus.14041. Choi BW, Song KJ, Chang H. Ossification of the posterior longitudinal ligament: a review of literature. Asian Spine J. 2011;5:267–76. https://doi.org/10.4184/asj.2011.5.4.267. Kawaguchi Y, Nakano M, Yasuda T, Seki S, Hori T, Kimura T.  Ossification of the posterior longitudinal ligament in not only the cervical spine, but also other spinal regions: analysis using multidetector computed tomography of the whole spine. Spine (Phila Pa 1976). 2013;38:E1477–82. https://doi.org/10.1097/ BRS.0b013e3182a54f00. Kim TJ, Kim TH, Jun JB, Joo KB, Uhm WS. Prevalence of ossification of posterior longitudinal ligament in patients with ankylosing spondylitis. J Rheumatol. 2007;34:2460–2. Liang H, Liu G, Lu S, Chen S, Jiang D, Shi H, et  al. Epidemiology of ossification of the spinal ligaments and associated factors in the Chinese population: a cross-sectional study of 2000 consecutive individuals. BMC Musculoskelet Disord. 2019;20:253. https://doi. org/10.1186/s12891-­019-­2569-­1. Nose T, Egashira T, Enomoto T, Maki Y.  Ossification of the posterior longitudinal ligament: a clinico-radiological study of 74 cases. J Neurol Neurosurg Psychiatry. 1987;50:321–6. https://doi. org/10.1136/jnnp.50.3.321. Okada S, Maeda T, Saiwai H, Ohkawa Y, Shiba K, Iwamoto Y.  Ossification of the posterior longitudinal ligament of the lumbar spine: a case series. Neurosurgery. 2010;67:1311–8. https://doi. org/10.1227/NEU.0b013e3181ef2806. Okumura T, Ohhira M, Kumei S, Nozu T. A higher frequency of lumbar ossification of the posterior longitudinal ligament in elderly in an outpatient clinic in Japan. Int J Gen Med. 2013;6:729–32. https:// doi.org/10.2147/IJGM.S48941.

867 Ramos-Remus C, Russell AS, Gomez-Vargas A, Hernandez-Chavez A, Maksymowych WP, Gamez-Nava JI, et al. Ossification of the posterior longitudinal ligament in three geographically and genetically different populations of ankylosing spondylitis and other spondyloarthropathies. Ann Rheum Dis. 1998;57:429–33. https://doi. org/10.1136/ard.57.7.429. Saetia K, Cho D, Lee S, Kim DH, Kim SD. Ossification of the posterior longitudinal ligament: a review. Neurosurg Focus. 2011;30:E1. https://doi.org/10.3171/2010.11.focus10276. Takahashi M, Kawanami H, Tomonaga M, Kitamura K. Ossification of the posterior longitudinal ligament--a roentgenologic and clinical investigation. Acta Radiol Diagn (Stockh). 1972;13:25–36. https:// doi.org/10.1177/02841851720130p105. Tamura M, Machida M, Aikawa D, Fukuda K, Kono H, Suda Y, et al. Surgical treatment of lumbar ossification of the posterior longitudinal ligament. Report of two cases and description of surgical technique. J Neurosurg Spine. 2005;3:230–3. https://doi.org/10.3171/ spi.2005.3.3.0230. Tong Y, Huang Z, Fan Z, Zhao C, Song Y.  Successful treatment of continuous ossification of the posterior longitudinal ligament in the lumbar spine using percutaneous transforaminal endoscopic spinal ­ decompression: a case report. J Int Med Res. 2021;49:493000605211004774. https://doi. org/10.1177/03000605211004774. Tsuji T, Chiba K, Hosogane N, Fujita N, Hikata T, Iwanami A, et al. Epidemiological survey of ossification of the posterior longitudinal ligament by using clinical investigation registration forms. J Orthop Sci. 2016;21:291–4. https://doi.org/10.1016/j.jos.2016.01.001. Wu D, Ba Z, Zhao W, Zhang Y, Liu J, Meng Y.  Ossification of the posterior longitudinal and yellow ligaments on the lumbar spine. Orthopedics. 2012;35:e298–301. https://doi. org/10.3928/01477447-­20120123-­22.

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Baastrup Disease

84.1 Generalities and Relevance Baastrup disease, also known as “kissing spines syndrome”, is a common but misdiagnosed clinical and radiological disorder of the lumbar spinal column first described in 1933 by the Danish radiologist Christian Ingerslev Baastrup (1885–1950). This entity is characterized by “interspinous bursitis” caused by contact between adjacent spinous processes as a result of degenerative modifications (Figs.  84.1 and 84.2). This may produce midline low back pain and clinically localized tenderness that is worsened with lumbar extension and released with flexion, anesthetic injections, or surgical excision. Sometimes, the disease is associated with neurologic signs and symptoms including neurogenic claudication and lumbosacral radiculopathy. Kissing spines are often associated with degenerative disc disease and variable degrees of lumbar stenosis, segmental instability, spondylolisthesis, and spondylosis with marked posterior facet degeneration. Histologically, there is a degeneration of interspinous and supraspinous ligaments with peripheral inflammation. The “bursitis” is related to the formation of a pseudarthrosis or a new synovial articulation with an interspinous fluid-filled cyst. Connections between bursitis and the posterior epidural space have been found in up to 50% of the patients. Sometimes, when the cyst is large enough, it could extend between the ligamentum flavum into the posterior spinal epidural space causing cauda equina nerve root compression. Baastrup cysts may change over time becoming progressively more fibrous. The etiology of kissing spines is supposed to be related to a hyperlordotic lumbar spine, repetitive trauma, obesity, and degenerative disc disease. Some iatrogenic cases have been described as secondary to anterior spinal lumbar approaches

Fig. 84.1  Lateral lumbosacral plain radiograph showing multilevel kissing spines (arrows) from L2 to L5

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syndrome, degenerative or congenital spondylolisthesis, spinal stenosis, or even lumbar disc herniation. Although rare, severe cases can present with more serious neurologic conditions such as partial or complete cauda equina syndrome (CES) due to large cyst compression or coexistence of lumbar spinal stenosis. If needed, a positive diagnostic test with local anesthetic injection may be used to confirm the Baastrup disease. Certainly, many patients with Baastrup disease will remain asymptomatic and the “kissing spines” with or without interspinous bursitis will be found only incidentally on neuroimaging.

84.3 Imaging Features The results of plain radiographs and computed tomography (CT) scan show a close approximation of adjacent spinous Fig. 84.2  Microscopic image of Baastrup’s disease showing a “bursite-­ processes. Flattening, hypertrophic, and reactive sclerosis of like lesion” with edema, sclerosis, and cystic degeneration of the new apposed interspinous surfaces can also be found especially at articulating surface (hematoxylin-eosin stain, original magnification the level of L4-L5 (Figs. 84.1 and 84.3). However, multilevel ×40). (Courtesy of Pr. Mohamed Amine Azami) kissing spines are not rare. Baastrup disease is often accomcausing increased lordosis. Also, Baastrup disease is one of panied by other degenerative spinal lesions (e.g., facet joints the potential risk factors for the reappearance of sciatica after degenerations, loss of intervertebral disc height, spinal steposterior lumbar spinal decompression by floating spinous nosis, and disc herniation). Dynamic flexion-extension radiographs may be used in process procedures for decompression surgery for lumbar the evaluation of variable degrees of adjacent segmental spinal stenosis. instability. The overall incidence of kissing spines syndrome was On MRI, an interspinous pseudocyst with fluid accumula8.2% among patients with low back or lower leg pain tion can extend into the spinal canal compressing the dural assessed on magnetic resonance imaging (MRI) with a slight sac posterolaterally (Fig. 84.4). The cyst content is hypoinmale predominance. However, this incidence increases with age, and also the cyst becomes multilevel. A peak incidence tense on T1-weighted sequence and hyperintense on of more than 80% was found in octogenarians. Young people T2-weighted sequence (Figs.  84.5, 84.6, and 84.7). Mural may also be affected because kissing spines syndrome has and interspinous enhancement may be present following intravenous gadolinium administration. Short tau inversion encountered in 6.3% of college athletes. recovery (STIR) sequences can be useful in evaluating bone edema at the level of new articulating surfaces. Intracystic contrast injection or “bursography” could be 84.2 Clinical Presentations useful in documenting the direct communication between Most symptomatic patients report lumbar midline pain which the interspinous bursa and the epidural posterior collection. The FDG-PET (fluorodeoxyglucose-positron emission radiates cephalad and caudal but rarely lateral or along the tomography) scan give more appropriate results when there lower limbs. Neurogenic claudication as well as unilateral or is an interspinous inflammation or bursitis. bilateral lumbosacral radicular pain are rare symptoms related Mainly because Baastrup disease is often underdiagnosed to the extension of cystic bursitis inside the spinal canal or or often missed, it can be confused with several other postesecondary to the co-existence of other degenerative diseases. rior lumbosacral lesions like: Typically, lumbar pain is relieved during flexion and aggravated during extension. During clinical examination, • Tarlov or arachnoid cysts the localized midline back pain is reproduced upon finger • Synovial cyst pressure at the level of posterior interspinous lesion (often on • Ligamentum flavum cyst L4-L5 vertebral level). • Meningocele Potential associated degenerative diseases and some pre• Posterior vertebral osteomyelitis disposing factors should be considered constantly. It is • Epidural abscess or hematoma important to determine if patients have other signs and symp• Primitive or secondary malignancies toms more typical of posterior facet (zygapophyseal) joint

84.3  Imaging Features Fig. 84.3 Anteroposterior lumbosacral X-ray (a) and sagittal reconstructions CT scan (b) revealing flattening, hypertrophic, and reactive sclerosis of L4-L5 apposed interspinous surfaces (arrows)

a

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b

b

Fig. 84.4  An L3-L4 interspinous pseudocyst with fluid accumulation extending into the spinal canal (posterior epidural space) and compressing the dural sac posterolaterally (arrows). Sagittal T1- (a) and T2- (b) weighted MRI as well as axial (c) T2-weighted. Note that the cyst con-

c

tent is hypointense on T1-weighted sequence and hyperintense on T2-weighted sequence. (Courtesy of Pr. Hatim Belfquih and Dr. Achraf Moussa)

872 Fig. 84.5 Lumbar interspinous bursitis (arrows) as seen on sagittal T2-weighted MR imaging (a, b)

Fig. 84.6  Axial T2-weighted MRI (a, b) showing flattening, hypertrophic, and reactive sclerosis of apposed interspinous surfaces between L4 and L5 (dotted lines). Note the posterior facet joint degeneration (arrows)

84  Baastrup Disease

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84.4  Treatment Options and Prognosis

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Fig. 84.7  Lumbosacral sagittal reconstruction CT scan (a), T1- (b), and T2-weighted MRI (c) showing L4-L5 kissing spines (arrowheads) due to grade I isthmic spondylolisthesis (arrows). Note the “bursite-like

lesion” hypointense on T1- (a) and hyperintense on T2-weighted (b) MRI (arrowheads)

84.4 Treatment Options and Prognosis

and partial or total removal of the spinous processes. If needed, a more extensive approach will be used such as laminectomy. Potential associated degenerative lesions will be treated accordingly. Interestingly, some patients with concurrent spinal stenosis were successfully treated by an interspinous posterior device (decompressive spacer) implanted between the spinous processes. This device is used as an alternative to lumbar laminectomy, principally in aging patients. Due to the important developments in spinal endoscopic techniques and equipment, recently, some authors reported their useful experience of percutaneous endoscopic ­decompression or interspinous plasty for the treatment of symptomatic patients with Baastrup disease. Post-operatively, there are many contrasting results found in the literature. Overall, the surgical success of patients undergoing open decompressive surgery in the setting of kissing interspinous processes is often less than satisfactory for a variable interval of time.

Therapies for Baastrup disease range from conservative measures to interventional radiology and surgical intervention. Initially, and outside any neurologic emergency, the pain may be managed conservatively. Conservative therapy includes bed rest, pain control medications, physiotherapy, and other physical modalities resulting in more or less control of the patient’s pain. If pain reduction fails following conservative treatments, percutaneous injections are then considered. Under fluoroscopy or CT-guided, the cyst can be aspired and followed by local anesthesia and corticosteroid injection. Recurrent cases may also undergo local thermal coagulation using a radiofrequency electrode. Traditional decompressive surgery is indicated for cases that failed to improve under conservative therapy or percutaneous interventional radiology. The common procedure includes the excision of the intraspinous/interspinous bursa

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Further Reading Akhaddar A.  Differential diagnosis of intraspinal arachnoid cysts. In: Turgut M, Akhaddar A, Turgut AT, Hall WA, editors. Arachnoid cysts: state-of-the-art concepts. Switzerland: Springer International Publishing; 2022. p.  311–26. https://doi. org/10.1007/978-­3-­030-­79371-­5_26. Alonso F, Bryant E, Iwanaga J, Chapman JR, Oskouian RJ, Tubbs RS. Baastrup’s disease: a comprehensive review of the extant literature. World Neurosurg. 2017;101:331–4. https://doi.org/10.1016/j. wneu.2017.02.004. Baastrup I.  The diagnosis and roentgen treatment of certain forms of lumbago. Acta Radiol. 1940;21:151–63. https://doi. org/10.1177/028418514002100204. Casuccio C, Scapinelli R. Clinical and anatomico-radiological studies of pathological changes in the vertebral spinous processes and adjacent soft tissues. J Bone Joint Surg (Br). 1962;44:218. Chen CK, Yeh L, Resnick D, Lai PH, Liang HL, Pan HB, et  al. Intraspinal posterior epidural cysts associated with Baastrup’s disease: report of 10 patients. AJR Am J Roentgenol. 2004;182:191–4. https://doi.org/10.2214/ajr.182.1.1820191. Egu CB, D’Aquino D, Mcculloch T, Pasku D.  Baastrup’s disease as a rare cause of cauda equina syndrome: a case report. JBJS case. Connect. 2022;12:12. https://doi.org/10.2106/JBJS.CC.22.00121. Filippiadis DK, Mazioti A, Argentos S, Anselmetti G, Papakonstantinou O, Kelekis N, et al. Baastrup’s disease (kissing spines syndrome): a pictorial review. Insights Imaging. 2015;6:123–8. https://doi. org/10.1007/s13244-­014-­0376-­7. Gold M, DeMattia J. Posterior epidural cyst associated with Baastrup disease. Spine J. 2016;16:e23–4. https://doi.org/10.1016/j. spinee.2015.08.044. Hatgis J, Granville M, Jacobson RE. Baastrup’s disease, interspinal bursitis, and dorsal epidural cysts: radiologic evaluation and impact on

84  Baastrup Disease treatment options. Cureus. 2017;9:e1449. https://doi.org/10.7759/ cureus.1449. Koda M, Mannoji C, Murakami M, Kinoshita T, Hirayama J, Miyashita T, et al. Baastrup’s disease is associated with recurrent of sciatica after posterior lumbar spinal decompressions utilizing floating spinous process procedures. Asian Spine J. 2016;10:1085–90. https:// doi.org/10.4184/asj.2016.10.6.1085. Lin WT, Xie FQ, Lin SH, Yang RB, Shen HW, Cai XF, et  al. Full-­ endoscopic approach forchronic low back pain from Baastrup’s disease: interspinous plasty. Orthop Surg. 2021;13:1102–10. https:// doi.org/10.1111/os.12988. Maes R, Morrison WB, Parker L, Schweitzer ME, Carrino JA. Lumbar interspinous bursitis (Baastrup disease) in a symptomatic population: prevalence on magnetic resonance imaging. Spine (Phila Pa 1976). 2008;33:E211–5. https://doi.org/10.1097/BRS.0b013e318169614a. Meluzio MC, Smakaj A, Perna A, Velluto C, Grillo G, Proietti L, et al. Epidemiology, diagnosis and management of Baastrup’s diseases: a systematic review. J Neurosurg Sci. 2021;66(6):519–25. https://doi. org/10.23736/S0390-­5616.21.05428-­X. Philipp LR, Baum GR, Grossberg JA, Ahmad FU. Baastrup’s disease: an often missed etiology for back pain. Cureus. 2016;8:e465. https:// doi.org/10.7759/cureus.465. Seo JS, Lee SH, Keum HJ, Eun SS.  Three cases of L4-5 Baastrup’s disease due to L5-S1 spondylolytic spondylolisthesis. Eur Spine J. 2017;26:186–91. https://doi.org/10.1007/s00586-­017-­5014-­x. Shukla K, Gosal JS, Garg M, Bhaskar S, Jha DK, Tiwari S. Atypical variant of Baastrup’s disease with lumbar stenosis and cauda equina syndrome. Surg Neurol Int. 2019;10:198. https://doi.org/10.25259/ SNI_467_2019. Spirollari E, Feldstein E, Ng C, Vazquez S, Kinon MD, Gandhi C, et al. Correction of sagittal balance with resection of kissing spines. Cureus. 2021;13:e16874. https://doi.org/10.7759/cureus.16874.

Spinal Epidural Gas Pseudocysts

85.1 Generalities and Relevance Gas formation within the intraspinal epidural space is an uncommon phenomenon mainly seen secondary to lumbar puncture, epidural anesthesia, spinal surgery, trauma, neoplasm, or epidural infection. More rarely, epidural gas can be related to degenerative disc disease due to a “vacuum phenomenon” (intradiscal gas) as a result of spine movement, especially in the lower lumbar spine. This juxta-discal degenerative herniated gas locule, first described by Gulati and Weinstein in 1980, is sometimes named “epidural gas pseudocyst.” Gulati and Weinstein in evaluating 79 symptomatic patients with lumbar spinal stenosis found a vacuum disc phenomenon on computed tomography scan in 22 patients but they observed also the presence of free spinal epidural gas in three cases. Other possible sources of epidural gas include degenerative apophyseal joints or juxtafacet cysts (including synovial cysts and ganglion cysts) and vertebral body pneumatocysts. Epidural gas pseudocyst can be found free in the epidural space of the lumbar spinal canal, but it can also be associated with a typical lumbar disc herniation or even be detected within the herniated disc itself. The combination of epidural gas pseudocyst and lumbar disc herniation is classically known as a “gas-containing prolapsed intervertebral disc.” This gaseous collection is often trapped within a thin layer of nonspecific tissue membrane undistinguishable from the posterior longitudinal ligament. Most authors suggest that the gas coming from the adjacent degenerative disc was trapped between the vertebral bone and the posterior longitudinal ligament. Migration of gas into the epidural space was thought to be secondary to the motion of the lumbosacral spine under important intradiscal pressure. Regarding the

85

gas itself, it was known to be composed of nitrogen and carbon dioxide. The incidence of this entity increases with age, particularly in patients over 40 years of age. An epidural gas pseudocyst is usually an asymptomatic and incidental imaging finding. However, it can be a rare source of lower limb radiculopathy, particularly as sciatic pain due to direct pneumatic nerve root compression.

85.2 Clinical Presentations The clinical importance of epidural gas pseudocyst is low because this entity is generally asymptomatic or can be indistinguishable from chronic symptoms attributed to pre-­ existing degenerative lower back problems. However, some patients might present with L5 or S1 radicular pain similar to that of any other discogenic sciatica. Sometimes, the radicular pain may increase when changing postural positions due to the free displacements and migrations of the gas inside the extradural spinal space. Uncommonly, there are severe neurological signs and symptoms such as an acute cauda equina syndrome suggesting significant radicular nerve compression especially when lumbar spinal stenosis is concomitant.

85.3 Imaging Features CT scan is the imaging modality of choice in the diagnosis of epidural gas pseudocyst either of small quantity due to negative Hounsfield unit value of the air. The accumulated gas may appear as single or multiple gas bubbles, sited in the lateral recess, or more rarely at the intervertebral foramina (Figs. 85.1, 85.2, 85.3, 85.4, and 85.5).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_85

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85  Spinal Epidural Gas Pseudocysts

Fig. 85.1  Axial CT scan on parenchymal (a) and bone (b) windows showing epidural gas pseudocysts (arrows) sited in right L5-S1 anterior paramedian space (a) and in left L4-L5 recess (b). Note some vertebral pneumatocysts (arrowhead)

a

Fig. 85.2  Axial CT scan (a, b) revealing an epidural gas pseudocyst sited in the left L5-S1 lateral recess (arrow) and compresses the S1 spinal nerve root. A vacuum phenomenon was seen within the degenerated disc (stars)

a

Fig. 85.3  Axial CT scan on parenchymal (a) and bone (b) windows showing an epidural gas pseudocyst (arrows) sited in right L3-L4 lateral recess

a

The existence of direct communication between the intervertebral disc gas and the epidural pseudocyst was previously demonstrated using CT discography. CT scan can also show associated degenerative lesions including spinal stenosis, osteophytes, and disc bulging or herniation.

b

b

b

On MRI, gas appears as a low signal intensity in both T1 and T2 weighted-images (Figs.  85.6 and 85.7); however, there is difficulty in differentiating between air and calcification because each lesion has similar signal intensity.

85.3  Imaging Features Fig. 85.4  Axial (a) and sagittal reconstruction (b) CT scan revealing a left epidural pseudocyst at the level of L5-S1 (arrows) which compresses the ipsilateral S1 spinal nerve root. The gaseous collection is associated with an adjacent prolapsed intervertebral disc (arrowhead) known as a “gas-containing prolapsed intervertebral disc.” (Courtesy of Pr. Nabil Hammoune)

Fig. 85.5 Sagittal reconstructions CT scan on bone (a) and parenchymal (b) showing an epidural gas pseudocyst (arrows) sited behind the vertebral body of S1. Note the vacuum phenomenon within L5-S1 degenerated disc (arrowheads)

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85  Spinal Epidural Gas Pseudocysts

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Fig. 85.6  Case A. Epidural gas pseudocyst (arrows) sited behind the vertebral body of L4 as seen on sagittal reconstructions CT scan on bone windows (a), on T1- (b), T2-weighted MR images (c), and on STIR sequences (d)

Fig. 85.7  Case A. The same epidural pseudocyst (arrows) as seen on axial CT scan (a), on T1- (b), and on T2-weighted MRI (c)

a

c

b

Further Reading

85.4 Treatment Options and Prognosis Most patients with lumbar epidural pseudocysts are managed conservatively. Indeed, many authors recommend bed rest, analgesics, non-steroidal anti-inflammatory drugs, myorelaxant drugs, and even epidural glucocorticoid injections to improve or resolve radiculopathies. Some authors suggest a preliminary period of observation in symptomatic patients because epidural gaseous collection may disappear naturally. The efficacy of CT-guided needle aspiration is usually reported despite the possibility of epidural gas recurrence and the high rate of sciatica relapse. Decompressive surgery is the ideal treatment for cases that failed to improve under conservative therapy. The common procedure combines gas evacuation with disc curettage of the contiguous disc to prevent a recurrence. Due to the important developments in endoscopic techniques and equipment, recently, some authors recently reported their useful experience of percutaneous endoscopic decompression for treating symptomatic patients with epidural gas pseudocyst.

Further Reading Akhaddar A, Eljebbouri B, Naama O, Boucetta M. Sciatica due to lumbar intraspinal gas pseudocyst. Intern Med. 2010;49:2647. https:// doi.org/10.2169/internalmedicine.49.4474. Bang WS, Lee W, Lee YS, Kang BU.  Dorsal epidural gas after lumbar microdiskectomy treated with CT-guided needle aspiration. Korean J Neurotrauma. 2020;16:305–12. https://doi.org/10.13004/ kjnt.2020.16.e25. Chen Y, Yu SD, Lu WZ, Ran JW, Yu KX. Epidural gas-containing pseudocyst leading to lumbar radiculopathy: a case report. World J Clin Cases. 2021;9:7279–84. https://doi.org/10.12998/wjcc.v9.i24.7279. Cheng TM, Link MJ, Onofrio BM. Pneumatic nerve root compression: epidural gas in association with lateral disc herniation. Report of two cases. J Neurosurg. 1994;81:453–8. https://doi.org/10.3171/ jns.1994.81.3.0453. Gulati AN, Weinstein ZR. Gas in the spinal canal in association with the lumbosacral vacuum phenomenon: CT findings. Neuroradiology. 1980;20:191–2. https://doi.org/10.1007/BF00336681. Guo J, Ma X, Liu Y, Li G, Wang D, Wang Z, Li S. Dura sac compression due to spinal epidural gas pseudocyst after lumbar decompression surgery: a case report. BMC Musculoskelet Disord. 2019;20:296. https://doi.org/10.1186/s12891-­019-­2682-­1. Kakitsubata Y, Theodorou SJ, Theodorou DJ, Yuko M, Ito Y, Yuki Y, et al. Symptomatic epidural gas cyst associated with discal vacuum

879 phenomenon. Spine (Phila Pa 1976). 2009;34:E784–9. https://doi. org/10.1097/BRS.0b013e3181b35301. Krishnan P.  Epidural gas pseudocyst: an uncommon cause of sciatica. Asian J Neurosurg. 2022;17:396–8. https://doi. org/10.1055/s-­0042-­1750809. Lassoued Ferjani H, Ben Ammar L, Kaffel D, Maatallah K, Triki W, Ben Nessib D, et al. Radiculopathies caused by spontaneous pneumorrachis: two case reports and review of literature. Clin Case Rep. 2021;9:e05061. https://doi.org/10.1002/ccr3.5061. Liu WC, Lee SH, Kwon AM, Lee SH, Park J, Park HS. Morphologic characteristics and clinical significance of computed tomography and magnetic resonance imaging findings of spinal epidural gas. World Neurosurg. 2020;141:e792–800. https://doi.org/10.1016/j. wneu.2020.06.009. Mehta TA, Sharp DJ. Acute cauda equina syndrome caused by a gas-­ containing prolapsed intervertebral disk. J Spinal Disord. 2000;13:532– 4. https://doi.org/10.1097/00002517-­200012000-­00013. Mortensen WW, Thorne RP, Donaldson WF 3rd. Symptomatic gas-containing disc herniation. Report of four cases. Spine (Phila Pa 1976). 1991;16:190–2. https://doi. org/10.1097/00007632-­199102000-­00017. Raynor RB, Saint-Louis L.  Postoperative gas bubble foot drop. A case report. Spine (Phila Pa 1976). 1999;24:299–301. https://doi. org/10.1097/00007632-­199902010-­00023. Şakir Ekşi M, Ece Özcan-Ekşi E, Orhun Ö, Akkaş A, Harun Yaşar A, Zarbizada M, et  al. Could gas-filled pseudocyst mimick extruded disc herniation? J Clin Neurosci. 2021;93:147–54. https://doi. org/10.1016/j.jocn.2021.09.023. Salpietro FM, Alafaci C, Collufio D, Passalacqua M, Puglisi E, Tripodo E, et al. Radicular compression by lumbar intraspinal epidural gas pseudocyst in association with lateral disc herniation. Role of the posterior longitudinal ligament. J Neurosurg Sci. 2002;46:93–5. Sasani M, Ozer AF, Oktenoglu T, Cosar M, Karaarslan E, Sarioglu AC.  Recurrent radiculopathy caused by epidural gas after spinal surgery: report of four cases and literature review. Spine (Phila Pa 1976). 2007;32:E320–5. https://doi.org/10.1097/01. brs.0000261565.76537.ea. Schömig F, Li Z, Becker L, Vu-Han TL, Pumberger M, Diekhoff T. Gas within the intervertebral disc does not rule out spinal infection-­a case series of 135 patients with spontaneous spondylodiscitis. Diagnostics (Basel). 2022;12:1089. https://doi.org/10.3390/ diagnostics12051089. Tsitouridis I, Sayegh FE, Papapostolou P, Chondromatidou S, Goutsaridou F, Emmanouilidou M, et al. Disc-like herniation in association with gas collection in the spinal canal: CT evaluation. Eur J Radiol. 2005;56:1–4. https://doi.org/10.1016/j.ejrad.2005.04.003. Yoshida H, Shinomiya K, Nakai O, Kurosa Y, Yamaura I.  Lumbar nerve root compression caused by lumbar intraspinal gas. Report of three cases. Spine (Phila Pa 1976). 1997;22:348–51. https://doi. org/10.1097/00007632-­199702010-­00021. Yun SM, Suh BS, Park JS.  Symptomatic epidural gas-containing cyst from intervertebral vacuum phenomenon. Korean J Spine. 2012;9:365–8. https://doi.org/10.14245/kjs.2012.9.4.365. Zhu B, Jiang L, Liu XG.  Transforaminal endoscopic decompression for a giant epidural gas-containing pseudocyst: a case report and literature review. Pain Physician. 2017;20:E445–9.

Part IV Extraspinal Intrapelvic Sciatica

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Sciatic Lumbosacral Plexopathies

86.1 Generalities and Relevance

the L4 to S3 distal nerve roots, and the proximal sciatic nerve trunk in the pelvis (Figs. 86.1 and 86.2). Sciatic pain related to lumbosacral plexopathy should be distinguished from other peripheral nervous system lesions involving the lower limbs such as L5 and/or S1 radiculopathy, sciatic peripheral

Sciatic lumbosacral plexopathy is the overarching condition describing lesions, dysfunctions, and pathologic changes of the nerves in the lumbar and particularly the sacral plexus,

Fig. 86.1  Configuration of the sacral plexus and its 12 branches. Superior gluteal nerve, inferior gluteal nerve, sciatic nerve, posterior femoral cutaneous nerve, pudendal nerve, nerve to lumbar plexus (a), nerve to perineum and levator ani (b), perforating cutaneous nerve (c), nerve to obturator internis and superior gemellus (d), nerve to quadratus femoris and inferior gemellus (e), and nerve to piriformis (f)

Lumbosacral trunk L4

a L5

S1

Superior gluteal nerve

S2

Inferior gluteal nerve S3

f

Peroneal nerve

Sciatic nerve

S4 Tibial nerve

e

d b

c Posterior femoral Cutaneous nerve

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_86

Pudendal nerve

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884 Fig. 86.2  Anterior view of the lumbosacral spine showing the origin of the sciatic nerve in the lumbosacral spinal canal from the fourth lumbar (L4) to the third sacral (S3) spinal nerves

86  Sciatic Lumbosacral Plexopathies

A portion of the lumbosacral plexus

Lumbar spine L4

L5 S1

IIiac bone

Sacrum

S2 S3 Sciatic nerve

Greater sciatic foramen Greater tronchanter Hip joint

Ischial tuberosity

neuropathy, tibial neuropathy, femoral neuropathy, and common peroneal neuropathy. Also, sciatic pain due to central (intraspinal and intracranial) funicular lesions, should be excluded. If the pathological involvement includes the nerve roots, nerves, and plexus, these conditions are not pure lumbosacral plexopathies but are known as lumbosacral radiculoplexus neuropathies. Pan-plexopathies including whole lumbar and sacral plexi are rare. Lumbosacral plexus neuropathies are uncommon, but when they occur, they generally present with a combination of pain, weakness, and sensory loss in the leg. Sphincter dysfunction may be seen but low back pain is unusual. Sometimes, the neurologic condition is confused and some clinical presentations are similar to diseases of the nerve roots or the sciatic trunk. Unlike sciatic radiculopathies and peripheral neuropathies, neurologic findings are mostly poorly defined and cannot be explained by a single nerve or single root lesion. Several pathologies and injuries contribute to lumbosacral plexopathies. The pathophysiology of this plexopathy is often multifactorial resulting from direct injury or traction on the plexus, direct infiltration, secondary invasion, microvascular disorders, chronic inflammatory changes, fibrosis, and ischemic damage.

Treatment is often limited and varies considerably depending on the underlying etiologies. However, early diagnosis and adequate management are critical in decreasing morbidity and mortality. Although sciatic lumbosacral plexopathies are far less common than sciatic radiculopathies and those secondary to peripheral neuropathies of the lower limbs, the prevalence of lumbosacral plexopathies is not well recognized for most causes. Diabetic amyotrophy occurs in less than 1% of cases with diabetes mellitus. Lumbosacral plexopathy reveals the diagnosis of cancer in 15% of cancer patients. Additionally, lumbosacral plexopathy occurs in approximately 0.7% of injured cases following a traumatic pelvic fracture and in 2% of cases sustained a sacral fracture. Lumbosacral plexopathy occurs in one case for every 2000–6000 deliveries. Overall, the median age for diagnosis is around 60 years with female predominance due to predisposing risk factors like gynecological neoplasms and pregnancy.

86.2 Etiologies There are multiple origins of lumbosacral plexopathies especially those secondary to neoplasms, intrapelvic compressive lesions, traumatic injuries whether exogenous or iatrogenic,

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86.2 Etiologies

and diabetes mellitus. Lumbosacral plexopathies are less common than brachial plexopathies, mostly because traumatic lumbosacral plexopathies are unusual. Nontraumatic lesions are the most common cause, especially malignant neoplasms that invade the plexus by direct extension in about 75% of cases.

Table 86.1 represents the most frequent causes of sciatic lumbosacral plexopathies previously published in the literature (Figs. 86.3, 86.4, 86.5, 86.6, 86.7, 86.8, 86.9, 86.10, and 86.11).

Table 86.1  The most frequent causes of sciatic lumbosacral plexopathies previously been published in the literature Tumor Trauma Iatrogenic Infection Inflammation Gyneco-­obstetric Digestive (bowel) Hematoma Vascular Radiation Diabetes Idiopathic

Intrapelvic and retroperitoneal benign and malignant invasions, schwannomas, neurofibromas, sarcoma, carcinoma, lymphoma, metastasis (colorectal, urologic, gynecologic…) [Figs. 86.3, 86.4, 86.5, 86.6, 86.7, 86.8, and 86.9] Pelvic fractures (including the sacrum), sacroiliac injuries, acetabulum, hip dislocation, hematoma [Fig. 86.10] Postoperative (scar tissue formation and bleeding), periacetabular osteotomy, post-biopsy, femoral artery catheter (damage to the vasculature innervating the lumbosacral plexus) Abscess [Fig. 86.11], hydatid cyst, herpes simplex virus, varicella zoster virus, HIV, mycobacterium tuberculosis Chronic inflammatory demyelinating polyneuropathy, vasculitis, sarcoidosis, amyloid, plexitis, diffuse infiltration lymphocytosis Pregnancy, labor and postpartum, endometriosis, uterine fibroid, hematometrocolpos Fecal impaction, idiopathic megacolon Spontaneous (anticoagulation), post-traumatic Ischemic, malformed, or dilated branches of iliac vessels (superior gluteal vein), aneurysms (common iliac artery) Post-radiotherapy Proximal diabetic neuropathy or plexopathy, diabetic amyotrophy From unknown cause

Fig. 86.3  Paravertebral and retroperitoneal intrapelvic sarcoma (stars) in a patient presenting with painful lumbosacral plexopathy on the right. Axial pelvic CT scan after contrast injection (a, b)

a

Fig. 86.4 Retroperitoneal intrapelvic neuroblastoma (dotted lines) in a young patient presenting with painful lumbosacral plexopathy on the left. Axial pelvic CT scan after contrast injection (a, b)

a

b

b

886 Fig. 86.5  Pelvic solitary plasmacytoma (stars) with sacroiliac involvement manifesting as a lumbosacral radicular pain on the left side. Axial post-gadolinium T1-weighted MRI (a) and coronal reconstructions CT scan (b)

Fig. 86.6  Schwannoma of the left lumbosacral plexus (stars) with homolateral L5 nerve root continuity (arrows). Axial CT scan (a), coronal T1-weighted MRI before (b) and after (c) gadolinium administration as well as on axial T2-weighted MRI (d)

86  Sciatic Lumbosacral Plexopathies

a

b

a

c

b

d

86.2 Etiologies Fig. 86.7 Intrapelvic lymphoma (circles) with paraspinal (triangles), iliac bone, and extrapelvic extension (stars) manifesting as a simple sciatic pain. Axial pelvic post-gadolinium T1- (a) and T2-weighted MRI (b) as well as post-contrast CT scan (c, d)

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a

c

Fig. 86.8 Retroperitoneal Ewing sarcoma next to the greater sciatic foramen (stars). Axial T1-weighted MRI before (a) and after (b) gadolinium administration as well as on T2-weighted MRI (c)

a

c

b

d

b

888 Fig. 86.9 Intrapelvic metastasis of a renal adenocarcinoma (stars) with extrapelvic extension through the right-sided greater sciatic foramen (arrows). This 65-year-old woman only had unilateral sciatic pain. Pelvic axial (a), coronal (b), and sagittal (c) post-contrast CT scan as well as 3D angio-CT scan (d). (Courtesy of Pr. Salah Bellasri)

Fig. 86.10 Post-traumatic right-sided lumbosacral plexopathy in a young man 11 months after a traffic road accident with pelvic penetrating injury (arrows) (a). Note the thigh muscles atrophy on the right (arrows) (b)

86  Sciatic Lumbosacral Plexopathies

a

b

c

d

a

b

86.4  Paraclinic Features Fig. 86.11  Large intrapelvic retroperitoneal abscess on the right side (stars) as seen on axial CT scan before (a) and after (b) contrast injection

889

a

86.3 Clinical Presentations The initial evaluation should include a detailed past medical history and physical exam. History would include questions about recent injuries, infections, surgeries, natal/deliveries, medications, or diabetic problems. Most patients with lumbosacral plexopathy present with a rapid onset of pseudo-radicular leg pain followed in days or a few weeks by weakness with or without atrophy (Fig. 86.10b). Sensory symptoms are less noticeable and typically involve paresthesias and dysesthesia. Symptoms are often unilateral; however, bilateral involvement can be seen in important traumas, diabetes mellitus, autoimmune diseases, and post-radiation plexopathies. In this latter condition, there is asymmetrical lower limb pain. Objective hypoesthesia and sphincter dysfunction are unusual and their existence should suspect a cauda equina syndrome. Lasègue test may sometimes be positive but sciatic pain rarely arise following back motion or Valsalva maneuver. The knee jerk reflex is abnormal in lumbar plexopathy and the ankle jerk is abnormal in sacral plexopathy. Cases with sacral plexus involvement present with sensory changes of the posterior thigh, dorsum of the foot, and perineum. Sciatic pain caused by traumatic injury or vascular etiologies presents acutely. Except that, most sciatic lumbosacral plexopathies present in a gradual subacute manner with mild or without low back pain. Sciatic pain related to lumbosacral plexopathy rarely exists in isolation but is often associated with other neurologic or non-neurologic symptoms linked with the underlying etiology and causative factors. Consequently, besides sciatica, other concomitant symptoms can include perineal or gluteal pain, anorectal dysfunction, rectal pain, and/ or lower urinary tract symptoms in the absence of pelvic organ prolapse or other recognizable reasons. Fever, chills, night sweats, fatigue, and weight loss should point toward malignancy or infection. Digital rectal examination and/or vaginal and transvaginal examination can be useful. When patients

b

present with sciatica but without obvious spinal or extrapelvic cause, it is important to consider these additional signs and symptoms, which may indicate an intrapelvic source of sciatica. In some cases, separating plexopathy from radiculopathy on clinical grounds can be difficult or impossible. Therefore, in such cases electrodiagnostic studies are decisive.

86.4 Paraclinic Features The diagnosis can be made on a clinical basis and may be confirmed with electrodiagnostic investigations such as nerve conduction explorations and electromyography. Differential diagnoses like lumbosacral radiculopathies and peripheral neuropathies should be ruled out. Imaging studies such as magnetic resonance (MR) imaging and ultrasound might help to localize the site of plexus damage and provide evidence for the etiology. Among all neuroimaging techniques, MR imaging remains the best method to detect lumbosacral plexopathy. However, the obliquity of the roots in the lumbar plexus makes them difficult to visualize on MR imaging. Complete assessment of the lumbosacral plexus should include both T1-weighted images (with and without gadolinium agent) and a fluid sensitive fat suppressed sequence like short tau inversion recovery (STIR). MR neurography is a useful technic in helping to clearly determine extraspinal injuries responsible for the plexopathy. Depending on the severity of the damage, T2-weighted MRI may show hyperintensity in the nerve fibers, abnormal fascicular appearance, nerve enlargement or deformation, and loss in nerve continuity. Additionally, affected muscles showed more edema, fatty infiltration, and muscular atrophy. When needed, an additional measurement may be performed based on data from the history and physical exam. The neurophysiologic evaluation plays a key role in the assessment of a possible lumbosacral plexopathy. The electrophysiologic approach evaluated and exclude disorders

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that can mimic sciatic neuropathy, including peroneal palsy at the fibular neck and lumbosacral radiculopathy. Nerve damage may be manifest on electromyography as fibrillation potentials, and motor unit potentials that are either decreased in number or increased in amplitude or duration and polyphasic. Needle examination is an important means of localizing the lesion. The involvement of gluteal muscles suggests either additional involvement of the gluteal nerves or of a lesion of the lumbosacral plexus. Concomitant involvement of femoral or obturator innervated muscles is indicative of a lumbosacral plexopathy. Denervation of the paraspinal muscles is generally encountered in radiculopathy and helps to separate from plexopathy. Compared to clinical and neurophysiological diagnostic methods, MRI neurography is a promising imaging tool for the assessment of lumbosacral plexus damage. Pelvic computer tomography, ultrasonography, positron emission tomography (PET), and angiographic studies as well as biological investigations may be indicated for specific cases in the search for an etiology. However, when paraclinical explorations are inconclusive, a biopsy of pelvic organs, as well as a biopsy of the suspected affected nerve root may be needed.

86.5 Treatment Options and Prognosis Identification of the origin of sciatic-related lumbosacral plexopathy is important for determining therapy and prognosis. Management depends on the underlying cause and includes conservative measures with physical therapy, analgesics, muscle relaxants, stretching local anesthetics, and non-­steroidal anti-­inflammatory drugs. Neuropathic pain is frequent in almost all causes of sciatic plexopathy and is commonly treated with neuropathic pain medications such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline), duloxetine, anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine), and even with transdermal lidocaine. Treatment of systemic illness commonly results in an improvement in sciatic neuropathic symptoms. Diabetic amyotrophy is a temporary disorder that frequently resolves with good glycemic control. Immune-mediated neuropathies would be treated with corticosteroids, immunosuppressant therapy, plasmapheresis, or intravenous immunoglobulin depending on the primary disease. Progestogens and gonadotropin-­releasing hormones may reverse sciatic neuropathy in endometriosis. Malignancy should be correctly managed by chemotherapy, surgery,

86  Sciatic Lumbosacral Plexopathies

and/or radiation therapy. Appropriate anti-infectious agents (e.g., antibiotics, anthelmintics, and antifungals) are required in infectious diseases. Surgery is indicated in patients with compressive mass lesions such as a tumor, hematoma, or abscess. Nerve repair and grafting may play a role in the treatment of severe sacral plexus injuries from trauma but is challenging. In individuals with poor recovery of sciatic pain with lumbosacral plexopathy, long-term complications may include bedsores and ulcerations, intractable pain, recurrent infections, progressive neurologic deterioration, retraction, and joint contractures. Some complications might necessitate further surgical procedures. In difficult and refractory forms, rhizotomy might be useful in specific cases. Recovery from pain generally precedes the reappearance of strength. Improvement is usually monophasic, slow (several months/years), and incomplete. The prognosis is variable depending on the underlying etiology, treatment response, and delay of treatment. The prognosis is good for patients with lumbosacral plexopathy secondary to pregnancy, retroperitoneal hematoma, and diabetic amyotrophy. Traumatic plexopathies are generally considered to have an unfavorable prognosis. Progressive neurological deterioration is common in patients with lumbosacral plexopathy secondary to malignancy with life-­ threatening consequences. Primary prevention is made through early intervention (e.g., post-traumatic, abdominal, or pelvic surgery) and close monitoring of disease progression (e.g., cancer metastasis, diabetes, systemic diseases).

Further Reading Ajala-Agbo T, Tang PT, Bat-Ulzii Davidson T.  Unilateral leg weakness and pain secondary to metastatic anal squamous cell carcinoma. BMJ Case Rep. 2019;12:e227563. https://doi.org/10.1136/ bcr-­2018-­227563. Alsever JD.  Lumbosacral plexopathy after gynecologic surgery: case report and review of the literature. Am J Obstet Gynecol. 1996;174:1769–77; discussion 1777–8. https://doi.org/10.1016/ s0002-­9378(96)70209-­0. Archer TM.  Varicella zoster lumbosacral plexopathy: a rare cause of lower limb weakness. BMJ Case Rep. 2018;2018:bcr2017223947. https://doi.org/10.1136/bcr-­2017-­223947. Babaei-Ghazani A, Eftekharsadat B, Samadirad B, Mamaghany V, Abdollahian S. Traumatic lower extremity and lumbosacral peripheral nerve injuries in adults: electrodiagnostic studies and patients symptoms. J Forensic Legal Med. 2017;52:89–92. https://doi. org/10.1016/j.jflm.2017.08.010. Babu MA, Spinner RJ, Dyck PJ, Amrami KK, Nathan MA, Kawashima A, et al. Recurrent prostatic adenocarcinoma with perineural spread to the lumbosacral plexus and sciatic nerve: comparing high resolution MRI with torso and endorectal coils and F-18 FDG and C-11

Further Reading choline PET/CT.  Abdom Imaging. 2013;38:1155–60. https://doi. org/10.1007/s00261-­013-­9991-­x. Brejt N, Berry J, Nisbet A, Bloomfield D, Burkill G.  Pelvic radiculopathies, lumbosacral plexopathies, and neuropathies in oncologic disease: a multidisciplinary approach to a diagnostic challenge. Cancer Imaging. 2013;13:591–601. https://doi. org/10.1102/1470-­7330.2013.0052. Capek S, Amrami KK, Howe BM, Collins MS, Sandroni P, Cheville JC, et al. Sequential imaging of intraneural sciatic nerve endometriosis provides insight into symptoms of cyclical sciatica. Acta Neurochir. 2016;158:507–12. https://doi.org/10.1007/s00701-­015-­2683-­2. Chahin N, Temesgen Z, Kurtin PJ, Spinner RJ, Dyck PJ. HIV lumbosacral radiculoplexus neuropathy mimicking lymphoma: diffuse infiltrative lymphocytosis syndrome (DILS) restricted to nerve? Muscle Nerve. 2010;41:276–82. https://doi.org/10.1002/mus.21507. Cimsit C, Yoldemir T, Akpinar IN.  Sciatic neuroendometriosis: magnetic resonance imaging defined perineural spread of endometriosis. J Obstet Gynaecol Res. 2016;42:890–4. https://doi.org/10.1111/ jog.12998. Delgado-García F, López-Domínguez JM, Casado-Chocán JL, Blanco-­ Ollero A, Robledo-Strauss A, Méndez-Sangil B, et al. Lumbosacral plexopathy as a form of presentation of an aneurysm of the iliac artery. Rev Neurol. 1999;28:1072–4. Dyck PJ, Windebank AJ. Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: new insights into pathophysiology and treatment. Muscle Nerve. 2002;25:477–91. https://doi.org/10.1002/ mus.10080. Ehler E, Vyšata O, Včelák R, Pazdera L. Painful lumbosacral plexopathy: a case report. Medicine (Baltimore). 2015;94:e766. https://doi. org/10.1097/MD.0000000000000766. Frischhut B, Ogon M, Trobos S, Judmaier W.  Sciatica as a manifestation of idiopathic megacolon: a previously undescribed causal relationship. J Pediatr. 1998;133:449. https://doi.org/10.1016/ s0022-­3476(98)70285-­9. Ge PS, Ng G, Ishaque BM, Gelabert H, de Virgilio C.  Iatrogenic pseudoaneurysm of the superior gluteal artery presenting as pelvic mass with foot drop and sciatica: case report and review of literature. Vasc Endovasc Surg. 2010;44:64–8. https://doi. org/10.1177/1538574409351990. Georgiou A, Grigsby PW, Perez CA.  Radiation induced lumbosacral plexopathy in gynecologic tumors: clinical findings and dosimetric analysis. Int J Radiat Oncol Biol Phys. 1993;26:479–82. https://doi. org/10.1016/0360-­3016(93)90966-­y. Ghijselings S, Bruyninckx F, Delport H, Corten K.  Inflammatory neuropathy of the lumbosacral plexus following Periacetabular osteotomy. Case Rep Orthop. 2016;2016:3632654. https://doi. org/10.1155/2016/3632654. Gujrathi R, Gupta K, Ravi C, Pai B. Sciatica: an extremely rare complication of the perianal abscess. Pol J Radiol. 2016;6(81):370–3. https://doi.org/10.12659/PJR.897269. Häckel S, Christen S, Vögelin E, Keel MJB. Exposure of the lumbosacral plexus by using the pararectus approach: a technical note. Oper Neurosurg (Hagerstown). 2023;24:e1–9. https://doi.org/10.1227/ ons.0000000000000418. Hébert-Blouin MN, Amrami KK, Myers RP, Hanna AS, Spinner RJ.  Adenocarcinoma of the prostate involving the lumbosacral plexus: MRI evidence to support direct perineural spread. Acta Neurochir. 2010;152:1567–76. https://doi.org/10.1007/ s00701-­010-­0682-­x. Hernalsteen D, Cosnard G, Peeters A, Duprez T.  Lumbar plexus involvement with chronic inflammatory demyelinating polyneu-

891 ropathy (CIDP): a variant case of the generic disorder. JBR-BTR. 2005;88:322–4. Howe BM, Amrami KK, Nathan MA, Garcia JJ, Spinner RJ. Perineural spread of cervical cancer to the sciatic nerve. Skelet Radiol. 2013;42:1627–31. https://doi.org/10.1007/s00256-­013-­1653-­0. Jo SY, Im SB, Jeong JH, Cha JG. Lumbosacral plexopathy caused by presacral recurrence of colon cancer mimicking degenerative spinal disease: a case report. Korean J Spine. 2015;12:103–6. https://doi. org/10.14245/kjs.2015.12.2.103. Katirji B, Wilbourn AJ, Scarberry SL, Preston DC. Intrapartum maternal lumbosacral plexopathy. Muscle Nerve. 2002;26:340–7. https:// doi.org/10.1002/mus.10216. Kutsy RL, Robinson LR, Routt ML Jr. Lumbosacral plexopathy in pelvic trauma. Muscle Nerve. 2000;23:1757–60. https://doi.org/10.1002/1097-­ 4598(200011)23:113.0.co;2-­m. Láinez JM, Yaya R, Lluch V, Casado I, Morera J, Sancho J. Lumbosacral plexopathy caused by aneurysms of the abdominal aorta. Med Clin (Barc). 1989;92:462–4. Laporte C, Albert JD, Duvauferrier R, Bertaud V, Gouillou M, Guillin R. MRI investigation of radiating pain in the lower limbs: value of an additional sequence dedicated to the lumbosacral plexus and pelvic girdle. AJR Am J Roentgenol. 2014;203:1280–5. https://doi. org/10.2214/AJR.13.11884. Lee JG, Peo H, Cho JH, Kim DH. Intraneural ganglion cyst of the lumbosacral plexus mimicking L5 radiculopathy: a case report. World J Clin Cases. 2021;9:4433–40. https://doi.org/10.12998/wjcc. v9.i17.4433. Lemos N, Cancelliere L, Li ALK, Moretti Marques R, Fernandes GL, Sermer C, et  al. Superior gluteal vein syndrome: an intrapelvic cause of sciatica. J Hip Preserv Surg. 2019;6:104–8. https://doi. org/10.1093/jhps/hnz012. London NJ, Sefton GK. Hematocolpos. An unusual cause of sciatica in an adolescent girl. Spine (Phila Pa 1976). 1996;21:1381–2. https:// doi.org/10.1097/00007632-­199606010-­00022. Luna R, Fayad LM, Rodriguez FJ, Ahlawat S.  Imaging of non-­ neurogenic peripheral nerve malignancy-a case series and systematic review. Skelet Radiol. 2021;50:201–15. https://doi.org/10.1007/ s00256-­020-­03556-­z. Melikoglu MA, Kocabas H, Sezer I, Akdag A, Gilgil E, Butun B. Internal iliac artery pseudoaneurysm: an unusual cause of sciatica and lumbosacral plexopathy. Am J Phys Med Rehabil. 2008;87:681–3. https://doi.org/10.1097/PHM.0b013e31816dca87. Muniz Neto FJ, Kihara Filho EN, Miranda FC, Rosemberg LA, Santos DCB, Taneja AK.  Demystifying MR neurography of the lumbosacral plexus: from protocols to pathologies. Biomed Res Int. 2018;2018:9608947. https://doi.org/10.1155/2018/9608947. Murata Y, Takahashi K, Murakami M, Moriya H.  An unusual cause of sciatic pain. J Bone Joint Surg Br. 2001;83:112–3. https://doi. org/10.1302/0301-­620x.83b1.10260. Myers MA, Harmon RL.  Sacral plexopathy and sciatic neuropathy after total knee arthroplasty. Electromyogr Clin Neurophysiol. 1998;38:423–6. Neufeld EA, Shen PY, Nidecker AE, Runner G, Bateni C, Tse G, et al. MR imaging of the lumbosacral plexus: a review of techniques and pathologies. J Neuroimaging. 2015;25:691–703. https://doi. org/10.1111/jon.12253. Ng PS, Dyck PJ, Laughlin RS, Thapa P, Pinto MV, Dyck PJB.  Lumbosacral radiculoplexus neuropathy: incidence and the association with diabetes mellitus. Neurology. 2019;92:e1188–94. https://doi.org/10.1212/WNL.0000000000007020.

892 Patel DK, Gwathmey KG.  Neoplastic nerve lesions. Neurol Sci. 2022;43:3019–38. https://doi.org/10.1007/s10072-­022-­05951-­x. Planner AC, Donaghy M, Moore NR. Causes of lumbosacral plexopathy. Clin Radiol. 2006;61:987–95. https://doi.org/10.1016/j. crad.2006.04.018. Rajashekhar RP, Herbison GJ.  Lumbosacral plexopathy caused by retroperitoneal hemorrhage, report of two cases. Arch Phys Med Rehabil. 1974;55:91–3. Richard A, Vellieux G, Abbou S, Benifla JL, Lozeron P, Kubis N. Good prognosis of postpartum lower limb sensorimotor deficit: a combined clinical, electrophysiological, and radiological follow-up. J Neurol. 2017;264:529–40. https://doi.org/10.1007/s00415-­016-­8388-­5. Sanal HT, Kocaoglu M, Bulakbasi N, Yildirim D. Pelvic hydatid disease: CT and MRI findings causing sciatica. Korean J Radiol. 2007;8:548–51. https://doi.org/10.3348/kjr.2007.8.6.548.

86  Sciatic Lumbosacral Plexopathies Stoeckli TC, Mackin GA, De Groote MA. Lumbosacral plexopathy in a patient with pulmonary tuberculosis. Clin Infect Dis. 2000;30:226– 7. https://doi.org/10.1086/313622. Tavee J, Mays M, Wilbourn AJ. Pitfalls in the electrodiagnostic studies of sacral plexopathies. Muscle Nerve. 2007;35:725–9. https://doi. org/10.1002/mus.20769. van Eijk J, Chan YC, Russell JW. Immunotherapy for idiopathic lumbosacral plexopathy. Cochrane Database Syst Rev. 2013;12:CD009722. https://doi.org/10.1002/14651858.CD009722.pub2. You JS, Park YS, Park S, Chung SP.  Lumbosacral plexopathy due to common iliac artery aneurysm misdiagnosed as intervertebral disc herniation. J Emerg Med. 2011;40:388–90. https://doi. org/10.1016/j.jemermed.2007.11.070.

Abdominopelvic and Retroperitoneal Tumors

87.1 Generalities and Relevance There are varying abdominopelvic or retroperitoneal tumors, benign or malignant, primary or secondary, associated with sciatic pain. These neoplasms may be originating from local or adjacent anatomic structures involving the nervous elements that cause the painful symptoms. Although clinical manifestations vary with the type of tumors and organs, the majority of patients suffering from sciatica present with a lumbosacral plexus neuropathy much more than a pure L5/ S1 radiculopathy or an isolated sciatic peripheral mononeuropathy. Regardless of their origin [Table 87.1], there are different types of primary or secondary intraabdominal or intrapelvic tumors causing sciatica as summarized in Table 87.2. Like the majority of lumbosacral plexopathies, the basic mechanism of intrapelvic tumors inducing sciatic pain may be multifactorial depending on their origin, size, and progression (acute, subacute, or chronic). However, most Table 87.1  Main anatomic structures involved in abdominopelvic tumors Abdomino-pelvic organs

Bones Joints Muscles

Nerves Other soft tissues

Colorectum Uterus Ovaries Prostate Sacrum Coccyx Iliac bone Sacroiliac Iliacus Piriformis Psoas Obturator internus Lumbosacral plexus and its branches Subcutaneous Adipose Lymph nodes

87

Table 87.2  Main sources of intraabdominal or intrapelvic tumors associated with sciatica Schwannoma, neurofibroma, neurofibromatosis, neurolymphomatosis, and malignant peripheral Malignant peripheral nerve sheath tumors (MPNST) (Figs. 87.1, 87.2, and 87.3) Intraabdominal and Benign or malignant uterine, intrapelvic tumors causing prostatic, and ovarian tumors. compression or invasion of the Lymphoma (Figs. 87.4, 87.5, and neural structures 87.6) Primary or secondary tumors  – Osseous structures originating from adjacent (osteochondroma, chordoma, pelvic structures osteosarcoma, chondrosarcoma…)  – Soft tissue structures (metastasis to muscle, sarcoma, lymphoma, lipoma, ganglion cyst…) (Figs. 87.7, 87.8, 87.9, 87.10, and 87.11) Tumors causing infiltration of  – Endoneural metastasis the nervous structure (melanomas, breast, lung, and kidney tumors)  – Lymphomatous involvement Primary tumors of the neural structures

tumoral lesions develop progressively and sciatica is explained through the following mechanisms: • Compression or Traction of the lumbosacral plexus or its components • Irritation and inflammation of the nervous elements • Infiltration and local destruction of underlying nervous elements • Ischemia secondary to microvascular disorders and even due to vascular ‘steal’ Some tumors may extend further downstream (toward extrapelvic deep gluteal area) or upstream (toward lateral

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_87

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894 Fig. 87.1  Case 1. Schwannoma (stars) of the left L4 nerve root (arrow) as seen on coronal (a) and axial (b) T2-weighted MRI

Fig. 87.2  Case 2. Malignant peripheral nerve sheath tumor of the left L4 nerve root (stars) with foraminal and retroperitoneal extension. Axial pelvic CT scan after contrast injection (a, b)

Fig. 87.3  Case 2. Malignant peripheral nerve sheath tumor depending on the left L4 nerve root (stars) as seen on axial (a) and coronal (b) T1-weighted MRI after gadolinium administration as well as on axial T2-weighted MRI (c) and on STIR sequence (d)

87  Abdominopelvic and Retroperitoneal Tumors

a

b

a

b

a

c

b d

87.1  Generalities and Relevance Fig. 87.4  Case 3. Large ovarian cyst (stars) in a 21-year-old woman manifesting as a left-sided sciatica. Axial T1-weighted MRI (a) and on STIR sequence (b) as well as on coronal (c) and sagittal T2-weighted MRI (d)

895

a

c

d

b

Fig. 87.5  Case 4. Intrapelvic tumor (star) in a 54-year-old man who presented with left-sided sciatica. Axial pelvic CT scan after contrast injection

lumbosacral foramen) causing deep gluteal syndrome or lumbosacral radiculoplexopathies, respectively. Tumors within the sciatic notch have the possibility to grow extremely great and develop wide dumbbell-shaped lesions. Treatment is not well codified due to the rarity of this clinical condition. Many therapeutic options have been proposed depending on the underlying etiologies and the patients’ conditions. However, early diagnosis and adequate management are critical in decreasing morbidity and even mortality. Although their prevalence is not well documented, digestive (e.g., colorectal carcinoma and sarcoma) and gynecologic (e.g., endometriosis) tumors represent the most frequent abdominal/pelvic tumoral lesions that cause lumbosacral plexopathy. Furthermore, lumbosacral plexopathy reveals the diagnosis of cancer in 15% of cancer patients. Neurogenic tumors are quite rare cause representing less than 2% of sciatica patients. Although schwannoma is the most common primary tumor of the peripheral nervous system, less than 1% originates from the sciatic nerve. Pelvic region schwan-

896 Fig. 87.6  Case 5. Uterine fibroid (leiomyoma) (stars) in a 59-year-old woman manifesting as left-sided sciatic pain as seen on axial CT scan (a–d)

Fig. 87.7  Case 6. Paraspinal lumbo-sacral tumor on the left side (stars) as seen on axial pelvic T2-weighted MRI (a, b)

87  Abdominopelvic and Retroperitoneal Tumors

a

b

c

d

a

b

87.1  Generalities and Relevance

897

a

b

Fig. 87.8  Case 7. This 60-year-old man presented with bilateral lumbosacral radicular pain (predominant on the left side). Sagittal T1- (a) and T2-weighted MRI (b, c) revealed a degenerative L3-L4 spinal ste-

Fig. 87.9  Case 7. Extensive type B lymphoma (stars) as seen on axial pelvic MRI on STIR sequences (a, b) and T2-weighted MRI (c, d)

c

nosis (arrow) and especially a sacral lesion with intravertebral, intrapelvic, and paraspinal extension (stars)

a

b

c

d

898 Fig. 87.10  Case 7. Extensive type B lymphoma (stars) as seen on axial pelvic CT scan following contrast administration (a–c)

87  Abdominopelvic and Retroperitoneal Tumors

a

b

c

Fig. 87.11  Case 8. Intrapelvic metastasis of a renal adenocarcinoma (stars) with extrapelvic extension through the right-sided greater sciatic foramen (arrows). This 65-year-old woman only had unilateral sciatic pain. Pelvic axial post-contrast CT scan (a) and 3D angio-CT scan (b). (Courtesy of Pr. Salah Bellasri)

a

nomas are rarer. Malignant peripheral nerve sheath tumors (MPNST) occur most often in patients with neurofibromatosis type 1 (NF-1), especially after radiation therapy. Among the remaining etiologies, endoneural metastases are often from melanomas and less commonly from breast, lung, or kidney tumors.

87.2 Clinical Presentations The majority of patients with sciatica related to tumoral lumbosacral plexopathy present in a gradual subacute/chronic manner with mild or without low back pain (c.f. Chap. 86 about Sciatic Lumbosacral Plexopathies). However, sciatic pain rarely exists in isolation but is often associated with other neurologic or non-neurologic symptoms in relation to

b

the underlying neoplastic diseases. Therefore, besides sciatica, other concomitant symptoms can comprise urinary, gynecologic, or colorectal dysfunctions. Physical examination may show lower abdominal pain with vague peritoneal signs of tenderness. Patients with sciatic pain but without recognizable spinal or extrapelvic causes should mention an intrapelvic source of sciatica. In addition to the neurological and general clinical examination, digital rectal examination and/or vaginal and transvaginal examination should not be left out. Indeed, some patients with intrapelvic sciatic schwannoma presented a positive Tinel’s sign during the digital rectal examination. More specifically, patients with malignant soft tissue or bone tumors present with initial insidious pelvic/perineal pain, being persistent, progressive, worsening at night, and not being relieved by changing position. The lag between

87.3  Paraclinic Features

initial pain and weakness or sensory loss may take weeks or months. In addition, fatigue and weight loss should point toward malignancy. Cases with malignant tumors infiltrating the lumbosacral plexus are more painful. A majority will also have other neurologic symptoms and signs such as weakness, paresthesia, and impaired reflexes. Half of the patients have tenderness over the sacrum or sciatic notch. Patients receiving pelvic irradiation for cancer may develop progressive leg weakness, often bilateral or more years later; imaging is crucial to the differential diagnosis from cancer recurrence. Young women with endometriosis present with sciatic pain classically starts a few days before menstruation, intensifies progressively, and shows some relief a week after the end of the menses (AKA catamenial sciatica). Clinical gynecological pelvic examination is usually unremarkable. However, response to hormonal treatment for endometriosis would provide further support for this unusual diagnosis. Patients with suspected neurogenic tumors should be investigated for possible association with neurofibromatosis. A deep neurocutaneous examination will be needed. Sometimes, the neurologic condition is confused and some clinical presentations are similar to diseases of the lumbosacral nerve roots or the sciatic trunk. Unlike sciatic radiculopathies and peripheral neuropathies, neurologic findings are mostly poorly defined and cannot be explained by a single nerve or single root lesion. However, separating plexopathy from radiculopathy on clinical grounds can be difficult or impossible in some cases. Therefore, in such cases, electrodiagnostic studies coupled with nerve conduction and needle electromyography will be decisive.

87.3 Paraclinic Features Pelvic magnetic resonance (MR) imaging, computed tomography (CT), ultrasonography, positron emission tomography (PET), and angiographic studies as well as biological investigations may be indicated for specific cases in the search for a tumoral lesion (Figs.  87.1, 87.2, 87.3, 87.4, 87.5, 87.6, 87.7, 87.8, 87.9, 87.10, and 87.11). However, among all neuroimaging techniques, magnetic resonance (MR) imaging remains the best method to detect lumbosacral plexopathy and provide evidence for the etiology. Complete assessment of the lumbosacral plexus should include both T1-weighted images (with and without gadolinium agent) and a fluid sensitive fat suppressed sequence like short tau inversion recovery (STIR) (Figs.  87.1, 87.3, 87.4, 87.7, 87.8, and 87.9). Furthermore, MR neurography becomes a useful technic for the assessment of lumbosacral plexus damage and its underlying causes [c.f. Chap. 86 about Sciatic Lumbosacral Plexopathies].

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Subtle pelvic bony destruction is better seen on a CT scan which is usually needed for the assessment of neoplasms involving bone. Most bony tumors are heterogeneous and may contain areas of calcifications (Figs. 87.2, 87.6, 87.10, and 87.11). However, when paraclinic explorations are inconclusive, a minimally invasive approach for performing image-guided percutaneous biopsies of pelvic organs, as well as a biopsy of the suspected affected nervous structure can be needed. Most endometriosis causing sciatic pain appears as a focal mass with a high signal intensity on both T1 and T2 weighted MR images, suggesting acute hemorrhage. However, signal intensities can vary depending on the nature of the hemoglobin breakdown products and the age of the lesion. On MR imaging, some gynecologic tumors can be misdiagnosed as retroversion of the uterus. Both schwannomas and solitary neurofibromas are often indistinguishable on imaging. Both tumors have a similar density on CT scan to that of adjacent muscles with various degrees of contrast enhancement. The majority of benign neural tumors are homogeneous and iso-hypointense with muscle on T1 and hyperintense on T2-weighted MR images. Interestingly, a central area of low-intensity signal may be seen (more commonly with neurofibromas), termed the “target sign”. About one-third of patients with neurofibroma are associated with NF-1. In such cases, neurofibromas are multiple and plexiform in appearance, with progressive diffuse involvement from the proximal to the distal part of the lumbosacral plexus (Fig. 87.1). The imaging features of malignant neural tumors may be similar to those of benign tumors, making differentiation between the two challenging. Findings that favor malignancy include large size, irregular margins, and heterogeneity. Signs of rapid enlarging mass in a patient are rather in favor of an MPNST (Figs. 87.1, 87.2, and 87.3). The appearance of soft tissue metastasis and sarcoma is variable. Often demonstrating low-attenuation mass in contrast CT scan with heterogeneous contrast enhancement. Calcification within the mass may be noticeable. On MR imaging, there are both high and low signal appearances when compared with surrounding muscle tissues depending on the existence of inflammation, hemorrhage, lobulation, or necrosis. However, necrosis, peritumoral edema, and lobulation are less commonly seen in soft-tissue sarcomas than in metastatic lesions. A histopathological analysis is required for a definitive diagnosis. Radiologists should be aware that in patients who have had previous surgery, postoperative fibrosis could mimic tumor recurrence. From this perspective, positron emission tomography (PET) could provide a better assessment in some difficult cases. Intrapelvic lymphoma may appear as an isolated entity, associated with systemic lesions, or in the context of primary

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central nervous system lymphoma. On neuroimaging, there are heterogeneous or focal low densities on CT scan, focal or diffuse low signal on T1-weighted images, and high signal on T2-weighted MR imaging. Contrast enhancement may be absent, ring-like, or uniform. These appearances in isolation may be impossible to distinguish from many focal pelvic or retroperitoneal lesions such as infection, MPNST, sarcoidosis, demyelinating and immune-mediated polyneuropathy, and hypertrophic neuropathy (Figs.  87.7, 87.8, 87.9, and 87.10). While very rare, direct lumbosacral plexus involvement with lymphoma has been reported.

87.4 Treatment Options Treatment of intrapelvic and intrabdominal tumors inducing sciatic pain is not well established and depends on many factors including but not limited to tumor origin, its size, grading, extension, intrinsic or extrinsic nature of the lesion in relation to the lumbosacral plexus, patient’s general condition, neurological disorders. Medication, conservative measures, surgery, laser ablation, radiotherapy, hormone therapy, and chemotherapy have been proposed. Several open surgical approaches have been proposed for tumors of intrapelvic and intraabdominal organs such as perineal approaches, anterior abdominal approaches, or mixed approaches, depending on the location and the size of the tumor, its potential malignant aspect, and whether or not contiguous organs are involved. Many authors suggested that abdominal approaches should be considered when the tumor is located and extended above the S3 vertebral level and perineal ones for tumors below S3. However, minimally invasive laparoscopic approaches are widely used nowadays. Most benign pelvic tumors may be directly dissected after the incision of the epineurium over the mass. Large tumors, especially double-shaped masses, demand the need for combined operative approaches because of the tumor’s dimension and the difficult anatomical relations between the tumors and the nervous structures. Regarding of their origins, malignancy should be correctly managed by chemotherapy, surgery, and/ or radiation therapy. The primary management of painful sciatic lumbosacral plexus endometriosis in the absence of neurological deficits is typically conservative. First-line therapy is represented by combined oral contraceptives and progestogens, whereas gonadotropin-releasing hormone agonists are second-line hormonal therapy. Surgery is indicated in patients who reported exponential worsening of gait disorders, lower limb weakness, foot drop, and neuropathic pain that became refractory to medical treatments. Laparoscopic retroperitoneal pelvic (surgical neuropelveology) resection is required

87  Abdominopelvic and Retroperitoneal Tumors

to obtain free margins but is still controversial owing to the risk of neurologic damage and irreversible gait disorders. The treatment of choice for a benign schwannoma is usually aggressive resection because of the high frequency of recurrence. However, large tumors or those that adhere to the retroperitoneal vessels may need only intralesional curettage and preserved the tumor capsule to prevent major vascular or nerve injury. As soon as the diagnosis of intrapelvic MPNST is suspected, surgical excision is the primary key to treatment. The aim of surgery is complete removal of the mass with tumor-­ free borders. Unfortunately, for MPNSTs that involve the lumbosacral plexus, it is difficult to achieve complete removal of the lesion with tumor-free borders without damaging the adjacent nervous structures.

87.5 Prognosis The prognosis is variable depending on the tumor’s nature and aggressiveness, initial neurological disorders, treatment response, delay of treatment, and the patient’s general condition. Prognosis is better for patients with benign neoplasm as well as for those without neural infiltration or invasion. Benign neurogenic tumors (schwannoma and neurofibroma) are generally considered to have a favorable prognosis if there are completely removed with nerve preservation. Progressive neurological deterioration is common in patients with lumbosacral plexopathy secondary to malignancy with life-threatening consequences. For example, in cases of MPNST, pulmonary metastasis is the main reason for death. Like other several causes of plexopathy, recovery from neurologic pain generally precede the reappearance of strength. Improvement is usually monophasic, slow (several months/years), and incomplete. In advanced cases with delayed management, complete recovery of motor function is rare, even after total surgical removal of the lesion. Fibrosis during the healing process is likely to induce permanent nerve damage. Whatever the results, careful clinical and paraclinical follow-up should be needed.

Further Reading Aguilera V, Calvo F, Nos P, Molla A, Esteban R, Ponce J.  Sciatica secondary to a presacral abscess as the first manifestation of Crohn’s disease. Gastroenterol Hepatol. 2002;25:505–7. https://doi. org/10.1016/s0210-­5705(02)70301-­4. Ajala-Agbo T, Tang PT, Bat-Ulzii DT. Unilateral leg weakness and pain secondary to metastatic anal squamous cell carcinoma. BMJ Case Rep. 2019;12:e227563. https://doi.org/10.1136/bcr-­2018-­227563. Akhaddar A, El-Asri AC.  Multiple massive neurofibromas of lumbosacral plexus with intraspinal and pelvic extension. Pan Afr Med J. 2014;17:67. https://doi.org/10.11604/pamj.2014.17.67.3869.

Further Reading Al-Khodairy AW, Bovay P, Gobelet C. Sciatica in the female patient: anatomical considerations, aetiology and review of the literature. Eur Spine J. 2007;16:721–31. https://doi.org/10.1007/ s00586-­006-­0074-­3. Bodack MP, Cole JC, Nagler W. Sciatic neuropathy secondary to a uterine fibroid: a case report. Am J Phys Med Rehabil. 1999;78:157–9. https://doi.org/10.1097/00002060-­199903000-­00015. Brejt N, Berry J, Nisbet A, Bloomfield D, Burkill G.  Pelvic radiculopathies, lumbosacral plexopathies, and neuropathies in oncologic disease: a multidisciplinary approach to a diagnostic challenge. Cancer Imaging. 2013;13:591–601. https://doi. org/10.1102/1470-­7330.2013.0052. Chitranjan, Kandpal H, Madhusudhan KS. Sciatic hernia causing sciatica: MRI and MR neurography showing entrapment of sciatic nerve. Br J Radiol. 2010;83:e65–6. https://doi.org/10.1259/bjr/47866965. Guedes F, Brown RS, Lourenço Torrão-Júnior FJ, Siquara-de-Sousa AC, Pires Amorim RM. Nondiscogenic sciatica: what clinical examination and imaging can tell us? World Neurosurg. 2020;134:e1053– 61. https://doi.org/10.1016/j.wneu.2019.11.083. Ichikawa J, Matsumoto S, Shimoji T, Tanizawa T, Gokita T, Hayakawa K, et  al. Intraneural metastasis of gastric carcinoma leads to sciatic nerve palsy. BMC Cancer. 2012;12:313. https://doi. org/10.1186/1471-­2407-­12-­313. Isiklar ZU, Lindsey RW, Tullos HS.  Sciatic neuropathy secondary to intrapelvic migration of an acetabular cup. A case report. J Bone Joint Surg Am. 1997;79:1395–7. https://doi. org/10.2106/00004623-­199709000-­00015. Jo SY, Im SB, Jeong JH, Cha JG. Lumbosacral plexopathy caused by presacral recurrence of colon cancer mimicking degenerative spinal disease: a case report. Korean J Spine. 2015;12:103–6. https://doi. org/10.14245/kjs.2015.12.2.103. Juković M, Koković T, Nikolić D, Ilić D, Till V.  Lower back pain— silent symptom of chronic infrarenal abdominal aneurysm rupture. Med Pregl. 2016;69:115–7. https://doi.org/10.2298/mpns1604115j. Kanaya K, Takebayashi T, Kawaguchi S, et al. Ovarian cyst presenting as sciatica: report of three cases. Seikei Geka. 2004;55:1311–4. Ladha SS, Spinner RJ, Suarez GA, Amrami KK, Dyck PJ. Neoplastic lumbosacral radiculoplexopathy in prostate cancer by direct perineural spread: an unusual entity. Muscle Nerve. 2006;34:659–65. https://doi.org/10.1002/mus.20597. Lee SE, Park HY, Kim S, Bang H, Min JH, Choi YL.  Epithelioid hemangioendothelioma with extensive cystic change and CAMTA1 rearrangement. Pathol Int. 2013;63:502–5. https://doi.org/10.1111/ pin.12097. Mavrogenis AF, Rossi G, Rimondi E, Calabrò T, Papagelopoulos PJ, Ruggieri P.  Palliative embolization for osteosarcoma. Eur J Orthop Surg Traumatol. 2014;24:1351–6. https://doi.org/10.1007/ s00590-­013-­1312-­0.

901 Mill CJ.  Case of sciatica depending on pressure by an Intrapelvic tumour. Edinb Med J. 1874;20:402–4. Murphy DR, Bender MI, Green G. Uterine fibroid mimicking lumbar radiculopathy: a case report. Spine (Phila Pa 1976). 2010;35:E1435– 7. https://doi.org/10.1097/BRS.0b013e3181e8ab84. Odell RT, Key JA. Lumbar disk syndrome caused by malignant tumors of bone. J Am Med Assoc. 1955;157:213–6. https://doi.org/10.1001/ jama.1955.02950200011003. Ortolan EG, Sola CA, Gruenberg MF, Carballo Vazquez F. Giant sacral schwannoma. A case report. Spine (Phila Pa 1976). 1996;21:522–6. https://doi.org/10.1097/00007632-­199602150-­00023. Planner AC, Donaghy M, Moore NR. Causes of lumbosacral plexopathy. Clin Radiol. 2006;61:987–95. https://doi.org/10.1016/j.crad. 2006.04.018. Robertson JH, Gropper GR, Dalrymple S, Acker JD, McClellan GA. Sacral plexus nerve sheath tumor: case report. Neurosurgery. 1983;13:78–81. https://doi.org/10.1227/00006123-­198307000-­ 00018. Sharifi G, Jahanbakhshi A.  Persistent L5 lumbosacral radiculopathy caused by lumbosacral trunk schwannoma. Asian J Neurosurg. 2017;12:51–4. https://doi.org/10.4103/1793-­5482.144158. Spinner RJ, Endo T, Amrami KK, Dozois EJ, Babovic-Vuksanovic D, Sim FH.  Resection of benign sciatic notch dumbbell-shaped tumors. J Neurosurg. 2006;105:873–80. https://doi.org/10.3171/ jns.2006.105.6.873. Topsakal C, Erol FS, Ozercan I, Murat A, Gurates B. Presacral solitary giant neurofibroma without neurofibromatosis type 1 presenting as pelvic mass—case report. Neurol Med Chir (Tokyo). 2001;41:620– 5. https://doi.org/10.2176/nmc.41.620. Wang J, Tang Q, Xie X, Yin J, Zhao Z, Li Z, et  al. Iliosacral resections of pelvic malignant tumors and reconstruction with nonvascular bilateral fibular autografts. Ann Surg Oncol. 2012;19:4043–51. https://doi.org/10.1245/s10434-­012-­2339-­x. Wang P, Chen C, Xin X, Liu B, Li W, Yin D, et al. Giant intrapelvic malignant peripheral nerve sheath tumor mimicking disc herniation: a case report. Mol Clin Oncol. 2016;5:653–6. https://doi. org/10.3892/mco.2016.1030. Woo PYM, Ho JMK, Ho JWK, Mak CHK, Wong AKS, Wong HT, et al. A rare cause of sciatica discovered during digital rectal examination: case report of an intrapelvic sciatic notch schwannoma. Br J Neurosurg. 2019;33(5):562–5. https://doi.org/10.1080/02688697.2 017.1378801. Yamada N, Kumagai M, Suzuki KS. A case of severe sciatica caused by a lymphocele after renal transplantation. JA Clin Rep. 2022;8:37. https://doi.org/10.1186/s40981-­022-­00527-­2. Ye BS, Sunwoo IN, Suh BC, Park JP, Shim DS, Kim SM. Diffuse large B-cell lymphoma presenting as piriformis syndrome. Muscle Nerve. 2010;41:419–22. https://doi.org/10.1002/mus.21538.

Intrapelvic and Retroperitoneal Vascular Lesions

88.1 Generalities and Relevance Among the abdominopelvic causes of sciatic pain, vascular lesions are sometimes developing diagnostic confusion with the traditional spinal causes. However, neurologic symptoms are mostly poorly defined and cannot be explained by a single nerve or single root lesion. Indeed, most patients present with a lumbosacral radiculoplexus neuropathy (including nerve roots, nerves, and lumbosacral plexus) much more than a pure L5/S1 radiculopathy or an isolated sacral plexopathy. These vascular lesions are variable. Regardless of their origin (arterial, venous, or arteriovenous), they frequently develop from the infrarenal abdominal aorta and iliac vessels, or their branches. The basic mechanism of vascular lesions-related sciatica may be multifactorial depending on their origin, size, and progression (acute, subacute, or chronic). However, most lesions develop progressively, finally leading to the development of symptoms and complications with time. Pathologic, structural, and hemodynamic changes may lead to: (a) (b) (c) (d)

Compression and mass effect on neural structures Irritation of neural elements Local destruction of underlying nerves Ischemia secondary to vasa vasorum compression and/ or due to vascular ‘steal’

The clinical presentation is variable and depends on the etiology. The majority of vascular lesions are chronic, and stable and may cause little if any, clinical symptoms, which are usually not manifested until later in life. An increase in size may enhance the risk of vascular rupture, which can be life-threatening. Besides neurologic pain and symptoms, they may produce a variety of symptoms referable to the urinary tract, digestive, gynecologic, or other adjacent pelvic structures.

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Treatment is often limited and varies considerably depending on the underlying etiologies and clinical presentations. However, early diagnosis and adequate management of vascular lesions are critical in decreasing morbidity and mortality. Vascular lesions can be congenital, acquired, or idiopathic. Acquired causes are trauma (including both penetrating and blunt), infection, inflammation, tumors eroding the vessels, and radiotherapy. Trauma also includes iatrogenic injury because of increasing minimally invasive needle biopsies and interventional surgical procedures. Table 88.1 represents the most frequent intrapelvic and abdominal vascular etiologies that contribute to sciatic pain previously published in the literature (Table 88.1). Other etiological factors have also been involved such as hypertension, arteriosclerosis, hypercholesterolemia, smoking, diabetes mellitus, and connective tissue disorders. Overall, the prevalence of chronic vascular lesions increases with age. Although rare, aneurysms arising from the iliac artery or its branches are the most frequent intrapelTable 88.1  The most frequent intrapelvic and abdominal vascular etiologies-related sciatica Arterial

Arteriovenous

Venous

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_88

Aorto-iliac obstruction (occlusive disease) Aneurysm Distal abdominal aorta Common iliac artery Internal iliac artery (AKA hypogastric artery) Pseudo-aneurysm Distal abdominal aorta Internal iliac artery Superior gluteal artery Inferior gluteal artery Arteriovenous fistula Arteriovenous Branches of the internal malformation (AVM) iliac artery and vein Aberrant superior gluteal vein (neurovascular conflict) Malformed vein from internal iliac vessels

903

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vic vascular lesions related to sciatica. The rest of the lesions rarely cause sciatic pain. Regarding aneurysms of the iliac arteries, they represent less than 2% of all aneurysmal diseases. Often uncomplicated, they are asymptomatic in up to 78% of affected cases. Patients with iliac artery aneurysms are usually elderly males occurring in the seventh to eighth decade of life.

88.2 Clinical Presentations The initial evaluation should include a detailed past medical history and careful neurological and vascular examination. History would include questions about recent injuries, infections, medical procedures, surgeries in the pelvic region, natal/deliveries, medications, or any previous medical problems. Classically, sciatic pain caused by traumatic injury or vascular etiologies presents acutely. However, there can be a significant delay between the initial trauma or iatrogenic procedure and the onset of symptoms in intrapelvic vascular-­ related sciatica. Indeed, most sciatic pain presents in a gradual subacute manner with mild or without low back pain. Within this context, abdominopelvic vascular lesions generally present with a combination of sciatic pain, progressive numbness and weakness, and sensory loss in the leg. Sphincter dysfunction may be seen but low back pain is unusual. Occasionally obturator neuralgia or foot drop have been reported. Neurological presentations are often unilateral but some lesions manifest bilaterally. Treating clinicians should look for an expanding vascular mass: a firm, non-tender mass with pulsation or thrill on palpation and a bruit on auscultation. However, unless they are large, it is almost impossible to examine them clinically because they are located deep within the pelvis. Some cases are usually incidentally discovered during abdominal imaging examinations or at the time of rupture. Additionally, in some patients, a pulsating mass can be palpated on a rectal or vaginal examination. More specifically, patients with aortoiliac occlusive disease present with a Leriche syndrome including fatigue of both lower limbs, intermittent bilateral claudication with ischemic pain, and absent or diminished femoral pulses. However, the symptoms resolve during rest after a predictable period. Advanced presentations will have an absence of penile erection in addition to pallor or coldness of both lower extremities. Dilated or malformed branches of the internal or external iliac vessels can entrap the nerves of the sacral plexus against the pelvic sidewalls, producing symptoms that are not commonly seen in gynecological practice, such as sciatica, perineal pain irradiating to the lower limbs, or refractory urinary

88  Intrapelvic and Retroperitoneal Vascular Lesions

and anorectal dysfunction in the absence of a spinal disorder or pelvic organ prolapse. Aneurysm and pseudoaneurysm may stay asymptomatic, but when ruptured the consequences can be life-threatening. Sciatic pain related to intrapelvic vascular lesions rarely exists in isolation but is often associated with other neurologic or non-neurologic symptoms linked with the primary etiology and relevant factors. Therefore, in addition to sciatica, other simultaneous symptoms can include perineal or gluteal pain, anorectal dysfunction, rectal pain and/or lower obstructive uropathy, leg edema, deep vein thrombosis, arterial insufficiency, fever, fatigue, and weight loss.

88.3 Paraclinic Features Because of the predominance of abdominopelvic symptoms, duplex ultrasonography permits confirmation of the vascular origin of the mass. If vascular etiology is not suspected, it may end in an imaging-guided biopsy resulting in a catastrophe. In cases of aneurysm or pseudoaneurysm, ultrasound examination would show turbulent bidirectional flow. Traditional lumbar computed tomography and magnetic resonance imaging are shown to be insufficient. However, the most satisfactory imaging technics for diagnosing these patients were retroperitoneal and pelvic computed tomography angiography (CTA) scan (Fig. 88.1) and magnetic resonance angiography (MRA) which would dem-

Fig. 88.1  Axial pelvic CT scan showing a retroperitoneal hematoma in red color

Further Reading

onstrate the vascular lesion clearly. They allow delineation of the true extent of the lesion, its topographic localization, and the involvement of adjacent pelvic structures. CTA and MRA will distinguish slow-flow venous malformations from high-flow arteriovenous malformations and arteriovenous fistulas. Dilatation in the artery may be surrounded by a calcified wall. Classically, the aneurysm had a large neck, and the pseudoaneurysm had a tight one. Sometimes, there is a thrombus formation within the aneurysm. Formal arteriography is both diagnostic and therapeutic. Imaging tools are also useful for monitoring these lesions. Sometimes, electrodiagnostic investigations such as nerve conduction explorations and electromyography can be useful in distinguishing lumbosacral radiculopathies from lumbosacral plexopathies and peripheral neuropathies. Further paraclinical and biological investigations may be indicated for specific cases in the search for an underlying etiology.

88.4 Treatment Options Treatment selection should consider the lesion size, angioarchitecture, hemodynamics, involvement of other vascular segments, presence of bilateral/unilateral lesion, compression symptoms, as well as the patient’s general conditions. There are different ways to treat these vascular lesions such as endovascular procedures, surgical repair (open or via laparoscopic retroperitoneal dissection), ultrasound-guided compression technique, thrombin injection, stereotactic body radiotherapy, or a combination of some of them. Nowadays, endovascular techniques are increasingly used and preferred because of fewer technical risks and complications. Anticoagulation therapy may also be required. For AVM, treatment options include endovascular embolization or repair, surgical excision, and stereotactic body radiotherapy (hypofractionated stereotactic body radiotherapy) alone or in combination. The goal of pseudoaneurysm and aneurysm treatment is exclusion from circulation. While management of iliac artery and gluteal artery aneurysm/pseudoaneurysm has undergone considerable evolution over the past century, endovascular coil embolization and stenting are the current procedures of choice. Open surgery to ligate the aneurysm/pseudoaneurysm and their parent arteries, remove a residual hematoma, or release compressed nerve tissue should only be indicated if endovascular management fails. Chronic contained abdomino-aortic aneurysm rupture warrants semi-emergency surgery. Aberrant and malformed venous lesions required surgical decompression (de-trapping the underlying nerves), coagulation, and ligation at best via laparoscopic retroperitoneal dissection.

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Treatment of systemic illness commonly results in an improvement in sciatic neuropathic symptoms. Malignancy should be correctly managed by chemotherapy, surgery, and/ or radiation therapy. Appropriate anti-infectious agents (e.g., antibiotics, anthelmintics, and antifungals) are required in infectious diseases.

88.5 Outcome and Prognosis The prognosis is variable depending on the underlying etiology, treatment response, and delay of treatment. The prognosis is better for patients with venous or arteriovenous lesions. Traumatic arterial lesions are generally considered to have a less favorable prognosis. Progressive neurological deterioration is common in patients with lumbosacral plexopathy secondary to malignancy with life-threatening consequences. The rupture of an abdominal aortic aneurysm is a severe surgical emergency condition with a high rate of mortality. If pressure symptoms are predominant, endovascular treatment compared to the open surgical method takes more time for resolving symptoms. As for other lumbosacral plexopathies, recovery from pain generally precedes the reappearance of strength. Improvement is usually monophasic, slow (several months/ years), and incomplete. In general, delayed diagnosis of vascular lesions and lack of response to initial traditional therapies are associated with poor prognosis.

Further Reading Ashleigh RJ, Marcuson RW. False aortic aneurysm presenting as sciatic nerve root pain. Eur J Vasc Surg. 1993;7:214–6. https://doi. org/10.1016/s0950-­821x(05)80767-­4. Boulouis G, Shotar E, Dangouloff-Ros V, Janklevicz PH, Boddaert N, Naggara O, et  al. Progressive paralyzing sciatica revealing a pelvic pseudoaneurysm a year after hip surgery in a 12yo boy. Eur J Paediatr Neurol. 2016;20:179–82. https://doi.org/10.1016/j. ejpn.2015.10.004. Delgado-García F, López-Domínguez JM, Casado-Chocán JL, Blanco-­ Ollero A, Robledo-Strauss A, Méndez-Sangil B, et al. Lumbosacral plexopathy as a form of presentation of an aneurysm of the iliac artery. Rev Neurol. 1999;28:1072–4. Ehler E, Vyšata O, Včelák R, Pazdera L. Painful lumbosacral plexopathy: a case report. Medicine (Baltimore). 2015;94:e766. https://doi. org/10.1097/MD.0000000000000766. Ge PS, Ng G, Ishaque BM, Gelabert H, de Virgilio C.  Iatrogenic pseudoaneurysm of the superior gluteal artery presenting as pelvic mass with foot drop and sciatica: case report and review of literature. Vasc Endovasc Surg. 2010;44:64–8. https://doi. org/10.1177/1538574409351990. Gutman H, Zelikovski A, Gadoth N, Lahav M, Reiss R. Sciatic pain: a diagnostic pitfall. J Cardiovasc Surg. 1987;28:204–5. Hatzidakis A, Touloupakis E, Charalambous S, Reppa D, Karagiannakidis E.  Giant internal iliac artery aneurysm success-

906 fully treated with endovascular stent-graft placement. Interv Med Appl Sci. 2018;10:54–8. https://doi.org/10.1556/1646.10.2018.04. Huang TY, Yeh CH, Wang YC, Cheng YT, Feng PC.  Progressing left-side sciatica revealing a common iliac artery mycotic aneurysm in an elderly patient: a CARE-compliant case report. Medicine (Baltimore). 2020;99:e22476. https://doi.org/10.1097/ MD.0000000000022476. Jo SY, Im SB, Jeong JH, Cha JG. Lumbosacral plexopathy caused by presacral recurrence of colon cancer mimicking degenerative spinal disease: a case report. Korean J Spine. 2015;12:103–6. https://doi. org/10.14245/kjs.2015.12.2.103. Jooya A, Simons ME, Tsang DS.  Stereotactic body radiotherapy (SBRT) for an extracranial arteriovenous malformation of the pelvis. Cureus. 2021;13:e18750. https://doi.org/10.7759/ cureus.18750. Kale A, Basol G, Topcu AC, Gundogdu EC, Usta T, Demirhan R.  Intrapelvic nerve entrapment syndrome caused by a variation of the Intrapelvic piriformis muscle and abnormal varicose vessels: a case report. Int Neurourol J. 2021;25:177–80. https://doi. org/10.5213/inj.2040232.116. Kale A, Basol G, Usta T, Cam I. Vascular entrapment of both the sciatic and pudendal nerves causing persistent sciatica and pudendal neuralgia. J Minim Invasive Gynecol. 2019;26:360–1. https://doi. org/10.1016/j.jmig.2018.04.014. Láinez JM, Yaya R, Lluch V, Casado I, Morera J, Sancho J. Lumbosacral plexopathy caused by aneurysms of the abdominal aorta. Med Clin (Barc). 1989;92:462–4. Lemos N, Cancelliere L, Li ALK, Moretti Marques R, Fernandes GL, Sermer C, et  al. Superior gluteal vein syndrome: an intrapelvic cause of sciatica. J Hip Preserv Surg. 2019;6:104–8. https://doi. org/10.1093/jhps/hnz012. Lemos N, Sermer C, Fernandes G, Morgado-Ribeiro A, Rossos A, Zhao ZY, et al. Laparoscopic approach to refractory extraspinal sciatica and pudendal pain caused by intrapelvic nerve entrapment. Sci Rep. 2021;11:10820. https://doi.org/10.1038/s41598-­021-­90319-­y. Levy LA.  Arteriosclerotic common iliac aneurysm causing sciatic pain. Arch Neurol. 1977;34:581. https://doi.org/10.1001/ archneur.1977.00500210083018.

88  Intrapelvic and Retroperitoneal Vascular Lesions Lowenthal RM, Taylor BV, Jones R, Beasley A. Severe persistent sciatic pain and weakness due to a gluteal artery pseudoaneurysm as a complication of bone marrow biopsy. J Clin Neurosci. 2006;13:384–5. https://doi.org/10.1016/j.jocn.2005.03.027. Melikoglu MA, Kocabas H, Sezer I, Akdag A, Gilgil E, Butun B. Internal iliac artery pseudoaneurysm: an unusual cause of sciatica and lumbosacral plexopathy. Am J Phys Med Rehabil. 2008;87:681–3. https://doi.org/10.1097/PHM.0b013e31816dca87. Mohan SR, Grimley RP. Common iliac artery aneurysm presenting as acute sciatic nerve compression. Postgrad Med J. 1987;63:903–4. https://doi.org/10.1136/pgmj.63.744.903. Nguyen TT, Le NT, Doan QH. Chronic contained abdominal aortic aneurysm rupture causing vertebral erosion. Asian Cardiovasc Thorac Ann. 2019;27:33–5. https://doi.org/10.1177/0218492318773237. Papadopoulos SM, McGillicuddy JE, Messina LM.  Pseudoaneurysm of the inferior gluteal artery presenting as sciatic nerve compression. Neurosurgery. 1989;24:926–8. https://doi. org/10.1227/00006123-­198906000-­00025. Planner AC, Donaghy M, Moore NR. Causes of lumbosacral plexopathy. Clin Radiol. 2006;61:987–95. https://doi.org/10.1016/j. crad.2006.04.018. Rajashekhar RP, Herbison GJ.  Lumbosacral plexopathy caused by retroperitoneal hemorrhage, report of two cases. Arch Phys Med Rehabil. 1974;55:91–3. Vos LD, Bom EP, Vroegindeweij D, Tielbeek AV.  Congenital pelvic arteriovenous malformation: a rare cause of sciatica. Clin Neurol Neurosurg. 1995;97:229–32. https://doi. org/10.1016/0303-­8467(95)00032-­f. You JS, Park YS, Park S, Chung SP.  Lumbosacral plexopathy due to common iliac artery aneurysm misdiagnosed as intervertebral disc herniation. J Emerg Med. 2011;40:388–90. https://doi. org/10.1016/j.jemermed.2007.11.070. Yurtseven T, Zileli M, Göker EN, Tavmergen E, Hoşcoşkun C, Parildar M. Gluteal artery pseudoaneurysm, a rare cause of sciatic pain: case report and literature review. J Spinal Disord Tech. 2002;15:330–3. https://doi.org/10.1097/00024720-­200208000-­00013. Zitouna K, Selmene MA, Derbel B, Rekik S, Drissi G, Barsaoui M. An unexpected etiology of lumbosciatica. Tunis Med. 2019;97:1415–8.

Pelvic and Intrapelvic Infections

89.1 Definition and Relevance Pelvic and intrapelvic infections may involve various anatomic structures including bones, joints, muscles, intrapelvic organs, vessels, and nerves (Table  89.1). Sometimes, these infectious lesions may cause sciatic pain, which is difficult to distinguish from traditional spinal sciatica. However, most patients with sciatica related to pelvic and intrapelvic infections present with a lumbosacral plexus neuropathy much more than an “isolated” L5/S1 radiculopathy or a “pure” sciatic peripheral mononeuropathy. In addition, further signs and symptoms of local and/or general infection are highly suggestive but may be lacking. Development of pelvic and intrapelvic infections may occur through three main contamination ways: • Contiguous extension of infection from adjacent surrounding areas

Table 89.1  Main anatomic structures involved in pelvic and intrapelvic infections Anatomic structures Bones Joints Muscles

Intrapelvic organs

Vessels Nerves

Organs Sacrum Coccyx Iliac bone Sacroiliac joints Psoas-Iliac Piriformis Obturator internus Levator ani muscles Bladder Rectum Uterus Ovaries Fallopian tubes Iliac artery and vein Lumbar and sacral plexus

Types of infection Osteomyelitis

Sacroiliitis Psoas abscess Myositis Pyomyositis Suppurative collections

Mycotic aneurysm Plexitis

89

• Direct inoculation from a trauma injury or iatrogenic procedure • Hematogenous spread (arterial or venous) from a remote infectious source Nevertheless, some cases remain “cryptogenic”. Gastrointestinal or genitourinary tract infections are by far the most common origin of pelvic and intrapelvic infections causing sciatic pain. Also, the iliopsoas muscle, and the iliac vessels, are the potential ways along which abdominal infections may spread into the pelvis. Furthermore, presacral abscesses related to sacral osteomyelitis or sacroiliac infection may directly affect the lumbosacral plexus and even the sciatic trunk and consequently cause sciatica. Other diseases like tuberculosis, Crohn, or Human Immunodeficiency Virus (HIV) can also determine the formation of perirectal or perianal suppurations (Table 89.2). There are variable pathogens involved whether bacterial, mycobacterial, fungal (mycotic), or parasitic.

Table 89.2  Main sources of infections in the pelvic area Iliopsoas muscle Lumbosacral spondylodiscitis Infectious sacroiliitis Pyomyositis Gastrointestinal infections (sigmoid diverticulitis, Crohn’s disease, appendicitis) Genitourinary infections (renal, vesical, tubo-ovarian infections) Pelvic inflammatory diseases (salpingitis) Hematogenous dissemination Infected hematomas Post-surgical infections (iatrogenic) Post-traumatic infections Tumors (colorectal carcinoma) Skin (perineum, primary staphylococcal abscess) Iatrogenic (e.g., “unsafe” abortions) Septic pelvic thrombophlebitis Idiopathic (unknown etiology)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_89

907

908

Many underlying diseases and some risk factors can be identified in the patients such as pelvic inflammatory disease, intrauterine device, immunocompromised states, diabetes mellitus, and trauma in addition to potential concomitant regional or general infections. Treatment varies considerably depending on the underlying etiologies, lesion size, the spread of disease, as well as the patient’s comorbidities and general conditions. However, early diagnosis and adequate management are critical in decreasing morbidity and even mortality. Most lesions develop acutely or subacutely, ultimately leading to the onset of symptoms and complications over time. Chronic forms are not rare, especially encountered with tuberculosis, brucellosis, fungal and parasitic pathogens. Pain in sciatic-related intrapelvic infections mainly results from: (a) Direct compression of the lumbosacral plexus including subsequent ischemia (b) Irritation of neural elements (c) Local destruction and invasion of neural structures (d) Acute or chronic inflammatory phenomena

89.2 Clinical Presentations The initial evaluation should include a detailed past medical history and a general physical exam to guide the diagnosis. Possible underlying diseases and some predisposing factors must be taken into consideration especially recent history of sepsis, invasive diagnosis technique, recent injuries, surgical procedures, and previous gastrointestinal or genitourinary diseases. Generally, clinical signs and symptoms of pelvic and intrapelvic infections are nonspecific and often related to gastrointestinal, gynecologic, or urologic problems. Physical examination may show lower abdominal pain with vague peritoneal signs of tenderness. More rarely, compression of the sciatic nerve can cause pain radiating down the posterior thigh that is typically aggravated by dorsiflexion, or sensory neuropathy related to lumbar and/or sacral plexopathies [c.f. Chap. 86 about Sciatic Lumbosacral Plexopathies]. Sciatic pain can rarely be the first and unique presenting symptom. In late clinical forms, neurologic deficits including leg weakness, sensory disturbance, foot drop, muscular atrophy, and gait difficulty would be found. Symptoms are often unilateral; however, bilateral involvement has been reported before. Clinical presentation can be fulminant, acute, subacute, or chronic. However, the course of these infectious diseases is often long and more indolent in granulomatous (mycobacteria, brucellosis, or mycosis) and hydatidosis than in pyogenic

89  Pelvic and Intrapelvic Infections

infections. Systemic findings including fever, chills, night sweats, weight loss, anorexia, and general malaise may be present but inconstant. Closer attention should be paid to local examination including pelvic, lumbosacral spine, sacroiliac joint, ­perineal, hip, and gluteal areas because pelvic infections may reach extra-pelvic sites by traveling via certain well-defined routes including the buttock and thigh. Digital rectal examination and/or vaginal and transvaginal examination can be helpful. In addition, the course of the sciatic nerve should be examined for extraspinal pathologies. However, in almost all cases, identifying the nature of the disease by examining the signs and symptoms is often impossible without additional endoscopic or imaging explorations. In some cases, separating a lumbosacral plexopathy from radiculopathies or peripheral neuropathies on clinical grounds can be difficult or impossible. Therefore, in such cases electrodiagnostic studies are decisive.

89.3 Imaging Features Due to the preponderance of abdominal and pelvic symptoms, ultrasonography is often the first imaging examination performed as part of the initial clinical examination. Also, transvaginal ultrasonography is more useful providing clear images of pelvic and vascular structures by means of color Doppler sonography. Typically, a tubo-ovarian abscess is seen as a complex cystic adnexal or cul-de-sac mass with thick irregular walls, septations, and internal echoes. Currently, CT scan and MRI are the modalities of choice in the assessment of pelvic and intrapelvic infectious disorders (Figs. 89.1, 89.2, 89.3, 89.4, 89.5, 89.6, 89.7, and 89.8). MRI has been shown to be better than or equal to CT for imaging soft tissue extent, bone marrow involvement, and neurovascular involvement. However, indirect bony erosion is better seen on CT scan which is usually required for surgical planning and performing image-guided percutaneous biopsies or abscess drainage if required. The presence of air in the abscess cavity and along the sciatic nerve is highly suggestive of the perineural spread of the abscess. On MRI, the abscesses appear as soft collections that are fluid-filled and thus easily drained tend to be high on T2-weighted images and will enhance peripherally following gadolinium administration around a central core of low on T1-weighted images. The diffusion weighted-image (DWI) sequence can help to differentiate between the acute and chronic stages of the infection: hyperintense in the acute stage and hypointense in the chronic stage. Differential diagnosis panels are extensive and include, cystic ovarian tumor, lymphangioma, presacral epidermoid/teratoma, and anterior sacral meningocele.

89.3  Imaging Features Fig. 89.1  Presacral abscess (stars) as seen on sagittal reconstructions (a) and axial (b) pelvic CT scan

909

a

b

a

b

c

d

Fig. 89.2  Unilateral infectious Sacroiliitis (arrows) with presacral abscess (stars). Axial pelvic CT scan (a, b), sagittal T1- (c) and T2-weighted MRI of the lumbosacral spine (d)

Classically, soft tissue hydatidosis presents as a uni- or multiloculated cystic lesion with thin uniform walls. Both on MRI and CT scan, the cyst content has similar features to cerebrospinal fluid (Fig. 89.7). A modification in the density or signal intensity may suggest inactivation of the cyst viability. Classically, no walls enhance following gadolinium administration. Adjacent bony involvement is possible. It is also necessary to look for concomitant pulmonary and hepatic cysts. MRI remains the best method to detect lumbosacral plexopathy. However, the obliquity of the roots in the lumbar plexus makes them difficult to visualize on MRI. Complete

assessment of the lumbosacral plexus should include both T1-weighted images (with and without gadolinium agent) and a fluid-sensitive fat-suppressed sequence like short tau inversion recovery (STIR). MR neurography is a useful technic in helping to clearly determine extraspinal injuries responsible for the plexopathy. Depending on the severity of the damage, T2-weighted MRI may show hyperintensity in the nerve fibers, abnormal fascicular appearance, nerve enlargement, or deformation. Further paraclinical (e.g., endoscopy) and biological investigations may be indicated for specific cases in the search for an underlying etiology.

910 Fig. 89.3  Case 1. Large intrapelvic retroperitoneal abscess on the right side (stars) as seen on axial CT scan before (a, b) and after (c, d) contrast injection

Fig. 89.4  Case 1. A great intrapelvic retroperitoneal abscess (stars) as seen on coronal (a) and sagittal (b) reconstructions

89  Pelvic and Intrapelvic Infections

a

b

c

d

a

b

89.3  Imaging Features

911

Fig. 89.5  Retroperitoneal tuberculous abscesses (stars) with extrapelvic extension through the right greater sciatic foramen (double arrows) as seen on axial pelvic CT scan Fig. 89.6  Axial (a) and coronal reconstructions (b) pelvic CT scan showing chronic sacroiliac osteomyelitis on the left side (arrows)

Fig. 89.7 Intrapelvic retroperitoneal multiloculated hydatidosis (stars) manifested as unilateral sciatic pain. Axial (a, b) and coronal reconstructions (c) CT scan

a

a

c

b

b

912 Fig. 89.8  Sacroiliac bone hydatidosis (arrows) as seen on axial pelvic CT scan (a, b)

89  Pelvic and Intrapelvic Infections

a

89.4 Laboratory Findings White blood cell count, erythrocyte sedimentation rate, and C-reactive protein are frequently found only moderately elevated. These results are not very sensitive nor specific indicators in establishing the diagnosis. However, elevated procalcitonin levels can be a strong indication for determining the presence of pyogenic bacterial infections. In addition, blood culture may be positive. Screen for other potential causes of infection is important for identifying the causative pathogens. The most common pathogen involved are Staphylococcus aureus, gram-negative rods (particularly Escherichia coli, Proteus species, and Bacteroides species), Streptococcus species, and Enterococcus species. Other pathogens are rare including Chlamydia trachomatis, Neisseria gonorrhea, and Actinomyces israelii). Mycobacterium tuberculosis is more common in many developing countries (especially from Asia and Africa); on the other side, brucellosis is seen in countries around the Mediterranean Sea and is related to animal contact or the consumption of raw milk or its derivatives. Fungal agents are rare but are more expected to be encountered in immunocompromised patients. Although unusual, hydatidosis (echinococcosis), is among the most common parasites involving the pelvic cavity. Pelvic infections are known to be polymicrobial. Interestingly, image-guided percutaneous biopsies or abscess drainage if required can be very helpful for the diagnosis (using ultrasonography or CT scan guidance). Histopathologic studies are an essential tool for identifying specific infections such as mycobacteria, fungi, and parasites. Serologic or antigen testing for specific bacteria, mycotic or parasitic infections may be useful in some patients from countries where these diseases are endemic.

89.5 Treatment Options and Prognosis The goal of treatment is to eradicate the infection definitely, decompress the nervous structures, manage the underlying cause, and preserve the neurologic function.

b

Identification of pathogens, underlying causes as well as the origin of sciatica related to intrapelvic infections is important for determining therapy and prognosis. For traditional bacterial infections, appropriate intravenous antibiotic agents are used for 1–2 weeks (empiric antibiotics include third-generation cephalosporin, vancomycin, and metronidazole), followed by additional 2–4  weeks of oral antibiotics. Antibiotic therapy should always be personalized according to culture results, antibiotic susceptibility testing, patient’s clinical conditions, and severity of the infection. Tuberculosis infection needs a first-line regimen of a combination of isoniazid, rifampicin, pyrazinamide, and ethambutol or streptomycin for 2 months followed by two drugs (isoniazid and rifampicin) for 6  months. Brucellosis infection is habitually treated with an association of doxycycline and rifampicin for 6 months. Fungal/mycotic infections must be treated with the appropriate anti-infectious agents (amphotericin B or azole drugs). Oral antihelminthic drugs such as albendazole/mebendazole are encouraging for hydatid disease. Surgical procedures (anterior, posterior, posterolateral, and lateral laparotomy or laparoscopy) are indicated to get diagnostic cultures, decompress lumbosacral plexus and nerve, drain associated suppurative collections, and debride infected and necrotic tissue when infection continues or deteriorates regardless of appropriate anti-infectious agents. Currently, laparoscopy is mostly used. Less invasive surgical procedures may be indicated such as percutaneous image-guided which is appropriate for draining uniloculated and multiloculated abscesses with few septations. The access routes were either the transabdominal, transgluteal, transrectal, or transvaginal. However, there is an increased risk of bowel injury with transabdominal drainage compared to the transvaginal route. Regarding hydatid cysts, biopsy sampling involves a high risk of anaphylactic reaction and contamination of adjacent tissues. According to many authors, there are five main indications for surgical treatment in patients with intrapelvic infections:

Further Reading

1. Surgical emergency (e.g., abscess rupture or bowel perforation) 2. Abscess material failed to drain 3. Unsuccessful response with anti-infectious agents and drainage 4. Doubt about the diagnosis 5. Hydatidosis During surgery, however, particular caution was necessary to separate the abscess from the iliac vessels and sacral nerve plexus that had closely adhered to the lesion. Conservative management with antimicrobial therapy alone can be proposed in some patients in the early stage of infection, with small abscesses (under 3 cm in diameter) those with poor clinical conditions, or those with wild neurologic disorders. The outcome depends mainly on the preoperative neurologic conditions of the patient, the delay in diagnosis and initiation of treatment, the potential underlying diseases, the associated lesions, the virulence of the causative pathogen(s), and the response to treatment. If treated timely and adequately, most cases of intrapelvic infections will be cured without additional complications or recurrent infections. Mortality is rare nowadays.

Further Reading Abbas TO.  Pelvic primary staphylococcal infection presenting as a thigh abscess. Case Rep Surg. 2013;2013:539737. https://doi. org/10.1155/2013/539737. Aguilera V, Calvo F, Nos P, Molla A, Esteban R, Ponce J.  Sciatica secondary to a presacral abscess as the first manifestation of Crohn’s disease. Gastroenterol Hepatol. 2002;25:505–7. https://doi. org/10.1016/s0210-­5705(02)70301-­4. Akhaddar A, Hall W, Ramraoui M, Nabil M, Elkhader A.  Primary tuberculous psoas abscess as a postpartum complication: case report and literature review. Surg Neurol Int. 2018;9:239. https:// doi.org/10.4103/sni.sni_329_18. Amato L, Valeri M, Emini P, Ciaccarini R, Petrina A, Ribacchi F, et  al. Retroperitoneal and iliopsoas abscess as Crohn’s disease onset mimicking a common lumbosciatic pain. Ann Ital Chir. 2022;11:S2239253X22037458. Andrews DW, Friedman NB, Heier L, Erickson A, Lavyne MH.  Tuboovarian abscess presenting as sciatic pain: case report. Neurosurgery. 1987;21:100–3. https://doi. org/10.1227/00006123-­198707000-­00024. Baba H, Okumura Y, Furusawa N, Omori H, Kawahara H, Fujita T, et al. Dumb-bell shaped tuberculous abscess across the greater sciatic notch compressing both sciatic nerves. Spinal Cord. 1998;36:584– 7. https://doi.org/10.1038/sj.sc.3100550. Casola G, vanSonnenberg E, D’Agostino HB, Harker CP, Varney RR, Smith D.  Percutaneous drainage of tubo-ovarian abscesses. Radiology. 1992;182:399–402. https://doi.org/10.1148/ radiology.182.2.1732956. Chen WS.  Chronic sciatica caused by tuberculous sacroiliitis. A case report. Spine (Phila Pa 1976). 1995;20:1194–6. https://doi. org/10.1097/00007632-­199505150-­00015.

913 Cohen BA, Lanzieri CF, Mendelson DS, Sacher M, Hermann G, Train JS, Rabinowitz JG. CT evaluation of the greater sciatic foramen in patients with sciatica. AJNR Am J Neuroradiol. 1986;7:337–42. Colmegna I, Justiniano M, Espinoza LR, Gimenez CR.  Piriformis pyomyositis with sciatica: an unrecognized complication of “unsafe” abortions. J Clin Rheumatol. 2007;13:87–8. https://doi. org/10.1097/01.rhu.0000260655.90449.7d. García-Mata S, Hidalgo-Ovejero A, Esparza-Estaun J.  Primary obturator-muscle pyomyositis in immunocompetent children. J Child Orthop. 2012;6:205–15. https://doi.org/10.1007/ s11832-­012-­0418-­y. Granberg S, Gjelland K, Ekerhovd E.  The management of pelvic abscess. Best Pract Res Clin Obstet Gynaecol. 2009;23:667–78. https://doi.org/10.1016/j.bpobgyn.2009.01.010. Gujrathi R, Gupta K, Ravi C, Pai B. Sciatica: an extremely rare complication of the perianal abscess. Pol J Radiol. 2016;81:370–3. https:// doi.org/10.12659/PJR.897269. Gupta A, Kakkar A, Chadha M, Sathaye CB.  A primary intrapelvic hydatid cyst presenting with foot drop and a gluteal swelling: a case report. J Bone Joint Surg Br. 1998;80:1037–9. https://doi. org/10.1302/0301-­620x.80b6.8793. Gurbani SG, Cho CT, Lee KR, Powell L. Gonococcal abscess of the obturator internal muscle: use of new diagnostic tools may eliminate the need for surgical intervention. Clin Infect Dis. 1995;20:1384–6. https://doi.org/10.1093/clinids/20.5.1384. Harisinghani MG, Gervais DA, Hahn PF, Cho CH, Jhaveri K, Varghese J, et al. CT-guided transgluteal drainage of deep pelvic abscesses: indications, technique, procedure-related complications, and clinical outcome. Radiographics. 2002;22:1353–67. https://doi. org/10.1148/rg.226025039. Hassan FO, Shannak A. Primary pelvic hydatid cyst: an unusual cause of sciatica and foot drop. Spine (Phila Pa 1976). 2001;26:230–2. https://doi.org/10.1097/00007632-­200101150-­00021. Herr CH, Williams JC.  Supralevator anorectal abscess presenting as acute low back pain and sciatica. Ann Emerg Med. 1994;23:132–5. https://doi.org/10.1016/s0196-­0644(94)70020-­6. Holtzman DM, Davis RE, Greco CM. Lumbosacral plexopathy secondary to perirectal abscess in a patient with HIV infection. Neurology. 1989;39:1400–1. https://doi.org/10.1212/wnl.39.10.1400-­a. Kalaci A, Sevinç TT, Yanat AN. Sciatica of nondisc origin: hydatid cyst of the sciatic nerve. Case report. J Neurosurg Spine. 2008;8:394–7. https://doi.org/10.3171/SPI/2008/8/4/394. Muniz Neto FJ, Kihara Filho EN, Miranda FC, Rosemberg LA, Santos DCB, Taneja AK.  Demystifying MR neurography of the lumbosacral plexus: from protocols to pathologies. Biomed Res Int. 2018;2018:9608947. https://doi.org/10.1155/2018/9608947. Negus S, Sidhu PS. MRI of retroperitoneal collections: a comparison with CT.  Br J Radiol. 2000;73:907–12. https://doi.org/10.1259/ bjr.73.872.11026872. Niazi A, Alibraheem A, Al-Mouakeh A, Abouzied MK, Basha SR, Suliman S, et al. Gluteal muscles primary hydatid cyst after cortical bone destruction in the sacrum. Ann Med Surg (Lond). 2020;59:89– 92. https://doi.org/10.1016/j.amsu.2020.09.019. Novoselova V, Lacasse A.  Acute diverticulitis masquerading as unilateral sciatica-like symptoms. J Community Hosp Intern Med Perspect. 2020;10:587–90. https://doi.org/10.1080/20009666.2020 .1804101. Ozgül A, Yazicioğlu K, Gündüz S, Kalyon TA, Arpacioğlu O. Acute brucella sacroiliitis: clinical features. Clin Rheumatol. 1998;17:521–3. https://doi.org/10.1007/BF01451292. Paley M, Sidhu PS, Evans RA, Karani JB. Retroperitoneal collections— aetiology and radiological implications. Clin Radiol. 1997;52:290– 4. https://doi.org/10.1016/s0009-­9260(97)80056-­6.

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Planner AC, Donaghy M, Moore NR. Causes of lumbosacral plexopPediatr Emerg Care. 2003;19:252–4. https://doi.org/10.1097/01. athy. Clin Radiol. 2006;61:987–95. https://doi.org/10.1016/j. pec.0000086237.54586.92. crad.2006.04.018. Shields DW, Robinson PG.  Iliopsoas abscess masquerading as ‘sciSanal HT, Kocaoglu M, Bulakbasi N, Yildirim D. Pelvic hydatid disatica’. BMJ Case Rep. 2012;2012:bcr2012007419. https://doi. ease: CT and MRI findings causing sciatica. Korean J Radiol. org/10.1136/bcr-­2012-­007419. 2007;8:548–51. https://doi.org/10.3348/kjr.2007.8.6.548. Stoeckli TC, Mackin GA, De Groote MA. Lumbosacral plexopathy in a Sharieff GQ, Lee DM, Anshus JS.  A rare case of salmonella-­ patient with pulmonary tuberculosis. Clin Infect Dis. 2000;30:226– mediated sacroiliitis, adjacent subperiosteal abscess, and myositis. 7. https://doi.org/10.1086/313622.

Non-discogenic Sciatica in Pregnancy

90

90.1 Generalities and Relevance A number of pregnant women will suffer from mild pain in the sciatic nerve, particularly in the second and third trimesters of pregnancy, as the fetus progressively grows more. This sciatic pain was unrelated to a compressive lumbar disc herniation (c.f. Chap. 25 about Pregnant Women with Lumbar Disc Herniations). The non-discogenic sciatic radicular pain can be unilateral or bilateral and may affect up to 22% of people in pregnancy. In some cases, simple low back pain can be associated with sciatica. Compression, over-stretching, or irritation of the sciatic nerve during pregnancy are often multifactorial, including:

Lumbosacral spine

Sacral plexus

Sciatic nerve

• Normal pregnancy-related changes due to the uterus’s expansion and the fetus’s. development • Postural changes and nutation of the pelvic girdle manifest as an increase in lumbar lordosis and an anterior tilt of the pelvis • Production of high concentrations of a hormone called “relaxin” which relaxes joints, muscles, and ligaments and helps the pelvis to expand • Fetal position within the uterine cavity and the abdomen (Fig. 90.1). The mechanism of injury likely involves compression of the fetal head against the underlying pelvis and lumbosacral plexus (Fig. 90.2) • Underlying spinal lumbosacral problems before the pregnancy • Lifestyle, psychological, and socioeconomic profiles

Fig. 90.1  Fetal position within the uterine cavity and the abdomen. Note the compression of the fetal head against the underlying pelvis and sacral plexus

Less often, other underlying causes have been suggested such as: –– Compression of vascular elements leading to neural hypoxia or ischemia –– Concomitant true lumbar disc herniation –– Excessive vomiting –– Sacral stress fracture (not associated with low bone mineral density) –– Extreme positions for prolonged periods of time

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90  Non-discogenic Sciatica in Pregnancy

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90.2 Clinical Presentations

90.4 Treatment Options

A pregnant woman’s sciatica is characterized by constant aching and stabbing pain of somewhat low to moderate intensity. This radicular symptom can be associated with low back pain, but a decline of lower-limb muscular strength is rarely encountered. In addition, sciatica pain exacerbates with sitting or standing for long periods. An important finding in patients presenting with sciatica without evidence of disc disease, and with prominent pain and local tenderness over the buttock muscles, the clinical examination should rule out “piriformis syndrome”. In this last situation, sciatic pain worsened on the FAIR test: representing hip Flexion, Adduction, and Internal Rotation.

There is limited evidence available regarding the optimal treatment of non-discogenic sciatica in pregnant women. Overall, the sciatic pain will frequently disappear naturally and generally will not require treatment. Sometimes, a variety of physiotherapies or self-care therapies may be helpful. This might comprise massage, stretching, swimming, hot/cold therapy, maternity support belts, and performing good posture and gentle exercises. If the pain causes functional limitations, appropriate treatment should be delivered. However, most of the analgesic medications habitually used to treat neuropathic pain are contraindicated in pregnancy. Some safety drugs can be used such as paracetamol (acetaminophen), antioxidants, and neurotrophic agents such as alpha-lipoic acid (known as thioctic acid) and its reduced form, dihydrolipoic acid. Surgery is usually not indicated unless a compressive lesion is clearly specified. In any case, surgical options remain a matter for debate in pregnant women (Please refer to Chap. 25 about LDH in Pregnant women). Sciatic pain often disappears after childbirth. However, in some patients, lumbosacral radicular pain tends to become chronic.

90.3 Imaging Features Classically, electromyography and lumbar magnetic resonance imaging are not requested for exploring traditional lumbosacral radicular pain in pregnant women. Indeed, during pregnancy, sciatic pain can be generated by muscle tension and/or unstable joints. However, in some atypical presentations, neuroimaging can be used for screening of lumbar spinal, lumbosacral plexus, or even sciatic nerve lesions causing potential sciatica.

Further Reading

Further Reading Al-Khodairy AW, Bovay P, Gobelet C. Sciatica in the female patient: anatomical considerations, aetiology and review of the literature. Eur Spine J. 2007;16:721–31. https://doi.org/10.1007/ s00586-­006-­0074-­3. Costantino M, Guaraldi C, Costantino D, De Grazia S, Unfer V.  Peripheral neuropathy in obstetrics: efficacy and safety of α-lipoic acid supplementation. Eur Rev. Med Pharmacol Sci. 2014;18:2766–71. Donaldson JO. Neurologic complications of pregnancy. In: Asbury AK, McKhann GM, McDonald WI, editors. Diseases of the nervous system clinical neurobiology, vol. 2. Philadelphia: Saunders; 1992. p. 1545–51. Gormus N, Ustun ME, Paksoy Y, Ogun TC, Solak H.  Acute thrombosis of inferior vena cava in a pregnant woman presenting with sciatica: a case report. Ann Vasc Surg. 2005;19:120–2. https://doi. org/10.1007/s10016-­004-­0142-­2. Güngör İ, Tezer T, Polat GG, Esen E, Günaydın B, Kaya K. Popliteal sciatic nerve block in a pregnant patient in the last trimester. Turk J Anaesthesiol Reanim. 2015;43:279–81. https://doi.org/10.5152/ TJAR.2014.87699. Hall H, Lauche R, Adams J, Steel A, Broom A, Sibbritt D. Healthcare utilisation of pregnant women who experience sciatica, leg cramps and/or varicose veins: a cross-sectional survey of 1835 pregnant women. Women Birth. 2016;29:35–40. https://doi.org/10.1016/j. wombi.2015.07.184. Hirabayashi Y, Shimizu R, Fukuda H, Saitoh K, Igarashi T. Effects of the pregnant uterus on the extradural venous plexus in the supine and lateral positions, as determined by magnetic resonance imaging. Br J Anaesth. 1997;78(3):317–9. https://doi.org/10.1093/ bja/78.3.317. Hope-Allan N, Adams J, Sibbritt D, Tracy S.  The use of acupuncture in maternity care: a pilot study evaluating the acupuncture

917 service in an Australian hospital antenatal clinic. Complement Ther Nurs Midwifery. 2004;10:229–32. https://doi.org/10.1016/j. ctnm.2004.07.001. Hu J, Jin X, Jiang Y, Li W, Hu J.  Ultrasound image characteristic analysis of sciatic nerve and Main branches in third trimester. World Neurosurg. 2021;149:316–24. https://doi.org/10.1016/j. wneu.2020.09.131. Nix K, Curtis H, Coolen J.  Venous thromboembolism manifesting as sciatica in two pregnant women. J Obstet Gynaecol Can. 2020;42:900–2. https://doi.org/10.1016/j.jogc.2019.08.031. Sencan S, Ozcan-Eksi EE, Cuce I, Guzel S, Erdem B. Pregnancy-related low back pain in women in Turkey: prevalence and risk factors. Ann Phys Rehabil Med. 2018;61:33–7. https://doi.org/10.1016/j. rehab.2017.09.005. Steel A, Adams J, Sibbritt D, Broom A, Gallois C, Frawley J. Utilisation of complementary and alternative medicine (CAM) practitioners within maternity care provision: results from a nationally representative cohort study of 1,835 pregnant women. BMC Pregnancy Childbirth. 2012;12:146. https://doi. org/10.1186/1471-­2393-­12-­146. Suntrup-Krueger S, Schilling M, Schwindt W, Wiendl H, Meuth SG. Case report of bilateral relapsing-remitting sciatic nerve palsy during two pregnancies. BMC Res Notes. 2015;8:654. https://doi. org/10.1186/s13104-­015-­1647-­1. Vermani E, Mittal R, Weeks A. Pelvic girdle pain and low back pain in pregnancy: a review. Pain Pract. 2010;10:60–71. https://doi. org/10.1111/j.1533-­2500.2009.00327.x. Wang SM, Dezinno P, Maranets I, Berman MR, Caldwell-Andrews AA, Kain ZN.  Low back pain during pregnancy: prevalence, risk factors, and outcomes. Obstet Gynecol. 2004;104:65–70. https://doi. org/10.1097/01.AOG.0000129403.54061.0e. Yoshimoto M, Kawaguchi S, Takebayashi T, Isogai S, Kurata Y, Nonaka S, et al. Diagnostic features of sciatica without lumbar nerve root compression. J Spinal Disord Tech. 2009;22:328–33. https://doi. org/10.1097/BSD.0b013e31817dc46d.

Sciatic Endometriosis

91.1 Generalities and Relevance Endometriosis is a common, chronic gynecological condition defined as the presence of ectopic functional endometrial tissue outside the uterine cavity. Endometriosis could be an important cause of pelvic chronic disease, and it is frequently associated with infertility. It manifests in three ways: superficial (peritoneal) disease, ovarian disease (endometriomas), and deep infiltrating endometriosis. In the nervous system, the most frequently involved site of endometriosis was the sacral plexus followed by the sciatic nerve. However, the sciatic nerve is rarely involved in endometriosis, and it is usually presented as “cyclic” or “catamenial sciatica.” Endometriosis is the most common obstetric or gynecological cause of sciatica in women (about 50% of cases) followed by pregnancy and labor-related sciatica (about 30%). The first description of cyclic sciatic pain in women was done by Carl Paul Schlicke (1910–2001) in 1946. This American surgeon excised an ectopic endometrial mass in the posterior part of the thigh of a woman; however, sciatic endometriosis was never confirmed. In 1955, Robert Officer Denton (1919–1999) described the first confirmed case of sciatic nerve endometriosis. Isolated endometriosis of the sciatic nerve is rare since less than 200 cases have been reported in the literature. The management of sciatic endometriosis is a true challenge due to diagnosis delay or misdiagnosis as well as elevated risk of surgical complications. Endometriotic involvement of the sciatic nerve may be intrapelvic, extrapelvic, or both. Indeed, in half of the cases, there is another concomitant localization, frequently in the pelvic cavity. However, the most common location of sciatic nerve endometriosis is over the lateral aspect proximal to the greater sciatic foramen. Endometriosis size is highly variable, ranging from microscopic endometriotic implants to large cysts (AKA endometriomas) and nodules. The lesion can be intraneural, perineural, or both, especially on the right side lower limb.

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The incidence of endometriosis varies from 5 to 20% of all women of reproductive age, more than 20% of whom present with infertility. The average age for endometriosis sciatica was about 35 years. Numerous theories have been suggested to explain the localization of endometrial tissue to the sciatic nerve: (a) The existence of a peritoneal diverticulum allows the endometrial tissue to migrate into the sciatic nerve from the site of genital endometriosis. (b) Retrograde menstruation: endometriosis foci arise because of the displacement of menstrual blood into the peritoneal cavity through the fallopian tubes. Then, endometrial cells extend into the periphery toward the sciatic notch. (c) Metaplastic theory (coelomic metaplasia): retroperitoneal deep endometriosis may originate from metaplasia of remnant Müller-type cells (embryonic cell rests) located in the rectovaginal septum under the influence of hormones. (d) Induction theory: endometrium releases elements that induce undifferentiated mesenchyme to form endometriotic tissue. Endometriosis is also considered a chronic inflammatory process associated with immune disorders. In addition, genetic and environmental factors may play a role. The genesis of pain in sciatic endometriosis is multivariable resulting from both compressive and inflammatory phenomena. The following factors are involved: –– –– –– ––

Perineural and intraneural spread and invasion Influence of activated mast cells on endometrial lesions Cyclic bleeding within endometrial tissues Impact of nerve growth factor in neuropathic pain.

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Imaging modalities are basic for both clinical practice and preoperative planning. However, the quality of imaging can Careful history in suspected patients may reveal antecedents be related to the phase of the menstrual cycle. Although there have been reports of using ultrasound and of pelvic endometriosis or the catamenial nature of sciatica computed tomography scan (CT) for the assessment of intrabut is rarely associated with lower back pain. pelvic and extrapelvic endometriosis affecting the sciatic Classically, young women present with limited pain in the nerve, MRI remains the imaging modality of choice for scihip and the gluteal area (particularly over the sciatic notch) radiating in the lower leg and foot a few days before men- atic endometriosis. Pelvic and hip MRI may provide direct struation, which becomes progressively more severe and information about the location, shape, and size of the sciatic subsides 2 days–2 weeks after the end of menses. About two-­ lesion as well as evidence about its relationship with the thirds of patients had right-side neurological signs. At a later adjacent tissues. Endometriosis exhibits hypersignal intensity on time, the duration of sciatic pain symptoms may increase T1-weighted images and hyper- to isosignal intensity on until they are continuously present with severe worsening T2-weighted images, depending on the stage of the blood during menstrual cycles. This truncal sciatica is characterproducts. Fat suppression sequences enhance the visibility of ized by the extensive distribution of the affected area (involving L5, S1, and S2 nerve roots) that is opposed to symptoms pelvic endometriosis, and gadolinium enhancement is helpof traditional discogenic sciatic pain (mostly limited to a ful (Fig. 91.1). MRI could also detect adjacent inflammatory processes and edema by showing high signal intensity on single nerve root compression). Clinical gynecological pelvic examination in patients T2-weighted images and diffuse gadolinium enhancement. with isolated sciatic endometriosis is usually unremarkable. In chronic forms, there are signs of gluteal and/or thigh musHowever, response to hormonal treatment for endometriosis cle denervation. Unfortunately, many cases of sciatic endometriosis will would provide further support for this unusual diagnosis. not be recognized on MRI. Sometimes, there are more severe neurological presentaClinical suspicion of intrapelvic endometriosis as a tions, such as leg weakness, foot drop, muscular atrophy, and gait difficulty. In some patients, local examination whether cause for cyclic sciatica may require not only routine pelextra-pelvic or intra-pelvic (transvaginal) will induce a trig- vic laparoscopy but also laparoscopy with the exploration ger pain with positive paresthesia sensation along the sciatic of the lateral pelvic wall, retroperitoneal space, and intrapelvic sciatic nerve. For extrapelvic endometriosis, transnerve (Hoffmann-Tinel-sign). gluteal CT-guided needle biopsy of the extrapelvic mass may provide a minimally invasive approach for diagnosis. However, such biopsies can be technically difficult to 91.3 Paraclinic Features achieve. Electromyography (EMG) findings can be variable but Clinical examination was able to suspect sciatic nerve pain but was not appropriate for etiological diagnosis. Magnetic may show signs of denervation in muscles innervated by the resonance imaging (MRI) was the first line modality for sciatic nerve, which can be either acute or chronic, dependevaluating sciatic nerve involvement followed by laparos- ing on the time from onset of symptoms. EMG can also help copy and neurophysiological exploration. However, the final differentiate between nerve root damage and peripheral nerve damage as well as follow nerve recovery. diagnosis is made histopathologically.

91.4  Treatment Options

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Fig. 91.1  MRI performed at 3.0 T in August 2015 during the pain-free week of the patient’s cycle. An axial T2 FS image (a) shows the enlarged and hyperintense L4–S1 spinal nerves (a; arrowheads) in higher resolution. An axial T2 FS image (b) demonstrates a hyperintense soft-tissue band (b; dashed arrow) extending from the uterus (b; letter U) to the left sciatic nerve and the soft-tissue mass in the sciatic notch. Atrophy of the gluteal musculature is compatible with chronic denervation (a, b; asterisks). An axial T2 FS image (c) demonstrates a partly intraneural and partly extraneural cyst of the left sciatic nerve (c; arrowhead: the sciatic

nerve and intraneural portion of the cyst; arrow: the extraneural portion of the cyst; and dashed line: borderline between the intraneural and extraneural portions). The same cyst is visualized on an axial T1 FS image (d; arrowhead) and showed a subacute hemorrhage (d; arrow). (Reproduced from Capek S, Amrami KK, Howe BM, Collins MS, Sandroni P, Cheville JC, Spinner RJ. Sequential imaging of intraneural sciatic nerve endometriosis provides insight into symptoms of cyclical sciatica. Acta Neurochir (Wien). 2016;158(3):507–12; discussion 512. https://doi.org/10.1007/s00701-­015-­2683-­2; with permission)

91.4 Treatment Options

non-steroidal anti-inflammatory drugs. First-line therapy is represented by combined oral contraceptives and progestogens, whereas gonadotropin-releasing hormone agonists are second-line hormonal therapy. Surgery is recommended for patients who have reported an exponential worsening of gait disorders, lower limb weakness, foot drop, and neuropathic pain that have become refractory to medical treatments. Surgical treatment is advisable to prevent further irreversible neurogenic damage. In cases of deep infiltrating intrapelvic endometriosis of the sciatic nerve, laparoscopic retroperitoneal pelvic (surgi-

Like other forms of deep infiltrative endometriosis, sciatic nerve endometriosis is difficult to treat. The treatment is dependent on the severity of the symptoms, the location of the lesions, and their extension. The therapy of endometriosis over the sciatic nerve can be medical, surgical, or a combination of these treatments. The primary management of painful sciatic nerve endometriosis in the absence of neurological deficits or signs of nerve injury on EMG is typically conservative and involves

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cal neuropelveology) resection is required to obtain free margins but is still controversial owing to the risk of neurologic damage and irreversible gait disorders. When the disease extends beyond the pelvis (i.e., extrapelvic) into the gluteal region, a transgluteal approach will be offered. Postoperative physiotherapy and medical treatment with neuroleptics must be started immediately after any surgical procedure.

91.5 Prognosis Surgical treatment can be done with great results in terms of pain improvement, recurrence, and functional outcome if the continuity of the nerve is preserved and patients are properly supported by intensive physiotherapy. In advanced cases with delayed management, complete recovery of motor function is rare, even after complete surgical removal of the lesion. Fibrosis during the healing process is likely to induce permanent nerve damage.

Further Reading Arányi Z, Polyák I, Tóth N, Vermes G, Göcsei Z. Ultrasonography of sciatic nerve endometriosis. Muscle Nerve. 2016;54:500–5. https:// doi.org/10.1002/mus.25152. Bindra V, Nori M, Reddy R, Reddy R, Satpathy G, Reddy CA. Sciatic nerve endometriosis—the correct approach matters: a case report. Case Rep Womens Health. 2023;38:e00515. https://doi. org/10.1016/j.crwh.2023.e00515. Capek S, Amrami KK, Howe BM, Collins MS, Sandroni P, Cheville JC, et al. Sequential imaging of intraneural sciatic nerve endometriosis provides insight into symptoms of cyclical sciatica. Acta Neurochir (Wien). 2016;158:507–12. https://doi.org/10.1007/ s00701-­015-­2683-­2. Cimsit C, Yoldemir T, Akpinar IN.  Sciatic neuroendometriosis: magnetic resonance imaging defined perineural spread of endometriosis. J Obstet Gynaecol Res. 2016;42:890–4. https://doi.org/10.1111/ jog.12998. Denton RO, Sherrill JD.  Sciatic syndrome due to endometriosis of sciatic nerve. South Med J. 1955;48:1027–31. https://doi. org/10.1097/00007611-­195510000-­00004. Floyd JR 2nd, Keeler ER, Euscher ED, McCutcheon IE.  Cyclic sciatica from extrapelvic endometriosis affecting the sciatic nerve. J Neurosurg Spine. 2011;14:281–9. https://doi.org/10.3171/2010.10. SPINE09162. Ghezzi L, Arighi A, Pietroboni AM, Jacini F, Fumagalli GG, Esposito A, et al. Sciatic endometriosis presenting as periodic (catamenial) sciatic radiculopathy. J Neurol. 2012;259:1470–1. https://doi. org/10.1007/s00415-­011-­6378-­1.

91  Sciatic Endometriosis Hughes MS, Burd TA, Allen WC.  Post-traumatic catamenial sciatica. Orthopedics. 2008;31:400. https://doi. org/10.3928/01477447-­20080401-­15. Jiang H, Liang Y, Li L, Gu L, Yao S. Cyclic sciatica due to endometriosis of the sciatic nerve: neurolysis with combined laparoscopic and transgluteal approaches: a case report. JBJS Case Connect. 2014;4:e11. https://doi.org/10.2106/JBJS.CC.M.00234. Koga K, Osuga Y, Harada M, Hirota Y, Yamada H, Akahane M, et al. Sciatic endometriosis diagnosed by computerized tomography-­ guided biopsy and CD10 immunohistochemical staining. Fertil Steril. 2005;84:1508. https://doi.org/10.1016/j.fertnstert.2005. 05.034. Lomoro P, Simonetti I, Nanni A, Cassone R, Di Pietto F, Vinci G, et  al. Extrapelvic sciatic nerve endometriosis, the role of magnetic resonance imaging: case report and systematic review. J Comput Assist Tomogr. 2019;43:976–80. https://doi.org/10.1097/ RCT.0000000000000916. Mannan K, Altaf F, Maniar S, Tirabosco R, Sinisi M, Carlstedt T. Cyclical sciatica: endometriosis of the sciatic nerve. J Bone Joint Surg Br. 2008;90:98–101. https://doi.org/10.1302/0301-­620X.90B1.19832. Motamedi M, Mousavinia F, Naser Moghadasi A, Talebpoor M, Hajimirzabeigi A. Endometriosis of the lumbosacral plexus: report of a case with foot drop and chronic pelvic pain. Acta Neurol Belg. 2015;115:851–2. https://doi.org/10.1007/s13760-­015-­0445-­9. Possover M, Chiantera V.  Isolated infiltrative endometriosis of the sciatic nerve: a report of three patients. Fertil Steril. 2007;87:417. e17–9. https://doi.org/10.1016/j.fertnstert.2006.05.084. Possover M. Five-year follow-up after laparoscopic large nerve resection for deep infiltrating sciatic nerve endometriosis. J Minim Invasive Gynecol. 2017;24:822–6. https://doi.org/10.1016/j. jmig.2017.02.027. Saar TD, Pacquée S, Conrad DH, Sarofim M, Rosnay P, Rosen D, et  al. Endometriosis involving the sciatic nerve: a case report of isolated endometriosis of the sciatic nerve and review of the literature. Gynecol Minim Invasive Ther. 2018;7:81–5. https://doi. org/10.4103/GMIT.GMIT_24_18. Schlicke CP.  Ectopic endometrial tissue in the thigh. J Am Med Assoc. 1946;132:445. https://doi.org/10.1001/ jama.1946.02870430025008. de Sousa ACS, Capek S, Howe BM, Jentoft ME, Amrami KK, Spinner RJ.  Magnetic resonance imaging evidence for perineural spread of endometriosis to the lumbosacral plexus: report of 2 cases. Neurosurg Focus. 2015;39:E15. https://doi.org/10.3171/2015.6.FO CUS15208. Smolarz B, Szyłło K, Romanowicz H.  Endometriosis: epidemiology, classification, pathogenesis, treatment and genetics (review of literature). Int J Mol Sci. 2021;22:10554. https://doi.org/10.3390/ ijms221910554. Vercellini P, Chapron C, Fedele L, Frontino G, Zaina B, Crosignani PG. Evidence for asymmetric distribution of sciatic nerve endometriosis. Obstet Gynecol. 2003;102:383–7. https://doi.org/10.1016/ s0029-­7844(03)00532-­5. Vinatier D, Orazi G, Cosson M, Dufour P. Theories of endometriosis. Eur J Obstet Gynecol Reprod Biol. 2001;96:21–34. https://doi. org/10.1016/s0301-­2115(00)00405-­x. Yekeler E, Kumbasar B, Tunaci A, Barman A, Bengisu E, Yavuz E, et  al. Cyclic sciatica caused by infiltrative endometriosis: MRI findings. Skeletal Radiol. 2004;33:165–8. https://doi.org/10.1007/ s00256-­003-­0663-­8.

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Sacroiliac Joint Disorders

92.1 Generalities and Relevance The pain generated from the sacroiliac joint results in postero-­superior iliac and back pain. Pain can also spread to the abdominal and groin area, leg, and even foot. About a third of patients with sacroiliac disorders have leg pain. Some cases may present symptoms similar to those of sciatic nerve impairment (Figs.  92.1, 92.2, 92.3, 92.4, 92.5, 92.6, 92.7, 92.8, 92.9, and 92.10). The sacroiliac joint is a synovial joint between the ilium and the sacrum. It represents the largest axial joint in the

human body. It has minimum movement, and its main function is to transfer load between the axial and lower skeletons. The sacroiliac joint is a symmetrical joint with an oblique coronal orientation and is located at the S1–S3 level. It has a close relationship with the piriformis muscle (attached to the anterior capsule), lumbosacral trunk, obturator nerve, iliac vessels, and ureter. In addition, the joint is closely related to the sciatic nerve anteriorly and inferiorly. In the 1920s, the sacroiliac joint was considered to be a significant cause of idiopathic sciatic pain. However, some years later, it became apparent that the lumbar disc could

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Fig. 92.1  Case 1. Right sided tuberculous sacroiliitis (arrows) with presacral abscess (stars) as seen on axial pelvic CT scan (a, b) and sagittal T1- (c) and T2-weighted MRI of the lumbosacral spine (d)

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Fig. 92.2  Case 2. Chronic Osteomyelitis of the ala of the sacrum on the left side (arrows) as seen on axial (a) and coronal reconstruction (b) pelvic CT scan on bone windows

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Fig. 92.3  Case 3. Sacral hydatid cyst on the right side (stars) with sacroiliac joint and proximal iliac bone involvement (arrows) as seen on axial pelvic CT scan on parenchymal (a) and bone (b) windows

produce sciatica. Recent medical literature has renewed interest in the sacroiliac joint as a source of pain in the leg known as “pseudo-sciatica” and even “true sciatic pain.” Due to the rarity of presentation and vague symptoms, the final diagnosis is habitually delayed. Numerous explanations have been suggested to clarify this radiating pain along the sciatic nerve, including the following: (a) The sacroiliac joint’s segmental nerve supply is directly derived from a division from L5–S3 spinal nerves. (b) The contiguous relationship between the anterior capsule of the sacroiliac joint and both L5 and S1 spinal nerves before they connect to form part of the sciatic nerve.

(c) Involvement of other adjacent lumbosacral structures, which are supplied by branches from the same spinal nerves (L5–S3). Some authors believed that in a traumatized and inflamed sacroiliac joint, extravasation of synovial fluid containing inflammatory mediators (e.g., substance P) might irritate one or more of the neural elements that constitute the sciatic nerve. Additionally, some other sacroiliac diseases may compress (e.g., tumor, injured lesion, or osteophytosis) or irritate (e.g., infection or acute inflammation) the surrounding structures. Pain in sciatic-related sacroiliac joint disease mainly results from the following:

92.1  Generalities and Relevance

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Fig. 92.4  Case 3. Sacral hydatidosis (stars) with sacroiliac joint and proximal iliac bone involvement (arrows) as seen on coronal reconstruction pelvic CT scan on parenchymal (a) and bone (b) windows

–– Direct compressive mechanism including subsequent ischemia –– Local musculoskeletal invasion –– Acute or chronic inflammatory phenomena The sacroiliac joint is a true synovial joint and is subject to infection, degenerative arthritis, trauma, and tumors as any other joint. The main pathologies and injuries that contribute to this unusual condition are summarized in Table 92.1. The incidence of this rare clinical entity is unknown but it seems more frequent in young adult women.

Fig. 92.5  Case 4. Anteroposterior pelvic plain radiography in a patient with bilateral sacroiliitis. The sacroiliac joints are seen as a thin line (arrows)

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Fig. 92.6  Case 4. Sacroiliac joint disorders in a patient with bilateral sciatic pain as seen on axial (a) and coronal reconstruction (b) CT scan (arrows). Note the subchondral erosions, sclerosis, and proliferation on both the iliac and sacral sides of the sacroiliac joints

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Fig. 92.7  Case 4. MRI disorders of the sacroiliac joints (arrows). Coronal T1-weighted MRI (a) and coronal (b) and axial (c) STIR sequences

92.1  Generalities and Relevance

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Fig. 92.8  Case 5. Bilateral sacroiliac joint inflammation as seen on axial (a–c) and coronal reconstruction (d) CT scan. There are subchondral erosions, sclerosis, and proliferation on the iliac side of the sacroiliac joints

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Fig. 92.9  Case 6. Left-sided transalar fracture (arrows) lateral to the sacral foramina as seen on axial pelvic CT scan (a–d)

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92.2  Clinical Presentations

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Fig. 92.10  Case 7. Right-sided iliac sarcoma (arrows) in a 16-year-old boy presented with sciatic pain as seen on axial pelvic CT scan on parenchymal (a, b) and bone (c) windows

Table 92.1  Main etiologies that contribute to sciatica related to sacroiliac joint Infection Inflammation Trauma Tumors Degenerative Idiopathic

Tuberculosis, brucellosis, non-specific pathogens, and hydatidosis (Figs. 92.1, 92.2, 92.3, and 92.4) Spondylarthropathies (ankylosing spondylitis, psoriasis arthritis, reactive arthritis, and Behcet’s disease) (Figs. 92.5, 92.6, 92.7, and 92.8) Pelvic fracture and sacroiliac injuries (Fig. 92.9) Primitive or metastatic neoplasms (Fig. 92.10) Sacroiliac osteoarthritis in older patients and osteophytosis From unknown cause

92.2 Clinical Presentations Factors from the medical history and general clinical examination may be helpful for differentiating between sacroiliac joint-related sciatica and other diseases. A thorough physical examination of the spine, sacroiliac joints, hips, and even the entire musculoskeletal system is required to exclude other concomitant causes. It seems that patients with sciatica derived from the sacroiliac joint are more often female, have lower stature, a shorter duration of symptoms, pain radiating to the groin, and a his-

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tory of a fall on the buttocks. Most neurogenic leg pains are unilateral and without additional sensitivo-motor deficits. Habitually, the straight leg raising test is positive. In bilateral forms, particularly in younger men, early ankylosing spondylitis needs to be suspected. Sometimes, the presenting symptoms are vague, and the distribution of pain varies considerably due to the close relationship between the sacroiliac joint, the lumbosacral plexus, and the ability of the underlying disease to track in any intrapelvic and/or extrapelvic direction. Sometimes, pain may exacerbate when using a tight belt.

92  Sacroiliac Joint Disorders

However, sciatic pain is rarely isolated. To make the correct diagnosis, we must find the following: (a) The radiating pain below the buttocks. (b) Pain presents in the region of the sacroiliac joint. The pain is typically perceived at or around the posterior-­ superior iliac spine. (c) Positive provocation sacroiliac maneuvers to attempt to replicate the patient’s symptoms (Table 92.2, Figs. 92.11, 92.12, and 92.13).

Table 92.2  Main provocative sacroiliac tests Distraction test (AKA gapping test)

The patient is in a supine position, and the clinician applies a vertically orientated, posteriorly directed force to both the anterior superior iliac spines (Fig. 92.11a) Compression test (AKA The patient is in side-lying, and the tester’s hands are placed over the upper part of the iliac crest (one approximation test) side), laterally directing force toward the floor. The movement causes forward pressure on the sacrum (Fig. 92.11b) Sacral thrust test (AKA sacral The patient is positioned prone, and the clinician applies an anteriorly directed pressure over the compression test, downwards sacrum. One hand is placed directly on the sacrum and is reinforced by the other tester’s hand pressure test, or sacral spring test) (Fig. 92.11c) Thigh thrust test (AKA posterior The patient is positioned supine, thigh, and knee are bent to 90°, and the tester’s hand is positioned on pelvic pain provocation, pppp test, p4 the sacral base: a vertical transmission of force through the thigh via the clinician’s body stresses the test, or posterior shear test) joint and tissues Gaenslen’s test/maneuver The patient is placed supine: pain referred to the back on hyperextension of the hip while flexing the opposite hip (Fig. 92.12). This test is named after the American orthopedic surgeon Frederick Julius Gaenslen (1877–1937) Yeoman’s test The patient is placed prone: the clinician stands at the painful side, flexes the patient’s knee to 90°, and extends the hip. Pain localized over the same-sided posterior sacroiliac joint area is indicative of a disorder in the anterior sacroiliac ligament. Anterior thigh paresthesia may indicate a femoral nerve stretch FABER test (AKA Patrick’s test, or The clinician practices a hip Flexion ABduction External Rotation test with the lateral malleolus Figure of 4 Test) placed on the contralateral knee (Fig. 92.13). This test is useful in diagnosing trochanteric bursitis, gluteal tendinopathy, sacroiliitis, or mechanical low back pain. However, the FABER test does not aggravate true lumbosacral nerve root compression. Patrick’s test was named after the American neurologist Hugh Talbot Patrick (1860–1939)

92.2  Clinical Presentations

a

931

b

c

Fig. 92.11  Some provocative sacroiliac joint tests. Distraction test (a), compression test (b), and sacral thrust test (c)

Fig. 92.13  FABER test: Hip Flexion ABduction External Rotation test

Fig. 92.12  Gaenslen’s test/maneuver for sacroiliac joint disorders

92  Sacroiliac Joint Disorders

932

92.3 Paraclinic Features Clinical examination was able to suspect sciatic nerve pain but was not appropriate for the etiological diagnosis. In the past, plain radiography was the gold standard for analysis of the sacroiliac joints. Currently, computed tomography (CT) scan and magnetic resonance imaging (MRI) are valuable techniques in the assessment of sacroiliac disorders. MRI has been shown to be better than or equal to CT for imaging soft tissue extent, bone marrow involvement, and neurovascular involvement. In addition, inflammatory disorders (sacroiliitis) are better assessed on STIR sequence (short tau inversion recovery sequence). However, subtle bony erosion is better seen on a CT scan, which is usually required for the description of neoplasms involving bone (Figs.  92.1, 92.2, 92.3, 92.4, 92.5, 92.6, 92.7, 92.8, 92.9, and 92.10). Scintigraphy can supplement classic imaging. Sacroiliac changes can be detected as increased uptake in bone scintigraphy. The appearance of the lesions on imaging will depend on the underlying cause, the stage of the disease, and the technic used. Occasionally, further imaging and biological tests are important to exclude other causes or to guide the diagnosis. Additionally, ultrasound and CT scans may provide a minimally invasive approach for performing image-guided percutaneous biopsies or abscess drainage if required. However, an open biopsy is essential when the histopathology study is inconclusive or the aspirate yields no growth. Except for infectious sacroiliitis, sacroiliac joint injection tests with corticosteroid and local anesthetic under fluoroscopic or CT scan guidance have a therapeutic function. Indeed, if a sacroiliac origin of the sciatic pain is suspected clinically, and even without imaging abnormalities, ­intra-­articular injection is currently the only means to confirm that diagnosis.

92.4 Treatment Options and Prognosis Identification of the origin of the sciatica-related sacroiliac joint is important for determining therapy and prognosis. Management depends on the underlying cause and includes conservative measures with physical therapy, manual therapy, analgesics, non-steroidal anti-inflammatory medications, muscle relaxants, and stretching. Other therapies include radiologically guided intra-articular injections with steroids and local anesthetics and radiofrequency denervation. Possible neuropathic pain is commonly treated with neuropathic pain medications, such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline), duloxetine, or anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine).

Specific medical or surgical methods depend on the cause. For example, treatment of ankylosing spondylitis disease focused on usual first (non-steroidal anti-inflammatory drugs and non-pharmacological measures) or second-line (TNF-­ alpha blockers and IL17 inhibitors) therapies. Malignancy should be correctly managed by chemotherapy, surgery, and/ or radiation therapy. Appropriate anti-infectious agents (e.g., antituberculosis, antibiotics) are required in infectious diseases. Surgery is indicated in patients with compressive mass lesions, such as a tumor, osteophytosis, hematoma, or abscess (surgical debridement with or without drainage). According to many authors, sacroiliac joint injection with corticosteroid and local anesthetic can be done with great results in terms of sciatic pain improvement and functional outcome. However, the prognosis depends also on causative etiology.

Further Reading Ahmed H, Siam AE, Gouda-Mohamed GM, Boehm H. Surgical treatment of sacroiliac joint infection. J Orthop Traumatol. 2013;14:121– 9. https://doi.org/10.1007/s10195-­013-­0233-­3. Buijs E, Visser L, Groen G. Sciatica and the sacroiliac joint: a forgotten concept. Br J Anaesth. 2007;99:713–6. https://doi.org/10.1093/bja/ aem257. Cai MD, Zhang HF, Fan YG, Su XJ, Xia L. Obturator nerve impingement caused by an osteophyte in the sacroiliac joint: a case report. World J Clin Cases. 2021;9:1168–74. https://doi.org/10.12998/ wjcc.v9.i5.1168. Carey I, Balagué F, Waldburger M. Pseudo-sciatica of neoplastic origin: a propos of an unusual case. Praxis (Bern 1994). 1995;84:197–9. Chen WS.  Chronic sciatica caused by tuberculous sacroiliitis. A case report. Spine (Phila Pa 1976). 1995;20:1194–6. https://doi. org/10.1097/00007632-­199505150-­00015. Fitzgerald O, Murphy SF. Lumbosarcal neuropathy and venous thrombosis complicating sacroilitis. Ir J Med Sci. 1983;152:456–8. https:// doi.org/10.1007/BF02958710. Fortin JD, Vilensky JA, Merkel GJ. Can the sacroiliac joint cause sciatica? Pain Physician. 2003;6:269–71. Hodge JC, Bessette B.  The incidence of sacroiliac joint disease in patients with low-back pain. Can Assoc Radiol J. 1999;50:321–3. Humphrey SM, Inman RD. Metastatic adenocarcinoma mimicking unilateral sacroiliitis. J Rheumatol. 1995;22:970–2. Kumar B, Sriram KG, George C. Osteophyte at the sacroiliac joint as a cause of sciatica: a report of four cases. J Orthop Surg (Hong Kong). 2002;10:73–6. https://doi.org/10.1177/230949900201000113. Liu XQ, Li FC, Wang JW, Wang S. Postpartum septic sacroiliitis misdiagnosed as sciatic neuropathy. Am J Med Sci. 2010;339:292–5. https://doi.org/10.1097/MAJ.0b013e3181c4b14a. Margules KR, Gall EP.  Sciatica-like pain arising in the sacroiliac joint. J Clin Rheumatol. 1997;3:9–15. https://doi. org/10.1097/00124743-­199702000-­00003. Millwala F, Chen S, Tsaltskan V, Simon G. Acupuncture and postpartum pyogenic sacroiliitis: a case report. J Med Case Rep. 2015;9:193. https://doi.org/10.1186/s13256-­015-­0676-­7. Murakami E, Aizawa T, Kurosawa D, Noguchi K.  Leg symptoms associated with sacroiliac joint disorder and related pain. Clin Neurol Neurosurg. 2017;157:55–8. https://doi.org/10.1016/j. clineuro.2017.03.020.

Further Reading Nejati P, Sartaj E, Imani F, Moeineddin R, Nejati L, Safavi M. Accuracy of the diagnostic tests of sacroiliac joint dysfunction. J Chiropr Med. 2020;19:28–37. https://doi.org/10.1016/j.jcm.2019.12.002. Ozgül A, Yazicioğlu K, Gündüz S, Kalyon TA, Arpacioğlu O. Acute brucella sacroiliitis: clinical features. Clin Rheumatol. 1998;17:521–3. https://doi.org/10.1007/BF01451292. Prakash J.  Sacroiliac tuberculosis—a neglected differential in refractory low back pain—our series of 35 patients. J Clin Orthop Trauma. 2014;5:146–53. https://doi.org/10.1016/j.jcot.2014.07.008. Silberstein M, Hennessy O, Lau L. Neoplastic involvement of the sacroiliac joint: MR and CT features. Australas Radiol. 1992;36:334–8. https://doi.org/10.1111/j.1440-­1673.1992.tb03215.x. Tekkök IH, Berker M, Ozcan OE, Ozgen T, Akalin E.  Brucellosis of the spine. Neurosurgery. 1993;33:838–44. https://doi. org/10.1227/00006123-­199311000-­00008. Thawrani DP, Agabegi SS, Asghar F. Diagnosing sacroiliac joint pain. J Am Acad Orthop Surg. 2019;27:85–93. https://doi.org/10.5435/ JAAOS-­D-­17-­00132.

933 Tsoi C, Griffith JF, Lee RKL, Wong PCH, Tam LS.  Imaging of sacroiliitis: current status, limitations and pitfalls. Quant Imaging Med Surg. 2019;9:318–35. https://doi.org/10.21037/qims.2018.11.10. Visser LH, Nijssen PG, Tijssen CC, van Middendorp JJ, Schieving J. Sciatica-like symptoms and the sacroiliac joint: clinical features and differential diagnosis. Eur Spine J. 2013;22:1657–64. https:// doi.org/10.1007/s00586-­013-­2660-­5. Wieczorek A, Campau E, Pionk E, Gabriel-Champine ME, Ríos-­ Bedoya CF. A closer look into the association between the sacroiliac joint and low back pain. Spartan Med Res J. 2021;6:21971. https:// doi.org/10.51894/001c.21971. Yilmaz N, Ozgocmen S, Kocakoc E, Kiris A.  Primary hydatid disease of sacrum affecting the sacroiliac joint: a case report. Spine (Phila Pa 1976). 2004;29:E88–90. https://doi.org/10.1097/01. brs.0000112073.58305.e2.

93

Sciatic Hernias

93.1 Generalities and Relevance Sciatic hernia (AKA sacrosciatic hernia, ischiatic hernia, gluteal hernia, hernia incisura ischiadica, or ischiocele) is one of the rarest types of hernia in the body with less than 120 cases reported in the literature since Papen first described it in 1750. A sciatic hernia is a type of pelvic floor hernia. It was defined as a herniation of the peritoneal sac and its contents through the greater or lesser sciatic foramen. For many authors, anatomic defect seen in sciatic hernias is the direct result of atrophy or abnormal development of the muscles lining the sciatic foramina, especially, the piriform muscle. Women are most commonly affected (75%) with more than one-third of patients being aged more than 60 years old.

Comprehensive knowledge of pelvic anatomy is essential for understanding this notion. The greater sciatic foramen, formed by the sacrotuberous and sacrospinous ligaments of the sciatic notch, is an opening in the posterior pelvis providing a passage for structures to pass from the pelvis (intrapelvic) into the gluteal (extrapelvic) region. The greater sciatic foramen is divided by the piriformis muscle on suprapiriform and infrapiriform spaces. Classically, the greater sciatic foramen is larger in females than in males. There are three types of sciatic hernias through the sciatic foramina: infrapiriform, suprapiriform, and subspinous (Fig. 93.1). The sciatic nerve, accompanying other neurovascular structures (Table  93.1), passes through the infrapiriform space below the piriformis. Sciatica occurs because of com-

Fig. 93.1  Anteromedial view of the pelvic cavity showing the three potential sciatic hernia sites through the sciatic foramina: infrapiriform, suprapiriform, and subspinous hernias. Hernia through the infrapiriform space is more likely to be involved when the sciatic nerve is compressed or entrapped in the sciatic foramen (arrow)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_93

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93  Sciatic Hernias

936 Table 93.1  Main neurovascular structures that travel within the infrapiriform space of the greater sciatic foramen (PIN PINS may be used as an acronym c.f. to Chap. 95 about Deep Gluteal Syndrome) Nerves Pudendal nerve Posterior femoral cutaneous nerve Inferior gluteal nerve Nerve to obturator internus Nerve to quadratus femoris Sciatic nerve

Vessels Inferior gluteal vessels Internal pudendal vessels

pression and/or entrapment of the sciatic nerve by the herniated sac and its contents. The contents of sciatic hernias are variables including small and large intestines, ovaries, fallopian tubes, ureters, bladder, Meckel’s diverticulum, omentum, and even tumors. Sometimes, the herniated sac may be found empty. The clinical presentation depends on the contents of the hernia sac and its compressive effect on the sciatic nerve within the infrapiriform space. Clinical diagnosis in patients with sciatica related to sciatic hernia can be challenging because of its rarity: just a dozen cases have been previously published.

93.2 Clinical Presentations The initial evaluation should include a detailed past medical history and physical examination. History would include questions about recent injuries, surgeries, natal/deliveries, ancient abdominopelvic hernias, and sepsis. The clinical symptoms of a sciatic hernia can vary greatly depending on the volume and anatomic structures that are entrapped in the greater sciatic foramen. However, about half of the patients report non-specific abdominal or pelvic pain, and one-third have a mass on clinical examination. Most symptoms are related to gastrointestinal or urologic symptoms, such as intestinal or ureteric obstruction, rectal tenesmus, urinary sepsis, and hydronephrosis. The majority of clinical presentations are subacute or chronic; however, some acute forms have also been reported because of bowel strangulation, perforation, or sepsis. Interestingly, patients may present with an uncomfortable mass in the gluteal area. On physical examination, this palpable mass is reducible with a cough impulse. However, because of the bulk of the gluteus maximus muscle covering the entire area of the sciatic foramen and the piriformis, an early hernia bulge is rarely evident. More rarely, compression of the sciatic nerve can cause pain radiating down the posterior thigh that is typically aggravated by dorsiflexion or sensory neuropathy. Sciatic pain can be the first presenting sign, especially if the hernia is not palpable. In late clinical forms, neurologic deficits, including muscle weakness or sensory disturbance, would be

expected. Symptoms are often unilateral; however, bilateral involvement has been seen before. Closer attention should be paid to pelvic, gluteal, and sciatic mononeuropathic pain to the lower extremities, even in the absence of obvious gluteal mass. Digital rectal examination or vaginal examination can facilitate the diagnosis if the examiner feels a mass in the sciatic region. In addition, the course of the sciatic nerve should be examined for extraspinal pathologies. However, in almost all cases, identifying the nature of the condition by examining the symptoms is often impossible without imaging explorations. Although rare, some patients with sciatic hernias can also have a coexisting or previously other hernia including inguinal, umbilical, femoral, obturator, or perineal hernia, and even genital prolapse.

93.3 Paraclinic Features Ultrasonography and computed tomography (CT) scans are the imaging techniques most frequently used to diagnose a sciatic hernia. Ultrasound is the preferred imaging modality when congenital sciatic hernias are suspected. Ultrasound may reveal bowel loops and peristalsis. Color Doppler study can be useful in studying the viability of herniated bowel, which is important for surgical planning. CT scan coupled with a barium enema exam is helpful in identifying underlying lesions and establishing the degree and level of bowel obstruction (Fig. 93.2). They also help to identify hernia contents. These methods are also valuable in describing surrounding or associated anatomic structures. Ureteric sciatic hernias are classically diagnosed with excretory urography. The radiologist should be aware of false negative CT scan results, as this is realized with the patient in a supine posi-

Fig. 93.2  Axial pelvic CT scan showing the typical site of the sciatic hernia (yellow). “P” corresponds to the piriformis muscle and the dotted line indicates the greater sciatic foramen

Further Reading

tion, potentially compressing the hernia. Faced with this problem, ultrasound evaluation may be a good alternative using a dynamic component to the assessment with the Valsalva maneuver and the patient in a standing position. Interestingly, six well-documented descriptions of a lipomatous tumor herniating through the sciatic foramen have been previously reported. The tumor might have its origin in the gluteus (extrapelvic) and extend through the sciatic foramen into the pelvis as an “inverted” or retrograde hernia. Traditional magnetic resonance (MR) imaging or even better MR neurography is the modality of choice to evaluate the lumbosacral plexus or the sciatic nerve in cases of sciatic pain. They can demonstrate entrapment of the sciatic trunk and highlight morphological changes in the nerve due to chronic compression. The MR neurography procedure uses high-resolution T1-weighted MR sequences to delineate anatomic detail and fat-suppressed T2-weighted or STIR sequences to detect abnormal nerve signal intensity. The electrophysiologic evaluation may play a role in the assessment of a possible sciatic peripheral mononeuropathy. The electrophysiologic approach evaluates and excludes disorders that can mimic lumbosacral plexopathy or radiculopathies. Nerve damage may be manifest on electromyography as fibrillation potentials, and motor unit potentials that are either decreased in number or increased in amplitude or duration and polyphasic.

93.4 Treatment Options and Prognosis The mainstay treatment of sciatic hernias, regardless of incarceration, is surgical reduction and repair because the risk of strangulation is high. However, there is no standardized surgical method for correcting sciatic hernias. Many authors have already used abdominal (transperitoneal or extraperitoneal), gluteal, and combined approaches (especially, both gluteal and abdominal transperitoneal methods). Prosthetic reinforcement is always needed for the best result. A transabdominal approach is recommended in patients who present signs of intestinal obstruction or strangulation or when the diagnosis is unclear. A transgluteal approach, through the gluteus maximus muscle, may be indicated when the herniated segments appear viable and reducible. To resect the herniated sac, the surgeon should always have in mind safe exposure of the sciatic nerve. The hernia defect can be restored with non-absorbable sutures, and synthetic mesh, and be covered with a peritoneal flap or bead of omentum. Recently, minimally invasive approaches using transperitoneal laparoscopic repair have been used successfully in some cases. When the ureter is the anatomic structure involved, it should be repaired solely with stent placements.

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The prognosis varies depending on the underlying etiology, hernia content, treatment response, and delay of treatment. Overall, the prognosis is good for patients with sciatica since the majority of them have pain relief and are without postoperative neurological disorders.

Further Reading Berman L, Aversa J, Abir F, Longo WE. Management of disorders of the posterior pelvic floor. Yale J Biol Med. 2005;78:211–21. Cai ZJ, Salem AE, Wagner-Bartak NA, Elsayes KM, Negm AS, Rezvani M, et al. Sciatic foramen anatomy and common pathologies: a pictorial review. Abdom Radiol (NY). 2022;47:378–98. https://doi. org/10.1007/s00261-­021-­03265-­8. Chitranjan KH, Madhusudhan KS. Sciatic hernia causing sciatica: MRI and MR neurography showing entrapment of sciatic nerve. Br J Radiol. 2010;83:e65–6. https://doi.org/10.1259/bjr/47866965. Dong ZP, She JJ, Sun XJ, Zheng JB. Sciatic hernia led to strangulated ileum and ipsilateral ovary: a case report and review of literature. Heliyon. 2023;9:e13904. https://doi.org/10.1016/j.heliyon.2023. e13904. Dulskas A, Poskus E, Jurevicius S, Strupas K. Giant gluteal lipoma presenting as a sciatic hernia. Hernia. 2015;19:857–60. Duran S, Cavusoglu M, Elverici E, Unal TD.  A giant retroperitoneal lipoma presenting as a sciatic hernia: MRI findings. JBR-BTR. 2015;98:32–3. https://doi.org/10.5334/jbr-­btr.749. Fadel MG, Louis C, Tay A, Bolgeri M.  Obstructive urosepsis secondary to ureteric herniation into the sciatic foramen. BMJ Case Rep. 2018;2018:bcr2018225523. https://doi.org/10.1136/ bcr-­2018-­225523. Gomez-Seoane A, Oyasiji T. Gluteal liposarcoma presenting as sciatic hernia: a case report and review of literature. Int J Surg Case Rep. 2020;67:25–9. https://doi.org/10.1016/j.ijscr.2020.01.015. Kaur N, Kaur N, Chhabra HS, Singh M, Singh P.  A case report of sciatic hernia as a cause of sciatica and lower back pain: diagnostic dilemma for family physicians. J Family Med Prim Care. 2022;11:3304–7. https://doi.org/10.4103/jfmpc.jfmpc_2057_21. Kim YU, Cho JH, Song PH. Ureterosciatic hernia causing obstructive uropathy successfully managed with minimally invasive procedures. Yeungnam Univ J Med. 2020;37:337–40. https://doi.org/10.12701/ yujm.2020.00402. Kimura J, Yoshikawa K, Sakamoto T, Lefor AK, Kubota T. Successful manual reduction for ureterosciatic hernia: a case report. Int J Surg Case Rep. 2019;57:145–51. https://doi.org/10.1016/j. ijscr.2019.03.036. Kostov D, Kostov V.  A Giant sciatic hernia. Eurasian J Med. 2017;49:222–3. https://doi.org/10.5152/eurasianjmed.2017.17189. Labib PL, Malik SN.  Choice of imaging modality in the diagnosis of sciatic hernia. J Surg Case Rep. 2013;2013:rjt102. https://doi. org/10.1093/jscr/rjt102. López-Tomassetti Fernández EM, Hernández JR, Esparragon JC, García AT, Jorge VN.  Intermuscular lipoma of the gluteus muscles compressing the sciatic nerve: an inverted sciatic hernia. J Neurosurg. 2012;117:795–9. https://doi.org/10.3171/2012.7.JNS111714. Losanoff JE, Basson MD, Gruber SA, Weaver DW. Sciatic hernia: a comprehensive review of the world literature (1900-2008). Am J Surg. 2010;199:52–9. https://doi.org/10.1016/j.amjsurg.2009.02.009. Martel L.  Pointe de hernie ischiatique: impotence fonctionelle du membre inferieur pendant 5 mois operation Guerison. Loire Med. 1900;19:165–74. [In French]. Miklos JR, O’Reilly MJ, Saye WB. Sciatic hernia as a cause of chronic pelvic pain in women. Obstet Gynecol. 1998;91:998–1001. https:// doi.org/10.1016/s0029-­7844(98)00085-­4.

938 Peters A, Reichelt A. “Lumbar intervertebral disk-induced sciatica” diagnostic error in extensive extra- and intrapelvic lipoma. Z Orthop Ihre Grenzgeb. 1999;137:362–5. https://doi. org/10.1055/s-­2008-­1039726. Salari K, Yura EM, Harisinghani M, Eisner BH. Evaluation and treatment of a ureterosciatic hernia causing hydronephrosis and renal colic. J Endourol Case Rep. 2015;1:1–2. https://doi.org/10.1089/ cren.2015.29005.sal. Shibata Y, Ueda T.  Ureterosciatic hernia with gluteal abscess: a case report. Urol Case Rep. 2023;47:102378. https://doi.org/10.1016/j. eucr.2023.102378. Servant CT.  An unusual cause of sciatica. A case report. Spine (Phila Pa 1976). 1998;23:2134–6. https://doi. org/10.1097/00007632-­199810010-­00019. Tokunaga M, Shirabe K, Yamashita N, Hiki N, Yamaguchi T.  Bowel obstruction due to sciatic hernia. Dig Surg. 2008;25:185–6. https:// doi.org/10.1159/000140685.

93  Sciatic Hernias Touloupidis S, Kalaitzis C, Schneider A, Patris E, Kolias A. Ureterosciatic hernia with compression of the sciatic nerve. Int Urol Nephrol. 2006;38:457–8. https://doi.org/10.1007/ s11255-­005-­4764-­2. van Langevelde K, Azzopardi C, Kiernan G, Gibbons M, Orosz Z, Teh J. The tip of the iceberg: lipomatous tumours presenting as abdominal or pelvic wall hernias. Insights Imaging. 2019;10:66. https://doi. org/10.1186/s13244-­019-­0739-­1. Vanneste JA, Butzelaar RM, Dicke HW. Ischiadic nerve entrapment by an extra- and intrapelvic lipoma: a rare cause of sciatica. Neurology. 1980;30:532–4. https://doi.org/10.1212/wnl.30.5.532. Zeng F, Shames B, Appel E, Varalakshmi N, Mortensen E, Maheshwari N. Bilateral sciatic hernias in an elderly woman successfully managed with robotic surgery: a case report and literature review. Int J Surg Case Rep. 2021;86:106333. https://doi.org/10.1016/j. ijscr.2021.106333.

Part V Extraspinal Extrapelvic Sciatica

Sciatic Peripheral Neuropathies

94.1 Generalities and Relevance Sciatic peripheral neuropathy or sciatic neuropathy is the overarching condition describing the damage, dysfunction, and pathologic changes of the sciatic nerve trunk along its complete course from the deep gluteal region to the popliteal fossa. Sciatic peripheral neuropathy should be distinguished from other peripheral nervous system lesions involving the lower limbs such as L5 and/or S1 radiculopathy, lumbosacral plexopathy, tibial neuropathy, and common peroneal neuropathy. Although rarer, central (intraspinal and intracranial) funicular presentations causing sciatic pain should also be mentioned (c.f. Chaps. 44 and 111, respectively). Sciatic neuropathy is the second most common neuropathy of the lower extremity, after common peroneal neuropathy. It may be seen at all ages, from neonates to the elderly with a slight male predominance. Pediatric sciatic neuropathies are uncommon, and the etiology is often traumatic or related to compression or stretch injury. However, pure and isolated sciatic neuropathy is an uncommon diagnosis in routine clinical practices and even in electrodiagnostic studies. When sciatic neuropathy is diagnosed, efforts need to be made to define the exact location of the nerve lesion, assess its significance and extension, identify the etiology of the damage, and treat it. Sometimes, surgical exploration may be required to attempt nerve repair.

94

The most common cause of sciatic neuropathy is traumatic injury whether exogenous or iatrogenic. Compressive sciatic neuropathies are also occasionally seen, while tumors and vascular lesions are rare but serious causes of this presentation. With the high prevalence of diabetes mellitus in the population, diabetic neuropathy should always be mentioned. In addition, some cases may be part of a systemic illness. Sometimes, multiple etiologies (including compressive causes) may simultaneously contribute to nerve disorder and its subsequent clinical symptoms, and this condition is so-­ called “multifocal neuropathy” or “Double Crush Syndrome Involving Different Sites” (c.f. Chap. 109).

94.2 Etiologies Sciatic neuropathy is any of numerous functional disturbances and pathologic changes in the sciatic nerve. The damage may include demyelinating lesions, axonal lesions, mixed axonal and demyelinating lesions, or partial or complete nerve discontinuity. Many and various etiologies are involved in sciatic neuropathy. However, traumatic, compressive, ischemic, neoplastic, diabetic, and idiopathic causes are among the most frequent etiologies. A useful mnemonic for remembering the various causes of this peripheral neuropathy is DANG CV THERAPIST (Table 94.1; Figs. 94.1, 94.2, and 94.3).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_94

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94  Sciatic Peripheral Neuropathies

942 Table 94.1  Various etiologies of sciatic peripheral neuropathies D

Diabetes mellitus Drugs Decompression sickness

A N G C

Alcohol abuse Nutritional Guillain-Barre syndrome Compressive

V

Vascular

T

Traumatic

I

Toxins Hereditary Hematologic Entrapment Endocrine Rheumatologic Recurrent Renal Radiation Amyloid Porphyric Psychiatric Paraneoplastic Pseudoneuropathy Pseudotumor Polymyalgia rheumatic Infectious

S

Inflammatory Iatrogenic Intoxication Idiopathic Systemic

T

Tumors

H E R

A P

Primary sensory neuropathy, diabetic amyotrophy, and diabetic proximal neuropathy Thalidomide, metronidazole, phenytoin, amitriptyline, dapsone, nitrofurantoin, cholesterol lowering drugs, isoniazid, gold salts, thallium, arsenic, and chemotherapy agents Underwater diving decompression, flying in an unpressurized aircraft, working in a caisson, and extra-vehicular activity from spacecraft Diffuse sensory neuropathy Vitamin B1, B6, B12, and E deficiency Acute Inflammatory Demyelinating Polyradiculopathy (AIDP) Acute, subacute, or chronic compression Prolonged immobilization, incorrect positioning, lotus position, lithotomy position, wallet neuritis, consciousness disorder, overdose, anesthesia, pressure palsies, severe weight loss, orthopedic casts, compartment syndromes, hematoma, hematocolpos, iliac artery aneurysm, pregnancy, endometriosis, during vaginal delivery, heterotopic calcification, abscess (Fig. 94.1), Parasitic cyst (Fig. 94.2), congenital iliac anomaly, abdominopelvic tumors, retroperitoneal lesions, and Baker’s cyst in the popliteal fossa Primary and secondary vasculitis (e.g., Churg–Strauss syndrome, microscopic polyangiitis, classic polyarteritis nodosa, and Wegener granulomatosis) Hematoma, aneurysm and pseudoaneurysm, ischemia, artery catheterization, embolization of vascular malformations, persistent congenital sciatic artery, and deep venous thrombosis Lower limb injuries (bone and/or soft tissues) (Fig. 94.3), penetrating injuries, gluteal intramuscular injections, crush injuries, traction injuries, compartment syndrome, and lacerations Heavy metals: Pb, As, Zn, and Hg Friedreich’s ataxia, Charcot-Marie-Tooth, Refsum’s disease, and hereditary compression neuropathy Paraproteins Deep gluteal syndrome, piriformis syndrome, wallet neuritis, and fibrovascular bands Hypothyroid Systemic lupus erythematosus, rheumatoid arthritis, and vasculitis Chronic inflammatory demyelinating polyneuropathy (CIDP) Uremic neuropathy in chronic renal failure Radiation-induced neuropathic (post radiotherapy) Familial, primitive, or secondary Metabolic disorders caused by specific enzyme deficiencies Related to a neuropsychiatric disorder Associated with cancer (carcinomatous) With psychogenic component (conversion-somatization-malingering) Endometriosis, ganglion cyst, lipomatosis, and fibromatosis PMR Leprosy, infectious mononucleosis, HIV, Lyme disease and borreliosis, diphtheria, syphilis, Herpes simplex/Varicella-zoster virus, hepatitis B and C, cytomegalovirus, Epstein-Barr virus, poliomyelitis, and Covid Sacroiliitis, osteoarthritis, and neuritis ossificans Hip and pelvic surgery, surgical positioning, and anesthesia Carbon monoxide and pyridoxine From unknown cause (up to 20% of cases) Sarcoidosis, Systemic lupus erythematosus, hypothyroidism, Sjögren’s syndrome, uremia, dysproteinemia, acromegaly, cryoglobulinemia, psoriasis, and hyper-­eosinophilic syndrome –  Nerve and nerve sheath tumors –  Benign and malignant neoplasms, schwannomas, perineurioma, neurofibromatosis, lymphoma, lipoma, neuroblastoma, rhabdomyosarcoma, paraneoplastic, multiple myeloma, and monoclonal gammopathy of undetermined significance (MGUS)

“DANG CV THERAPIST” can be used as an acronym

a

b

Fig. 94.1  Right sciatic neuropathy secondary to gluteal abscess compression (stars) as seen on axial pelvic CT scan with contrast injection (a, b)

94.5  Treatment Options and Prognosis

a

c

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b

d

Fig. 94.2  Popliteal hydatid cyst (stars) manifesting as sciatic pain. Sagittal (a, b) and axial (c, d) MR imaging. Note the proximity of the popliteal artery and vein and the tibial nerve (dotted lines)

944 Fig. 94.3  Left peroneal (fibular) nerve neuropathy secondary to a lower limb injury (a, b)

94  Sciatic Peripheral Neuropathies

a

94.3 Clinic Presentations Sciatic peripheral neuropathies caused by traumatic injury, compression, or vascular etiologies present acutely. Apart from that, most sciatic neuropathies present in a gradual subacute manner without low back pain. Initially, the clinical symptoms are less obvious and most often mistaken for peroneal neuropathy due to incomplete injury to the sciatic nerve. Indeed, many patients with sciatic neuropathy may present with a foot drop and sensory disturbance over the dorsal part of the foot and lateral calf. However, patients with complete sciatic neuropathy have paralysis of knee flexion and all movements about the ankle and toes. Sometimes, there is weakness in hip extension due to hamstring muscle damage. Furthermore, hypoesthesia may be seen in several areas including the lateral knee and lateral calf, dorsum of the foot, web space of the great toe, posterior calf, lateral foot, and plantar foot. Achilles and hamstring reflexes are depressed or absent on the involved side. Pain in the gluteal area, proximal thigh, and the postero-­ lateral part of the leg radiating into the lateral and plantar aspects of the foot are more evocative of sciatic neuropathy than radiculopathy. Additional palpation, compression, or percussion over the sciatic nerve trunk may produce pain and paresthesias extending on the course of the nerve (Valleix Phenomenon). In severe cases, there is dysesthesic pain and numbness in the lateral lower leg, as well as the sole and dorsal part of the foot.

b

Many other concomitant symptoms related to underlying etiologies or systemic diseases should be considered in clinical presentations.

94.4 Paraclinic Features The diagnosis can be made on a clinical basis and may be confirmed with electrodiagnostic tests, such as nerve conduction explorations and electromyography. In contrast to the intraspinal origin of sciatic pain, the majority of peripheral neuropathies may be difficult to image. Differential diagnoses like lumbosacral radiculopathies and plexopathies should be ruled out. Imaging studies, such as magnetic resonance imaging (MRI) and ultrasound, might show denervation changes in the involved muscles, help to localize the site of sciatic nerve damage, and provide pieces of evidence for the etiology. When needed, an additional measurement may be performed based on data from the history and physical exam. The electrophysiological investigation, including conduction explorations and electromyography, plays a key role in the assessment of possible sciatic neuropathy. The electrophysiologic approach evaluates and excludes disorders that can mimic sciatic neuropathy, including peroneal palsy at the fibular neck, lumbosacral plexopathy, and lumbosacral radiculopathy. Needle examination is an important means of localizing the lesion. Involvement of tibial and peroneal supplied muscles distally in the leg, but not the hamstring muscles,

Further Reading

restricts the lesion to the distal part of the sciatic nerve. Involvement of the hamstrings, but not the glutei or vastus lateralis muscles, limits the lesion to the proximal part of the sciatic nerve. The involvement of gluteal muscles suggests either additional involvement of the gluteal nerves or of a lesion of the lumbosacral plexus. Concomitant involvement of femoral or obturator innervated muscles is indicative of a lumbosacral plexopathy. Abnormalities of the paraspinal muscles suggest an intraspinal or nerve root lesion. Chronicity of nerve injury may be decided by analysis of the amplitude, duration, and configuration of the motor unit. In some specific etiologies, such as entrapment neuropathies, tumors of the sciatic nerve, Herpes Zoster-related sciatica, and post-traumatic sciatica, peripheral nervous ultrasonography has shown sciatic nerve enlargement and swelling of the symptomatic sciatic nerve compared to the contralateral asymptomatic side. This swelling occurs more frequently in patients with acute forms of sciatica. Among all neuroimaging techniques, MRI seems to be the best method to detect sciatic nerve neuropathy. Depending on the severity of the damage, T2-weighted MRI may show hyperintensity in the nerve fibers, loss of the normal fascicular appearance, blurring of perifascicular fat, nerve enlargement or deformation, and loss in nerve continuity. The size and extent of the lesion will be better seen on short tau inversion recovery (STIR) sequences. In addition, there are some indirect signs seen in the muscles supplied by the nerve such as increased signal intensity (related to edema) followed by fatty infiltration and muscular atrophy. MRI neurography is a new promising imaging tool for the assessment of peripheral nerve damage. CT, ultrasonographic, and angiographic studies as well as biological explorations can be useful in the search for a potential etiology. However, when paraclinical explorations are inconclusive, surgical exploration may be needed in order to eliminate the possibility of a curable lesion.

94.5 Treatment Options and Prognosis

945

Treatment should be tailored to each site and etiology to ensure patient safety. Management of systemic illness commonly results in an improvement in sciatic neuropathic symptoms. Diabetic amyotrophy is a temporary disorder that frequently resolves with good glycemic control. Progestogens and gonadotropin-releasing hormones may reverse sciatic neuropathy in endometriosis. Immune-mediated neuropathies would be treated with corticosteroids, immunosuppressant therapy, plasmapheresis, or intravenous immunoglobulin depending on the primary disease. Surgery is indicated in patients with compartment syndrome, hip/femoral fracture or dislocation, in refractory cases with a deep gluteal syndrome, and in those with compressive mass lesions, such as a tumor, hematoma, abscess, or heterotopic ossification. Nerve grafting and anastomosis may play a role in the treatment of severe sciatic nerve injuries from trauma but is challenging. Bracing may be used to support weak muscles. For example, an ankle foot orthosis is recommended to improve walking or support the foot and ankle when the tibialis anterior muscle is weak. Physical therapy may help to reinforce muscles, preserve the range of motion, decrease pain, and improve walking. At large, the prognosis for sciatic neuropathy is chiefly dependent on the causal etiology and severity of the lesion. Most patients with sciatic neuropathy had a good outcome at 3 years, whereas only one-third had a good or better recovery at 1 year. Good but incomplete recovery occurred principally in individuals who did not show severe motor axonal loss on the electromyographic study. In patients with an acute or subacute onset, a moderate or better recovery occurred in most cases. Depending on the surgical technique used, partial recovery was seen in more than 70% of patients enduring neurolysis, 30–90% of cases undergoing end-to-end suture reparation, and 25–80% of patients treated with nerve grafts. In individuals with poor recovery of sciatic neuropathies, long-term complications may include, pes cavus, lesions related to sensory loss in the feet (e.g., ulcerations), tendon shortening, retraction, and growth failure of the affected limb in the pediatric population. Some complications might necessitate further orthopedic or surgical procedures.

Identification of the origin of sciatic peripheral neuropathy is important for determining therapy and prognosis. Management depends on the underlying cause and includes conservative measures with physical therapy, analgesics, muscle relaxants, stretching, local anesthetics, and non-­ Further Reading steroidal anti-inflammatory drugs. Neuropathic pain is frequent in almost all causes of sci- Abdallah IE, Ayoub R, Sawaya R, Saba SC.  Iatrogenic sciatic nerve injury during liposuction and fat tissue grafting: a preventable suratic neuropathy and is commonly treated with neuropathic gical complication with devastating patient outcomes. Patient Saf pain medications, such as tricyclic antidepressants (e.g., Surg. 2020;14:40. https://doi.org/10.1186/s13037-­020-­00265-­3. amitriptyline or nortriptyline), anticonvulsants (e.g., gaba- Adib F, Posner AD, O’Hara NN, O’Toole RV.  Gluteal compartment syndrome: a systematic review and meta-analysis. Injury. pentin, pregabalin, or carbamazepine), and transdermal 2022;53:1209–17. https://doi.org/10.1016/j.injury.2021.09.019. lidocaine.

946 Asagai Y, Minamikawa S, Ueshima E, Aida Y, Nakagishi Y.  Sciatic neuropathy caused by forced stretching exercise. Pediatr Int. 2022;64:e15387. https://doi.org/10.1111/ped.15387. Bodur H, Eser F, Dedeoglu M, Yilmaz O. Nontraumatic focal neuropathies: distribution and retrospective analysis of the cases. Turk J Phys Med Rehab. 2012;58:114–20. https://doi.org/10.4274/tftr.46503. Cherian RP, Li Y.  Clinical and electrodiagnostic features of nontraumatic sciatic neuropathy. Muscle Nerve. 2019;59:309–14. https:// doi.org/10.1002/mus.26380. De Mulder P, Harth C, Ide L, Vallaeys J, Baelde N, De Bo T. An uncommon cause of sciatic pain: tuberculous osteomyelitis of the ischial tuberosity. Acta Clin Belg. 2017;72:357–60. https://doi.org/10.1080 /17843286.2016.1271499. Devlieger BK, Drees P, Mattyasovszky S, Özalp C, Rommens PM.  Impingement of the sciatic nerve due to a protruding acetabular cage rim. Arthroplast Today. 2020;6:825–9. https://doi. org/10.1016/j.artd.2020.08.005. Distad BJ, Weiss MD.  Clinical and electrodiagnostic features of sciatic neuropathies. Phys Med Rehabil Clin N Am. 2013;24:107–20. https://doi.org/10.1016/j.pmr.2012.08.023. Feinberg J, Sethi S.  Sciatic neuropathy: case report and discussion of the literature on postoperative sciatic neuropathy and sciatic nerve tumors. HSS J. 2006;2:181–7. https://doi.org/10.1007/ s11420-­006-­9018-­z. Flug JA, Burge A, Melisaratos D, Miller TT, Carrino JA. Post-operative extra-spinal etiologies of sciatic nerve impingement. Skeletal Radiol. 2018;47:913–21. https://doi.org/10.1007/s00256-­018-­2879-­7. Galluzzo M, Talamonti M, Di Stefani A, Chimenti S. Linear psoriasis following the typical distribution of the sciatic nerve. J Dermatol Case Rep. 2015;9:6–11. https://doi.org/10.3315/jdcr.2015.1189. Jeon SY, Moon HS, Han YJ, Sung CH. Post-radiation piriformis syndrome in a cervical cancer patient—a case report. Korean J Pain. 2010;23:88–91. https://doi.org/10.3344/kjp.2010.23.1.88. Kim DH, Murovic JA, Tiel R, Kline DG.  Management and outcomes in 353 surgically treated sciatic nerve lesions. J Neurosurg. 2004;101:8–17. https://doi.org/10.3171/jns.2004.101.1.0008. Koh E.  Imaging of peripheral nerve causes of chronic buttock pain and sciatica. Clin Radiol. 2021;76:626.e1–626.e11. https://doi. org/10.1016/j.crad.2021.03.005. Louw JA.  The differential diagnosis of neurogenic and referred leg pain. SA Orthop J. 2014;13:5256. Mannan K, Altaf F, Maniar S, Tirabosco R, Sinisi M, Carlstedt T. Cyclical sciatica: endometriosis of the sciatic nerve. J Bone Joint Surg Br. 2008;90:98–101. https://doi.org/10.1302/0301-­620X.90B1.19832. McMillan HJ, Srinivasan J, Darras BT, Ryan MM, Davis J, Lidov HG, et  al. Pediatric sciatic neuropathy associated with neoplasms. Muscle Nerve. 2011;43:183–8. https://doi.org/10.1002/ mus.21867. Mert M, Oztürkmen Y, Unkar EA, Erdoğan S, Uzümcügil O.  Sciatic nerve compression by an extrapelvic cyst secondary to wear

94  Sciatic Peripheral Neuropathies debris after a cementless total hip arthroplasty: a case report and literature review. Int J Surg Case Rep. 2013;4:805–8. https://doi. org/10.1016/j.ijscr.2013.07.008. Michaelson NM, Malhotra A, Wang Z, Heier L, Tanji K, Wolfe S, et al. Peripheral neurological complications during COVID-19: a single center experience. J Neurol Sci. 2022;434:120118. https://doi. org/10.1016/j.jns.2021.120118. Mishra P, Stringer MD. Sciatic nerve injury from intramuscular injection: a persistent and global problem. Int J Clin Pract. 2010;64:1573– 9. https://doi.org/10.1111/j.1742-­1241.2009.02177.x. Pérez D, de la Torre RG, Carrio I, Pinto J, Morís G. Cryoglobulinaemic neuropathy: a further cause of bilateral sciatic neuropathy. Int Arch Med. 2008;1:18. https://doi.org/10.1186/1755-­7682-­1-­18. Prasad M, Babiker M, Rao G, Rittey C.  Pediatric sciatic neuropathy presenting as painful leg: a case report and review of literature. J Pediatr Neurosci. 2013;8:161–4. https://doi. org/10.4103/1817-­1745.117858. Srinivasan J, Ryan MM, Escolar DM, Darras B, Jones HR.  Pediatric sciatic neuropathies: a 30-year prospective study. Neurology. 2011;76:976–80. https://doi.org/10.1212/ WNL.0b013e3182104394. Stewart JD, Angus E, Gendron D.  Sciatic neuropathies. Br Med J (Clin Res Ed). 1983;287:1108–9. https://doi.org/10.1136/ bmj.287.6399.1108. Son BC, Kim DR, Jeun SS, Lee SW.  Decompression of the sciatic nerve entrapment caused by post-inflammatory scarring. J Korean Neurosurg Soc. 2015;57:123–6. https://doi.org/10.3340/ jkns.2015.57.2.123. Wang JC, Wong TT, Chen HH, Chang PY, Yang TF.  Bilateral sciatic neuropathy as a complication of craniotomy performed in the sitting position: localization of nerve injury by using magnetic resonance imaging. Childs Nerv Syst. 2012;28:159–63. https://doi. org/10.1007/s00381-­011-­1597-­4. Weil Y, Mattan Y, Goldman V, Liebergall M. Sciatic nerve palsy due to hematoma after thrombolysis therapy for acute pulmonary embolism after total hip arthroplasty. J Arthroplasty. 2006;21:456–9. https://doi.org/10.1016/j.arth.2005.03.042. Yamauchi Y, Abe S, Sudo S, Kimura S, Nagaro T, Arai T.  A case of Guillain-Barre syndrome with severe sciatica preceding motor paralysis in the lower extremities. Masui. 1999;48:198–200. Yoon SJ, Park MS, Matsuda DK, Choi YH.  Endoscopic resection of acetabular screw tip to decompress sciatic nerve following total hip arthroplasty. BMC Musculoskelet Disord. 2018;19:184. https://doi. org/10.1186/s12891-­018-­2091-­x. Yoshimoto M, Kawaguchi S, Takebayashi T, Isogai S, Kurata Y, Nonaka S, et al. Diagnostic features of sciatica without lumbar nerve root compression. J Spinal Disord Tech. 2009;22:328–33. https://doi. org/10.1097/BSD.0b013e31817dc46d. Yuen EC, So YT.  Sciatic neuropathy. Neurol Clin. 1999;17:617–31, viii. https://doi.org/10.1016/s0733-­8619(05)70155-­9.

95

Deep Gluteal Syndrome (Including Piriformis Syndrome)

95.1 Generalities and Relevance Classically, the term “piriformis syndrome” has been used to define an entrapment neuropathy involving compression of the sciatic nerve by the piriformis (AKA pyramidal) muscle causing buttock pain, sciatic pain, or both. The sciatic nerve has a close relationship to the piriformis muscle, exiting the pelvis frequently below the muscle at the greater sciatic foramen (notch) (Figs. 95.1 and 95.2; Table 95.1). However, the relationship between these two anatomic structures is variable, as the nerve occasionally passes through the muscle, or splits early, with part of it passing through the muscle (Fig. 95.3; Table 95.2). Fig. 95.1  Posterior view of the pelvis showing the relationship between sciatic nerve and piriformis muscle

With time, it becomes clear that other different conditions can cause entrapment of the sciatic nerve in the deep gluteal region (Table 95.3) besides the piriformis muscle including: • • • • •

Gemelli-obturator internus syndrome Quadratus femoris/ischiofemoral impingement Proximal hamstring syndrome Gluteal contracture Some orthopedic conditions such as changes in the osseous alignment of the pelvis, femur, and spine

Lumbar spine

IIiac bone

Sacrum Greater sciatic foramen Hip joint

Piriformis muscle Greater tronchanter Sciatic nerve Ischial tuberosity

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_95

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95  Deep Gluteal Syndrome (Including Piriformis Syndrome) Table 95.1  The anatomic structures (PIN PINS is used as an acronym) that pass from the greater sciatic notch below the piriformis muscle P I N P I N S

Posterior femoral cutaneous nerve Inferior gluteal artery and nerve Nerve to quadratus femoris Pudendal nerve Internal pudendal artery and vein Nerve to obturator internus Sciatic nerve

Fig. 95.2  Axial pelvic CT scan showing the location of the piriformis muscle (in red color), the greater sciatic foramen (double arrow), and the internal iliac vessels with the sciatic nerve (dotted circle)

Fig. 95.3  Posterior view of the pelvis showing the six main variations of the sciatic nerve in relation to the piriformis muscle (from type a to type f)

Type a

Type b

Type c

Type d

Type e

Type f

95.1  Generalities and Relevance

949

Table 95.2  The main anatomical variants related to the division of the sciatic nerve about the piriformis muscle in the deep gluteal region (according to Beaton and Anson) Type of variation a b

c d e f

Reported Description incidence (%) An undivided nerve below undivided 83.1 the piriformis muscle (normal course) A divided sciatic nerve passing 13.7 through and below the piriformis muscle A divided nerve passing above and 1.3 below an undivided muscle An undivided sciatic nerve passing 0.5 through the piriformis muscle heads A divided nerve passing through and 0.08 above the muscle heads An undivided sciatic nerve passing 0.08 above the undivided muscle

Wallet

Table 95.3  Limitations of the deep gluteal space Anterior border Posterior border Medial border Lateral border Superior border Inferior border

Posterior acetabular column Gluteus maximus muscle Sacro-tuberous ligament Gluteal tuberosity Sciatic notch Ischial tuberosity

For that reason, the wide-ranging and more accurate term “deep gluteal syndrome” (DGS) has been proposed to include all these subtypes. The first description of sciatic nerve entrapment by the piriformis muscle was given by Yeoman in 1928. However, it was only in 1947 that Robinson named the clinical entity the “piriformis syndrome.” In 1938, Beaton and Anson classified the variations of anatomical relationship between the piriformis muscle and the sciatic nerve into six types. In 1966, Battle described “credit-carditis” to describe wallet sciatica. Nevertheless, it was only in 1978 that Lutz first demonstrated that the ipsilateral sciatic nerve gets compressed from the exogenous wallet beneath the piriformis muscle, mimicking discogenic sciatica, and named this condition “credit-card-­ wallet sciatica.” Since then, several names have been used such as “wallet neuritis,” “fat wallet syndrome,” or “back-­ pocket sciatica” (Fig.  95.4). In 1999, McCrory and Bell introduced the concept of “Deep Gluteal Syndrome,” which include piriformis syndrome and other gluteal conditions that could result from the entrapment of the sciatic nerves by different structures in the deep gluteal space. Numerous etiologies may be situated in the subgluteal space and can produce DGS, such as traumatic, iatrogenic, tumoral, vascular, inflammatory, infectious, gynecologic (particularly endometriosis), and malformative lesions. DGS may occur after overuse or repetitive microtrauma to the buttock region, and several cases with post-traumatic entrapment of the sciatic nerve have constricting fibrous membranes

Fig. 95.4  An overloaded wallet may initiate gluteal pain (arrow) with sciatic neuritis known as “wallet neuritis” (AKA walletosis, fat-wallet syndrome, or credit-carditis)

or fibrovascular bands between the muscles and the sciatic nerve. However, in most patients, the compression is originally muscular, and the piriformis muscle is frequently involved. Macroscopically, a normal sciatic nerve will have good epineural blood flow and epineural fat, whereas an abnormal sciatic nerve will seem white without or with poor epineural blood flow. There are two types of piriformis syndrome, primary (15%) and secondary (85%). Primary piriformis syndrome has anatomic causes such as: –– Hypertrophy of the piriformis muscle –– Dynamic sciatic nerve entrapment by the piriformis muscle –– Anomalous course of the sciatic nerve (anatomical variations) (Fig. 95.3; Table 95.3) The secondary piriformis syndrome occurs as a result of a precipitating cause including direct trauma (whether macro-­

950

traumatisms or micro-traumatisms), ischemic mass effect, and local ischemia. Piriformis syndrome is much more prevalent than that of other subtypes of DGS. Several reviews described the piriformis syndrome as having an estimated prevalence of up to 10%. Overall, DGS is an under-recognized and multifactorial entity often present in the adult population in their fifth decade without distinct gender predilection.

95.2 Clinical Presentations Clinical evaluation of patients with DGS is often difficult since symptoms are inaccurate and may be mistaken with many other spinal, intrapelvic, and especially peri-articular hip diseases. The most common symptoms include posterior hip or buttock pain, tenderness in the gluteal and retro-trochanteric region, and sciatic nerve pain, often unilateral (Fig.  95.5), exacerbated with rotation of the hip in flexion and knee extension. Classically, the pain worsened when sitting for more than 30  min. Sometimes patients report neurogenic claudication, nocturnal lower limb pain, and disturbed or loss of sensation in the leg. Lumbago, lower back pain, and foot drop are unusual findings. In addition, several patients may adopt an antalgic position. Patients with ischiofemoral impingement typically experience worsening pain during running or taking bigger steps. Patients with proximal hamstring syndrome may complain of ischial pain during the initial heel strike. Pain in the region of the ischial tuberosity may radiate down to the posterior aspect of the thigh. This pain gets worse while running (especially in athletes) or exercising and sometimes even when sitting.

Fig. 95.5  Clinical evaluation of patients with deep gluteal syndrome: there is often unilateral buttock pain, tenderness in the gluteal, and sciatic nerve pain

95  Deep Gluteal Syndrome (Including Piriformis Syndrome)

Many other associated symptoms related to underlying causes should be considered in addition to the DGS. In physical examination, tenderness in deep gluteal space (Fig. 95.5) and some maneuvers or tests are considered suggestive of piriformis syndrome. A positive provocative test reproduces gluteal and neurologic pain. (a) The FAIR test is a Flexion Adduction and Internal Rotation test performed with the patient in the lateral decubitus position on the unaffected side (Fig. 95.6) (b) Freiberg test: internal rotation of the hip of the affected side with the patient in a supine position (stretching the piriformis muscle) (Fig. 95.7) (c) Pace sign: active or resisted abduction and external rotation of the hip in a sitting position (activating the piriformis muscle) (Fig. 95.8)

Fig. 95.6  The FAIR test (Flexion Adduction and Internal Rotation test) is a provocative test for deep gluteal syndrome (In a lateral position)

Fig. 95.7  Freiberg test (internal rotation of the hip of the affected side) is a provocative test for deep gluteal syndrome (Stretching the piriformis muscle in a supine position)

95.3  Paraclinic Features

951

Cases with hamstring injuries can present a thickened hamstring tendon or muscular defect over the ischial tuberosity.

95.3 Paraclinic Features

Fig. 95.8  Pace sign (active or resisted abduction and external rotation of the hip) is a provocative test for deep gluteal syndrome (activating the piriformis muscle in a sitting position)

(d) The seated piriformis stretch test: the examiner extends the knee and passively moves the flexed hip into adduction with internal rotation in a seated position. (e) Beatty test: with the patient in the lateral decubitus position on the unaffected side, both the hip and knee are flexed. Abducting the affected lower limb produces deep buttock pain (contracting the piriformis muscle) (f) Lasègue test (AKA straight leg raise test): the patient reports buttock and leg pain during this traditional passive test. The ischiofemoral impingement test induces pain lateral to the ischium when the hip is extended with adduction and relieves it when the hip is abducted with extension. In people with proximal hamstring syndrome, weakness of knee flexion and re-creation of pain on resisted knee flexion may be found in a seating position during resisted knee flexion at 30°, but not at 90°. Patients with piriformis syndrome may present a palpable sausage-shaped mass over the piriformis muscle region or ipsilateral gluteal atrophy (depending on the duration) in comparison to the contralateral side.

Magnetic resonance imaging (MRI) is the diagnostic procedure of choice for assessing deep gluteal syndrome and may substantially influence the management of these patients. A pelvic MRI is performed to confirm the presence of nerve entrapment in the deep gluteal space and excludes the probability of intra-pelvic lesions. Neural enlargement, abnormal fascicular appearance, increased perifascicular and intraneural signal intensity on T2-weighted or short tau inversion recovery (STIR) sequences, and perifascicular fat blurring are morphologic alterations that suggest neural damage. Longitudinal high-contrast isotropic 3D images reconstructed along the path of the sciatic nerve can help detect the presence of perineural fibrovascular bands. Unfortunately, many cases of DGS will not be documented on MRI. Furthermore, patients should be assessed by appropriate biologic and imaging tools to exclude hip, sacroiliac joint, and lumbar spine disorders. Consultations with experts, such as neurologists, orthopedists, and gynecologists, can aid in differential diagnoses. Electromyography (EMG) findings can be valuable in rejecting lumbosacral radiculopathy. Although EMG tests are often normal in DGS, peripheral nerve damage can be diagnosed by detecting decreased conduction velocities or amplitude of action potentials in a nerve conduction study or by detecting a denervation pattern (Table 95.4). However, in patients with an axonotmetic or neurotmetic lesion, it is problematic to recognize the damaged site using EMG studies. It seems that there was a significant association between the clinical symptoms and EMG findings in patients necessitating sciatic nerve neurolysis. Perineural injection tests of the sciatic nerve with corticosteroid and local anesthetic under ultrasound or CT guidance have both a diagnostic and therapeutic function. Table 95.4  Some neurophysiological features associated with deep gluteal syndrome –  Waste of hamstring muscles –  Denervation of hamstring muscles (particularly biceps femoris) – Delayed latency of sciatic nerve from sciatic notch to hamstring muscles –  Positive Tinel’s sign in the buttock – Numbness in the distribution of the posterior cutaneous nerve of the thigh – Denervation in the tibial nerve distribution affecting the calf (plantar flexors of the ankle)

952

95  Deep Gluteal Syndrome (Including Piriformis Syndrome)

95.4 Treatment Options and Prognosis

Specific surgical methods of sciatic nerve decompression depend on the cause:

First-line treatment of DGS consists of conservative measures, including rest, oral anti-inflammatories agents, neuropathic drugs, muscle relaxants, stretching, and physical therapy to enhance mobility. The perineural infiltration test with lidocaine and corticosteroid is valid for diagnosis and treatment. In refractory cases, intramuscular infiltration with botulinum toxin under fluoroscopic, ultrasonographic, or CT scan guidance represents the next stage. At the ultimate phase (about 50% of cases), surgical decompression is finally needed. For a long time, open surgery was the only surgical option. Nevertheless, for about 20  years, endoscopic access to decompress the sciatic nerve within the subgluteal space appears as an important alternative to the open approach with a success rate. a

• Piriformis syndrome: release or piriformis tenotomy • Gemelli-obturator internus syndrome: obturator internus sectioning • Proximal hamstring syndrome: proximal hamstring release or debridement with primary hamstring tendon repair • Ischiofemoral impingement: lesser trochanter resection • Sciatic nerve injuries following trauma or heterotrophic neurogenic ossification: neurolysis or repair with sutures or grafts Overall, surgery is reserved for people who did not show improvement in their symptoms following conservative measures and those with more severe or recurring symptoms. However, in patients with compressive mass lesions, such as a tumor, hematoma, abscess (Figs. 95.9 and 95.10), pyomyob

Fig. 95.9  Axial pelvic CT scan with contrast injection (a, b) showing left-sided abscess and pyomyositis of the piriformis muscle (arrows) causing sciatic pain

a

b

Fig. 95.10  Large buttock abscess (dotted circle) causing sciatica (a). Axial pelvic CT scan with contrast injection showing right-sided gluteal abscess/pyomyositis (star) extended to the greater sciatic notch (arrow) (b)

Further Reading

sitis, or heterotopic ossification, surgery is indicated without preoperative conservative management. For tumor localization, intraoperative ultrasonography may be helpful when using the transgluteal approach as the working passageway can be disorienting when normal anatomical piriformis muscle margins are detached. Conservative treatment in patients with piriformis syndrome led to the resolution of symptoms in about 50% following 3 months. Both open and endoscopic procedures had good postoperative results, although endoscopic surgery needs a high level of expertise. However, it seems that open procedures have more postoperative complications and residual pain than mini-invasive endoscopic techniques.

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Hernando MF, Cerezal L, Pérez-Carro L, Abascal F, Canga A.  Deep gluteal syndrome: anatomy, imaging, and management of sciatic nerve entrapments in the subgluteal space. Skeletal Radiol. 2015;44:919–34. https://doi.org/10.1007/s00256-­015-­2124-­6. Hogan E, Vora D, Sherman JH.  A minimally invasive surgical approach for the treatment of piriformis syndrome: a case series. Chin Neurosurg J. 2020;6:8. https://doi.org/10.1186/ s41016-­020-­00189-­y. Hopayian K, Danielyan A. Four symptoms define the Piriformis syndrome: an updated systematic review of its clinical features. Eur J Orthop Surg Traumatol. 2018;28:155–64. https://doi.org/10.1007/ s00590-­017-­2031-­8. Hopayian K, Heathcote J. Deep gluteal syndrome: an overlooked cause of sciatica. Br J Gen Pract. 2019;69:485–6. https://doi.org/10.3399/ bjgp19X705653. Kamal T, Hall M, Moharam A, Sharr M, Walczak J. Gluteal pyomyositis in a non-tropical region as a rare cause of sciatic nerve compression: a case report. J Med Case Rep. 2008;2:204. https://doi. org/10.1186/1752-­1947-­2-­204. Kay J, de Sa D, Morrison L, Fejtek E, Simunovic N, Martin HD, et al. Surgical management of deep gluteal syndrome causing sciatic Further Reading nerve entrapment: a systematic review. Arthroscopy. 2017;33:2263– 78.e1. https://doi.org/10.1016/j.arthro.2017.06.041. Akremi MSE, Bellil M, Souissi M, Zaibi M, Balti W, Salah MB. Sciatica Kizaki K, Uchida S, Shanmugaraj A, Aquino CC, Duong A, Simunovic and femoral head osteonecrosis complicating a gluteal hydatid cyst: N, Martin HD, Ayeni OR. Deep gluteal syndrome is defined as a non-­ a case report. Int J Surg Case Rep. 2022;92:106841. https://doi. discogenic sciatic nerve disorder with entrapment in the deep gluteal org/10.1016/j.ijscr.2022.106841. space: a systematic review. Knee Surg Sports Traumatol Arthrosc. Atıcı A, Külcü DG, Akpınar P, Urgun DA.  A rare cause of non-­ 2020;28:3354–64. https://doi.org/10.1007/s00167-­020-­05966-­x. discogenic sciatica; musculus gemellus inferior: a case report. Turk J Phys Med Rehabil. 2017;63:355–6. https://doi.org/10.5606/ Knudsen JS, Mei-Dan O, Brick MJ.  Piriformis syndrome and endoscopic sciatic neurolysis. Sports Med Arthrosc Rev. 2016;24:e1–7. tftrd.2017.684. https://doi.org/10.1097/JSA.0000000000000088. Battle JD.  Credit-carditis: a new clinical entity? N Engl J Med. Lutz EG. Credit-card-wallet sciatica. JAMA. 1978;240:738. 1966;274:467. https://doi.org/10.1056/NEJM196602242740820. Beaton LE, Anson BJ. The relation of the sciatic nerve and its subdivi- McCrory P, Bell S. Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock. Sports Med. 1999;27:261–74. https://doi. sions to the piriformis muscle. Anat Rec. 1937;70:1–5. org/10.2165/00007256-­199927040-­00005. Beatty RA.  The piriformis muscle syndrome: a simple diagMetikala S, Sharma V. Endoscopic sciatic neurolysis for deep gluteal nostic maneuver. Neurosurgery. 1994;34:512–4. https://doi. syndrome: a systematic review. Cureus. 2022;14:e23153. https:// org/10.1227/00006123-­199403000-­00018. doi.org/10.7759/cureus.23153. Brown JA, Braun MA, Namey TC.  Pyriformis syndrome in a 10-year-old boy as a complication of operation with the patient Michel F, Decavel P, Toussirot E, Tatu L, Aleton E, Monnier G, et al. The piriformis muscle syndrome: an exploration of anatomical in the sitting position. Neurosurgery. 1988;23:117–9. https://doi. context, pathophysiological hypotheses and diagnostic criteria. org/10.1227/00006123-­198807000-­00023. Ann Phys Rehabil Med. 2013;56:300–11. https://doi.org/10.1016/j. Cai ZJ, Salem AE, Wagner-Bartak NA, Elsayes KM, Negm AS, Rezvani rehab.2013.03.006. M, et al. Sciatic foramen anatomy and common pathologies: a picMurata Y, Ogata S, Ikeda Y, Yamagata M.  An unusual cause of scitorial review. Abdom Radiol (NY). 2022;47:378–98. https://doi. atic pain as a result of the dynamic motion of the obturator interorg/10.1007/s00261-­021-­03265-­8. nus muscle. Spine J. 2009;9:e16–8. https://doi.org/10.1016/j. Carro LP, Hernando MF, Cerezal L, Navarro IS, Fernandez AA, spinee.2009.01.004. Castillo AO.  Deep gluteal space problems: piriformis syndrome, Natsis K, Totlis T, Konstantinidis GA, Paraskevas G, Piagkou M, ischiofemoral impingement and sciatic nerve release. Muscles Koebke J.  Anatomical variations between the sciatic nerve and Ligaments Tendons J. 2016;6:384–96. https://doi.org/10.11138/ the piriformis muscle: a contribution to surgical anatomy in pirimltj/2016.6.3.384. formis syndrome. Surg Radiol Anat. 2014;36:273–80. https://doi. Charalambous GK, Katergiannakis VA, Manouras AJ.  Three cases org/10.1007/s00276-­013-­1180-­7. of primary hydatidosis of the gluteus muscle: our experience in clinical, diagnostic and treatment aspects. Chirurgia (Bucur). Park JW, Lee YK, Lee YJ, Shin S, Kang Y, Koo KH.  Deep gluteal syndrome as a cause of posterior hip pain and sciatica-like pain. 2014;109:555–8. Bone Joint J. 2020;102-B:556–67. https://doi.org/10.1302/0301-­ Giebaly DE, Horriat S, Sinha A, Mangaleshkar S.  Pyomyositis of 620X.102B5.BJJ-­2019-­1212.R1. the piriformis muscle presenting with sciatica in a teenage rugby player. BMJ Case Rep. 2012;2012:bcr1220115392. https://doi. Peh WC, Reinus WR.  Piriformis bursitis causing sciatic neuropathy. Skeletal Radiol. 1995;24:474–6. https://doi.org/10.1007/ org/10.1136/bcr.12.2011.5392. BF00941253. Güvençer M, Iyem C, Akyer P, Tetik S, Naderi S. Variations in the high Probst D, Stout A, Hunt D.  Piriformis syndrome: a narrative review division of the sciatic nerve and relationship between the sciatic of the anatomy, diagnosis, and treatment. PM R. 2019;11(Suppl nerve and the piriformis. Turk Neurosurg. 2009;19:139–44. 1):S54–63. https://doi.org/10.1002/pmrj.12189. Hermann W. The piriformis syndrome-a special indication for botulinum toxin. Nervenarzt. 2020;91:99–106. https://doi.org/10.1007/ Robinson DR. Pyriformis syndrome in relation to sciatic pain. Am J Surg. 1947;73:355–8. https://doi.org/10.1016/0002-­9610(47)90345-­0. s00115-­020-­00866-­4.

954 Shah SS, Consuegra JM, Subhawong TK, Urakov TM, Manzano GR.  Epidemiology and etiology of secondary piriformis syndrome: a single-institution retrospective study. J Clin Neurosci. 2019;59:209–12. https://doi.org/10.1016/j.jocn.2018.10.069. Shanmuga Jayanthan S, Rajkumar SS, Kumar VS, Shalini M. Pyomyositis of the piriformis muscle-a case of piriformis syndrome. Indian J Radiol Imaging. 2021;31:1023–6. https://doi. org/10.1055/s-­0041-­1739183. Sharma S, Kaur H, Verma N, Adhya B. Looking beyond piriformis syndrome: is it really the piriformis? Hip Pelvis. 2023;35:1–5. https:// doi.org/10.5371/hp.2023.35.1.1. Siddiq MAB, Jahan I, Masihuzzaman S. Wallet neuritis—an example of peripheral sensitization. Curr Rheumatol Rev. 2018;14:279–83. https://doi.org/10.2174/1573397113666170310100851. Siddiq MAB, Rasker JJ.  Piriformis pyomyositis, a cause of piriformis syndrome—a systematic search and review. Clin Rheumatol. 2019;38:1811–21. https://doi.org/10.1007/s10067-­019-­04552-­y. Vallejo MC, Mariano DJ, Kaul B, Sah N, Ramanathan S.  Piriformis syndrome in a patient after cesarean section under spinal anesthesia.

95  Deep Gluteal Syndrome (Including Piriformis Syndrome) Reg Anesth Pain Med. 2004;29:364–7. https://doi.org/10.1016/j. rapm.2004.01.014. Vassalou EE, Katonis P, Karantanas AH. Piriformis muscle syndrome: a cross-sectional imaging study in 116 patients and evaluation of therapeutic outcome. Eur Radiol. 2018;28:447–58. https://doi. org/10.1007/s00330-­017-­4982-­x. Vij N, Kiernan H, Bisht R, Singleton I, Cornett EM, Kaye AD, et  al. Surgical and non-surgical treatment options for piriformis ­syndrome: a literature review. Anesth Pain Med. 2021;11:e112825. https://doi.org/10.5812/aapm.112825. Yan K, Xi Y, Hlis R, Chhabra A. Piriformis syndrome: pain response outcomes following CT-guided injection and incremental value of botulinum toxin injection. Diagn Interv Radiol. 2021;27:126–33. https://doi.org/10.5152/dir.2020.19444. Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica, with an analysis of 100 cases. Lancet. 1928;212:1119–23. https:// doi.org/10.1016/S0140-­6736(00)84887-­4.

Gluteal Intramuscular Injections

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96.1 Generalities and Relevance

Most of the medications being administered were analgesics, antibiotics, or antiemetic drugs but a broad range of Sciatic pain can be the consequence of iatrogenic injury to therapeutic agents may be involved. It seems that benzylthe sciatic nerve resulting from a misplaced gluteal intramus- penicillin, diazepam, and chlorpromazine were the most cular injection (GIMIJ). The sciatic nerve is the most usually intraneural/perineural neurotoxic substances. injured nerve following intramuscular injection because of This injury occurs in all age groups but it is more comits large size and the fact that the buttock is a common injec- mon in the pediatric population, elderly individuals, and tion site. This iatrogenic complication leads to temporary or underweight patients due to the higher nerve anatomic vulpermanent neurologic disability that can result in medico-­ nerability. In addition, there is a male predominance (about legal claims. 2/3 proportion) probably because the subcutaneous adipose Since first reported by Arnozan in 1882 as “sciatic neuri- tissue of the gluteal area of women is larger than that of men. tis due to injection,” this avoidable complication remains a persistent universal problem (about 2.7% of all GIMIJ) that affects patients in both developed and developing healthcare 96.2 Clinical Presentations systems. However, according to some authors, sciatic nerve injection injury appears to be a much more frequent problem The initial evaluation should include a detailed history and in developing countries because of the high use of intramus- physical exam. Recent intragluteal injections and no back cular injections for treating common diseases as well as the pain were helpful for the diagnosis. intragluteal injections had been administered by inadequately Most of the patients (almost 90%) have an instantaneous trained or unqualified staff. onset of symptoms, whereas 10% of the cases have a delayed The proposed mechanisms of nerve injury include the onset of symptoms that appears minutes to hours following the following: injection. This variability depends on the site of the injection being either intrafascicular or extrafascicular in location. • Direct needle trauma Classically, there was no tender area in the lumbosacral • Intramuscular hematoma pressure region. • Secondary circumferential constriction by scar Intrafascicular needle placement may result in immediate • Neurotoxic chemical destruction by agents injected sciatic pain, paresthesia, and variable motor and sensory into or near the nerve trunk. deficits. However, motor function is usually more severely impaired than sensory function. In some cases, symptoms Damage may be minimal or may result in severe axonal may worsen more gradually and be exacerbated by secondand myelin degeneration. In addition, it is important to con- ary fibrosis. sider some neurologic/muscular anatomic variations in the Obach and his colleagues described four types of paralybuttock area. sis resulting from GIMIJ: The most destructive mechanism is the result of direct intrafascicular injection into the sciatic nerve. Extrafascicular (a) Immediate neurogenic involvement with instant pain injection causes no or minor neuropathy. In addition, the (b) Obvious paralysis without pain (the most frequent peroneal nerve is most often involved in GIMIJ because the type) peroneal component is located more laterally and superfi- (c) Subacute or late paralysis without immediate pain cially than the tibial nerve division. (d) Late paralysis with immediate pain © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_96

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956

Paralytic foot drop is a frequent presentation (deficit of dorsiflexion and eversion) because the peroneal nerve division is commonly injured. Patients with tibial neuropathy may result in the loss of foot plantar flexion, loss of toe flexion, and weakened inversion of the foot. Some patients may present with symptoms of a complete sciatic nerve injury.

96.3 Paraclinic Features Apart from the clinical examination, electrodiagnostic and imaging studies provide valuable information in the assessment and management of injured sciatic nerves secondary to GIMIJ. On magnetic resonance imaging (MRI), an altered signal intensity, especially high signal intensity on T2-weighted images, may be seen in the injured segment of the sciatic nerve in the gluteal area associated with nerve thickening or post-injury neuroma formation. In addition, secondary signs of denervation may be found in the muscles supplied by the affected nerve. MRI can also have a prognostic value regarding nerve injury. When there is diffuse thickening of the nerve with signal alteration, recovery is usually complete. While if there is a formation of a neuroma-in-continuity, recovery is incomplete/poor. Unfortunately, no recovery is expected if there is end neuroma formation or complete transection of the nerve. Both nerve conduction studies and needle electromyography can define axonal damage in the nerve but may not be able to determine the exact location of the lesion. Like other types of traumatic peripheral nerve injury, the differentiation of neuropraxia from neurotmesis and axonotmesis is decisive.

96.4 Treatment Options and Prognosis Sciatic neuropathy secondary to intragluteal injection can be managed conservatively or surgically. Conservative treatment includes symptomatic medications, physiotherapy, and foot braces. While surgical treatment ranges from immediate operative exposure and irrigation with normal saline to early neurolysis or delayed exploration with neurolysis or resection and anastomosis (with or without grafting). An operation is a reasonable option whenever there is a realistic chance that the nerve will functionally improve.

Sunderland classified nerve injection injury (NII) and its treatment as follows: • First-degree NII (reversible conduction block): conservative management is sufficient • Second-degree NII (Wallerian degeneration with reactive fibrosis, slow recovery, often incomplete): neurolysis is indicated • Third-degree NII (necrosis and fibrosis due to neurotoxicity of the agent, no spontaneous recovery): flushing is indicated to limit the toxicity, but the drug has often already been completely reabsorbed at the time of surgery During surgical exploration, it is important to assess the presence or absence of the nerve action potential (NAP) distal to the injury location. If NAP is present beyond the lesion, external neurolysis alone or with internal neurolysis is indicated. However, if there is no NAP beyond the lesion, suture or graft repair is required for many authors. Many authors usually recommend waiting for 3–6 months before surgical exploration if the injury is not severely weakening and the pain is minor. The extent of recovery depends on the severity of the initial injury. Neurapraxia carries a good prognosis, but if the diagnosis is in doubt, a delay may cause continuing compression or ischemia and so extend the lesion to axonotmesis or even neurotmesis.

96.5 Prevention The implications for nurses include the need to learn and practice safe intragluteal injection techniques. The sciatic nerve courses through the middle of the gluteal region, for that reason injections, should be administered in the upper outer quadrant of the buttock to avoid hitting the sciatic nerve (it can be remembered using the sentence “Shut up and butt out”) (Fig. 96.1). However, for many practitioners and even nurses, this area lacks precision. The ventrogluteal region (between the iliac crest, greater trochanter of the femur, and anterior superior iliac spine) is considered safer because of the relatively thick bulk of the underlying muscle away from significant neurologic structures. In addition, gluteal intramuscular injections should be performed with the patient lying rather than sitting or standing since the normal anatomical landmarks become distorted in some unusual positions.

Further Reading

957

Fig. 96.1  The buttock quadrant is safest for needle insertion. The upper lateral (outer) quadrant of the buttock safely avoids hitting the sciatic nerve

Further Reading Agarwal A, Mirza A, Gulati A, Gulati P.  Post-injection sciatic nerve injury: MRI.  Neurol India. 2019;67:S157–8. https://doi. org/10.4103/0028-­3886.250726. Altıntaş A, Gündüz A, Kantarcı F, Gözübatık Çelik G, Koçer N, Kızıltan ME. Sciatic neuropathy developed after injection during curettage. Agri. 2016;28:46–8. https://doi.org/10.5505/agri.2014.30974. Arnozan, quoted by Wexburg E. Neuritis und polyneuritis. In: Bumke O, Foerster O, editors. Handbuch der neurologie, vol. 9. Berlin: Springer; 1935. p. 87. Coskun H, Kilic C, Senture C.  The evaluation of dorsogluteal and ventrogluteal injection sites: a cadaver study. J Clin Nurs. 2016;25:1112–9. https://doi.org/10.1111/jocn.13171. Fidancı H, Öztürk İ. The relationship between nerve conduction studies and neuropathic pain in sciatic nerve injury due to intramuscular injection. Korean J Pain. 2021;34:124–31. https://doi.org/10.3344/ kjp.2021.34.1.124. Geyik S, Geyik M, Yigiter R, Kuzudisli S, Saglam S, Elci MA, et al. Preventing sciatic nerve injury due to intramuscular injection: ten-year single-center experience and literature review. Turk Neurosurg. 2017;27:636–40. https://doi.org/10.5137/1019-­5149. JTN.16956-­16.1. Kadioglu HH.  Sciatic nerve injuries from gluteal intramuscular injection according to records of the High Health Council. Turk Neurosurg. 2018;28:474–8. https://doi.org/10.5137/1019-­5149. JTN.19789-­16.4. Kim DH, Murovic JA, Tiel R, Kline DG.  Management and outcomes in 353 surgically treated sciatic nerve lesions. J Neurosurg. 2004;101:8–17. https://doi.org/10.3171/jns.2004.101.1.0008. Kim HJ, Park SH.  Sciatic nerve injection injury. J Int Med Res. 2014;42:887–97. https://doi.org/10.1177/0300060514531924. Kim YS, Nam YS, Kim DI.  Evaluating the effectiveness of gluteal intramuscular injection sites: a cadaveric study. Anat Cell Biol. 2022;55:48–54. https://doi.org/10.5115/acb.21.223. Kline DG, Kim D, Midha R, Harsh C, Tiel R.  Management and results of sciatic nerve injuries: a 24-year experience. J Neurosurg. 1998;89:13–23. https://doi.org/10.3171/jns.1998.89.1.0013. Mishra P, Stringer MD. Sciatic nerve injury from intramuscular injection: a persistent and global problem. Int J Clin Pract. 2010;64:1573– 9. https://doi.org/10.1111/j.1742-­1241.2009.02177.x. Obach J, Aragones JM, Ruano D. The infrapiriformis foramen syndrome resulting from intragluteal injection. J Neurol Sci. 1983;58:135–42. https://doi.org/10.1016/0022-­510x(83)90116-­8.

Ong MJ, Lim GH, Kei PL.  Clinics in diagnostic imaging (140). Iatrogenic sciatic nerve injury secondary to intramuscular injection. Singapore Med J. 2012;53:551–4. Park CW, Cho WC, Son BC. Iatrogenic injury to the sciatic nerve due to intramuscular injection: a case report. Korean J Neurotrauma. 2019;15:61–6. https://doi.org/10.13004/kjnt.2019.15.e4. Pham M, Wessig C, Brinkhoff J, Reiners K, Stoll G, Bendszus M.  MR neurography of sciatic nerve injection injury. J Neurol. 2011;258:1120–5. https://doi.org/10.1007/ s00415-­0 10-­5 895-­7 . Ramtahal J, Ramlakhan S, Singh K.  Sciatic nerve injury following intramuscular injection: a case report and review of the literature. J Neurosci Nurs. 2006;38:238–40. https://doi. org/10.1097/01376517-­200608000-­00006. Ripellino P, Mazzini L, Comi C, Perchinunno M, Stecco A, Cantello R.  MRI imaging and clinical features of sciatic nerve injection injury. Int J Neurosci. 2016;126:658–9. https://doi.org/10.3109/00 207454.2015.1046066. Small SP.  Preventing sciatic nerve injury from intramuscular injections: literature review. J Adv Nurs. 2004;47:287–96. https://doi. org/10.1111/j.1365-­2648.2004.03092.x. Sunderland S. Miscellaneous causes of nerve injury. In: Nerve injuries and their repair. A critical appraisal. London: Churchill Livingstone; 1991. p. 193–9. Topuz K, Kutlay M, Simşek H, Atabey C, Demircan M, Senol GM. Early surgical treatment protocol for sciatic nerve injury due to injection—a retrospective study. Br J Neurosurg. 2011;25:509–15. https://doi.org/10.3109/02688697.2011.566380. Turner GG.  The site for intramuscular injections. Lancet. 1920;196:819. Yaffe B, Pri-Chen S, Lin E, Engel J, Modan M.  Peripheral nerve injection injury: an experimental pilot study of treatment modalities. J Reconstr Microsurg. 1986;3:33–7. https://doi. org/10.1055/s-­2007-­1007036. Yeremeyeva E, Kline DG, Kim DH. Iatrogenic sciatic nerve injuries at buttock and thigh levels: the Louisiana State University experience review. Neurosurgery. 2009;65:A63–6. https://doi.org/10.1227/01. NEU.0000346265.17661.1E. Zhuo P, Gao D, Xia Q, Ran D, Xia W.  Sciatic nerve injury in children after gluteal intramuscular injection: case reports on medical malpractice. Med Sci Law. 2019;59:139–42. https://doi. org/10.1177/0025802419851980.

Prolonged Immobilization and Incorrect Positioning

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97.1 Generalities and Relevance Sciatic neuropathy due to external nerve pressure is a rare but severe complication following prolonged immobilization and incorrect positioning. This condition can be unilateral or bilateral. Generally, most clinical presentations are transient and rarely definitive; however, some complications may occur such as gluteal or thigh compartment syndromes with subsequent life-threatening impacts if not managed promptly (c.f. Chap. 98 about Lower Limb Compartment Syndrome). Early diagnosis is difficult and sometimes delayed or overlooked because of poor physical signs resulting from altered mental status and inappropriate diagnosis by clinicians. Direct compression injury of the sciatic nerve may occur as the consequence of a variety of prolonged immobilization and unusual positioning. A significant number of cases would be related to an iatrogenic cause, particularly due to surgical positioning. The most non-iatrogenic causes are secondary to prolonged immobilization due to drug abuse or alcoholic intoxication. Overall, the most known etiologies are as follows: (a) Prolonged or incorrect surgical patient positioning, especially during orthopedic, obstetric, lithotomy, neurosurgical, spinal, urologic, bariatric, or cardiac surgery. Nerve sciatic damage can be encountered in variable positions including supine, lateral, knee-chest/elbow, or sitting positions (b) Prolonged toilet seat position resulting in a “toilet bowl neuropathy” (AKA Toilet seat neuropathy) (Fig. 97.1) (c) Following performing the lotus position in yoga (Padmasana) or its variant causing a “lotus neuropathy” (Fig. 97.2) (d) Overloaded wallet initiating gluteal pain with sciatic neuritis known as “wallet neuritis,” walletosis, fat-wallet

Fig. 97.1  Prolonged toilet seat position (arrows) resulting in a “toilet bowl neuropathy” (AKA toilet seat neuropathy)

syndrome, and credit-carditis. Classically, developing wallet neuritis features may take a long time. (Fig. 97.3) (e) Sitting for a long time (f) Crossing one leg over the other. However, this position induces a peroneal nerve neuropathy rather than a sciatic nerve lesion (Fig. 97.4)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_97

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97  Prolonged Immobilization and Incorrect Positioning

Wallet

Fig. 97.2  Illustration of a “Lotus position” in yoga (Padmasana). This position or its variant may cause “lotus neuropathy”

Some predisposing factors should be considered for such sciatic neuropathy including: • • • • • •

Low body mass index Advanced age Alcohol intoxication Illicit drug use Cigarette smoking Preexisting peripheral neuropathy due to diabetes or vascular diseases • Presence of anatomic anomalies • Long operating time • Epidural anesthesia

Fig. 97.3 An overloaded wallet may initiate gluteal pain (arrow) with sciatic neuritis known as “wallet neuritis” (AKA walletosis, fat-wallet syndrome, or credit-carditis)

The two main mechanisms of sciatic nerve damage following prolonged immobilization or incorrect positioning include stretch injury (overstretching) and/or direct nerve compression. Damage may be minimal or may result in severe axonal and myelin degeneration. An incomplete injury is expected to eventually heal with a good return of

neurologic function, although a complete return of function is not always predictable. The global incidence of sciatic neuropathy secondary to prolonged immobilization or incorrect positioning is unknown; only sporadic cases have been reported in the literature. According to some authors, lower-extremity nerve neuropathy is a rare complication secondary to postoperative positioning, with an incidence of 2–3 cases per 10,000 surgical procedures, most of them related to peroneal nerve injury.

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97.4  Treatment Options

compressive tenseness, and swelling of the buttock as well as numbness and weakness from the sciatic nerve. Moreover, on examination, the clinician can report tenderness to touch, hardness of tissues, erythema, pain on passive motion of the hip joint in any direction, and sensory and motor deficits in the sciatic nerve distribution. Several patients will present a rhabdomyolysis that manifests as the following triad of symptoms: myalgia, muscle weakness, and dark-tea-colored urine (c.f. Chap. 98).

97.3 Paraclinic Features

Fig. 97.4  Illustration of a young woman sitting with crossed legs. This position may induce a peroneal nerve (arrow) or a sciatic nerve neuropathy

97.2 Clinical Presentations Sciatic injury secondary to prolonged immobilization and incorrect positioning should be suspected in cases of neuropathic pain in the gluteal or thigh region with severe dysesthesia. Neurological examination disclosed sensory and motor dysfunctions (particularly weakness or sensory loss) in the sciatic nerve distribution areas. Other non-specific symptoms may be seen such as swelling of the buttocks or thigh area with possible skin changes (erythema). These non-specific symptoms often lead to a misdiagnosis, such as venous thrombosis, abscess, or bleeding. Habitually, transient benign forms have no neurologic deficits but the pain did not improve with traditional analgesics. More seriously, patients with gluteal or thigh compartment syndromes can present with more severe pain, non-­

Electromyogram is often abnormal, showing muscle membrane instability and active denervation changes in the sciatic-­innervated muscle distribution. However, nerve conduction studies are relatively normal except for no conduction along the tibial and peroneal nerves. Electrodiagnostic studies are useful to differentiate between sciatic neuropathy and common peroneal neuropathy. Magnetic resonance imaging (MRI) and ultrasound (US) may be normal or show muscle mild degree of edema and swelling. The normal fascicular architecture is rarely lost. Classically, there are no signs of ischemia. MRI can help accurately localize the level of the nerve injury. Diagnosis of lower limb compartment syndrome is often clinical, but measurement of gluteal or high intracompartmental pressure may be very useful. Imaging studies, including US, computed tomography (CT) scans, and MRI, are usually omitted to prevent any delay in surgical treatment (c.f. Chap. 98). When used, MRI and US may show muscle severe edema, swelling, loss of normal fascicular architecture, and patterns of myonecrosis. When rhabdomyolysis occurs, biological studies show myoglobinemia, myoglobinuria, acidosis, hyperkaliemia, and acute kidney failure with elevated blood urea, nitrogen, and serum creatinine levels. In addition, creatinine kinase was markedly elevated in most patients with compartment syndrome.

97.4 Treatment Options As mentioned previously, most benign clinical presentations are transient and rarely definitive. Improvement with conservative treatment is recognized. Acetaminophen (paracetamol), nonsteroidal anti-­ inflammatory drugs, adjacent analgesics, and physiotherapy sessions could give some relief. However, radical “wallectomy” is the most appropriate intervention for Wallet Neuritis. For acute gluteal or thigh compartment syndrome, once the diagnosis is made, the patient should undergo prompt

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fasciotomy. Many authors suggest fasciotomy for pressures greater than 30  mmHg. The goal of surgery is to open all fascial sheaths of the involved muscles for limb salvage (c.f. Chap. 98). Rhabdomyolysis should be managed in the intensive care unit (fluid resuscitation, urine alkalinization, and so on) with hemodialysis sessions if needed. In addition, hyperbaric oxygen therapy could be considered adjuvant therapy. Appropriate patient positioning during surgical procedures, avoidance of extrinsic pressure on the legs, and minimization of operating time are needed to minimize the risk of intraoperative sciatic injuries.

97.5 Prognosis Most patients usually recover from position-related sciatic nerve palsy within a few weeks under conservative therapy. However, in some cases, recovery may be complicated by some degree of neuropathic pain in the sciatic nerve distribution, Achilles tendon contracture, and even variable degrees of sciatic paralysis or foot drop. On the contrary, people with acute compartment syndrome have a high morbidity and mortality rate (especially in cases complicated by Crush syndrome). The most important prognostic factors in such patients are the time to diagnosis, the severity of the initial injury, and subsequent surgical fasciotomy (c.f. Chap. 98). Despite the fasciotomy, some signs and symptoms may be permanent depending on factors such as which topographic compartment, the time until fasciotomy, and the extent of muscle necrosis. These may include muscle atrophy, muscle contracture, sciatic paralysis, foot drop, leg numbness, pain, scarring, and dystrophic calcification. Iatrogenic-related forms can result in medico-legal claims. Prolonged positioning using a posture that can induce nerve compression or stretching should be avoided.

Further Reading Bosma JW, Wijntjes J, Hilgevoord TA, Veenstra J. Severe isolated sciatic neuropathy due to a modified lotus position. World J Clin Cases. 2014;2:39–41. https://doi.org/10.12998/wjcc.v2.i2.39. Brown JA, Braun MA, Namey TC.  Pyriformis syndrome in a 10-year-old boy as a complication of operation with the patient in the sitting position. Neurosurgery. 1988;23:117–9. https://doi. org/10.1227/00006123-­198807000-­00023. Chusid J. Yoga foot drop. JAMA. 1971;217:827–8. Dacci P, Amadio S, Gerevini S, Moiola L, Del Carro U, Radaelli M, et  al. Practice of yoga may cause damage of both sciatic nerves: a case report. Neurol Sci. 2013;34:393–6. https://doi.org/10.1007/ s10072-­012-­0998-­9.

97  Prolonged Immobilization and Incorrect Positioning Dimachkie MM, Ohanian S, Groves MD, Vriesendorp FJ.  Peripheral nerve injury after brief lithotomy for transurethral collagen injection. Urology. 2000;56:669. https://doi.org/10.1016/ s0090-­4295(00)00741-­x. Dubil EA, Dahle JM, Owens MD. Bilateral sciatic nerve palsy: a new presentation of toilet bowl neuropathy. J Emerg Med. 2012;43:622– 4. https://doi.org/10.1016/j.jemermed.2010.04.009. Gleich J, Fürmetz J, Kamla C, Pedersen V, Böcker W, Keppler AM. Gluteal compartment syndrome after immobilization following opioid abuse. Unfallchirurg. 2020;123:496–500. https://doi. org/10.1007/s00113-­020-­00792-­9. Gozal Y, Pomeranz S.  Sciatic nerve palsy as a complication after acoustic neurinoma resection in the sitting position. J Neurosurg Anesthesiol. 1994;6:40–2. https://doi. org/10.1097/00008506-­199401000-­00006. Heyn J, Ladurner R, Ozimek A, Vogel T, Hallfeldt KK, Mussack T.  Gluteal compartment syndrome after prostatectomy caused by incorrect positioning. Eur J Med Res. 2006;11:170–3. Iizuka S, Miura N, Fukushima T, Seki T, Sugimoto K, Inokuchi S.  Gluteal compartment syndrome due to prolonged immobilization after alcohol intoxication: a case report. Tokai J Exp Clin Med. 2011;36:25–8. Khalifa R, Craft MR, Wey AJ, Thabet AM, Abdelgawad A.  Missed positional gluteal compartment syndrome in an obese patient after foot surgery: a case report. Patient Saf Surg. 2020;14:35. https://doi. org/10.1186/s13037-­020-­00260-­8. Kim D, Kwon OY, Kim Y, Hye KS, Son S, Park KJ, Choi NC, Lim B. A case of bilateral sciatic neuropathy caused by lotus position. J Korean Neurol Assoc. 2004;22:418–20. Ley L, Ikhouane M, Staiti G, Benhamou D.  Neurological complication after the “tailor posture” during labour with epidural analgesia. Ann Fr Anesth Reanim. 2007;26:666–9. https://doi.org/10.1016/j. annfar.2007.04.012. Lutz EG. Credit-card-wallet sciatica. JAMA. 1978;240:738. Poppi M, Giuliani G, Gambari PI, Acciarri N, Gaist G, Calbucci F. A hazard of craniotomy in the sitting position: the posterior compartment syndrome of the thigh. Case report. J Neurosurg. 1989;71:618– 9. https://doi.org/10.3171/jns.1989.71.4.0618. Reel BA, Odedokun TA, Simmons DB, Hong L. Bilateral sciatic neuropathies as a complication of positioning during neuraxial anesthesia for cesarean delivery: a case report. A A Pract. 2019;13:173–5. https://doi.org/10.1213/XAA.0000000000001026. Sancineto C, Godoy MD.  Compartment syndrome of the thigh: an unusual complication after spinal surgery. J Spinal Disord Tech. 2004;17:336–8. https://doi.org/10.1097/01.bsd.0000097252.54459. ef. Shimada T, Tsunemi T, Hattori A, Nakazato-Taniguchi T, Yasuhara H, Ogaki K, et  al. Bilateral thigh compartment syndromes from extended sitting with forward bending. J Clin Neurosci. 2019;64:35– 7. https://doi.org/10.1016/j.jocn.2019.03.027. Siddiq MAB.  Piriformis syndrome and wallet neuritis: are they the same? Cureus. 2018;10:e2606. https://doi.org/10.7759/cureus.2606. Vallejo MC, Mariano DJ, Kaul B, Sah N, Ramanathan S.  Piriformis syndrome in a patient after cesarean section under spinal anesthesia. Reg Anesth Pain Med. 2004;29:364–7. https://doi.org/10.1016/j. rapm.2004.01.014. Wang JC, Wong TT, Chen HH, Chang PY, Yang TF.  Bilateral sciatic neuropathy as a complication of craniotomy performed in the sitting position: localization of nerve injury by using magnetic resonance imaging. Childs Nerv Syst. 2012;28:159–63. https://doi. org/10.1007/s00381-­011-­1597-­4. Young Cho J, Lee JW, Jung Cho E, Kim MG, Jo SK, Yong Cho W, et al. Bilateral gluteal compartment syndrome complicated by rhabdomyolysis and acute kidney injury in a patient with alcohol intoxication. Kidney Res Clin Pract. 2012;31:246–8. https://doi.org/10.1016/j. krcp.2012.07.005.

Lower Limb Compartment Syndromes

98.1 Generalities and Relevance A compartment syndrome occurs when pressure within a closed muscle compartment goes beyond the perfusion pressure and results in muscle and nerve ischemia, creating a varying degree of deficit that may be neuropathic, myopathic, or mixed. In the lower limb, the sciatic nerve trunk may be compressed due to limited space and the increased pressure in the buttock (gluteal) or the thigh. There are two different types of compartment syndromes: acute and chronic (exertional). However, the acute one is by far the most severe form and constitutes a medico-surgical emergency. It is accepted that a muscle can survive 4 h of temporary ischemia with only minor functional and histological damage. However, 8  h of ischemia is generally definitive and may be fatal. The neuron is more vulnerable to hypoxia, and the first sensory deficits can occur at the end of the first half hour. A significant number of cases with acute presentations can develop sciatic neuropathy, rhabdomyolysis (Crush or Bywater’s syndrome), and acidosis with subsequent renal failure. Some other complications may occur such as sepsis and contiguous necrotizing fasciitis (Fig. 98.1). If not treated promptly, the disorder can cause complete and definitive neurologic dysfunction of the lower limb, gangrene, and even life-threatening consequences. There are multiple causes inducing lower limb compartment syndromes. They can be classified into different categories such as traumatic or atraumatic causes and following iatrogenic or non-iatrogenic immobilizations (Table 98.1). Chronic form (AKA Chronic exertional compartment syndrome) is a common condition seen especially in athletes, following physical overuse or sporting activity. In this chronic condition, there is commonly leg pain with physical exercise but the pain dissipates with rest. Normally, this situation does not produce permanent damage.

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a

b

Fig. 98.1  Gluteal compartment syndrome with contiguous necrotizing fasciitis (a, b). This complex gluteal wound was treated with debridement and skin grafting. (Courtesy of Pr. Hassan Baallal)

The global incidence of compartment syndromes in the literature is 7.3 per 100,000 in men and 0.7 per 100,000 in women. The most common spaces involved are the lower extremity followed by the abdomen, upper extremity, and rarely the gluteal and thigh region. In the lower limb, compartment syndromes are noted to be found in young male patients with fewer medical comorbidities in traumatic presentations than in non-traumatic ones. In acute forms, most cases are unilateral. However, in chronic compartment syndrome, bilateral lower limb involvement has been reported to be as high as 80%.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_98

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964 Table 98.1 Most known etiologies of lower limb compartment syndromes •  Limb trauma including crush injuries • Overexertion and endurance athletes (particularly for chronic forms) • Burn • Infection •  Muscle hypertrophy • Obesity •  Ehlers-Danlos syndrome •  Vascular damage, hematoma, and coagulation disorders •  Carbon monoxide poisoning •  Spinal anesthesia •  Intraoperative hypoperfusion •  Surgical procedures •  Gluteal intramuscular injection •  Bone marrow biopsy complication •  Incorrect surgical positioning •  Prolonged immobilization •  Drug abuse and alcohol intoxication

98  Lower Limb Compartment Syndromes

stops. Additional symptoms may occur, including muscle weakness and paresthesias. The findings of neurologic examination typically are normal if the patient is inactive and asymptomatic. However, if the physical examination is done during symptom reproduction, then abnormal findings of a neurologic examination in the distribution of the nerve within the affected compartment may be found including passive stretching of the involved muscles.

98.3 Paraclinic Features

Lower limb compartment syndrome diagnosis is often clinical, but measurement of gluteal or high intracompartmental pressure may be very useful. A transducer connected to a catheter is inserted 5 cm into the zone of injury. Normal values have been reported to be 13–14  mmHg. Noninvasive methods of diagnosis such as near-infrared-spectroscopy that uses sensors on the skin are promising techniques. Imaging studies, including ultrasound (US), computed 98.2 Clinical Presentations tomography (CT) scan, and magnetic resonance imaging Compartment syndrome is a truly challenging diagnosis to (MRI), are usually omitted to prevent any delay in surgical make with diverse clinical variety. Often, a high index of treatment. When used, MRI and US may show muscle edema clinical suspicion is required especially in spontaneous non-­ and swelling. The normal fascicular architecture is often lost. In myonecrosis, muscle enhancement on T1 post gadolinium traumatic forms. In acute forms of lower limb compartment syndrome, sequences is absent and decreased in ischemia. There is a limited role for electromyoneurography, which there are five distinctive signs and symptoms (known as the is impractical to organize in urgent situations and likely to be 5 Ps), and they generally develop gradually: insufficiently sensitive. Severe rhabdomyolysis is characterized by myoglo• Pain: deep and burning in nature. Pain severity is out of binemia, myoglobinuria, acidosis, hyperkaliemia, and acute proportion to the apparent injury. kidney failure with elevated blood urea nitrogen, and serum • Paresthesia: suggesting ischemic nerve damage. • Pallor: (uncommon) discoloration due to vascular creatinine level. In addition, creatinine kinase was markedly elevated in most patients. insufficiency. Chronic exertional compartment syndrome is usually a • Pulselessness (uncommon). diagnosis of elimination, with the mark finding being the • Paralysis: a rare late finding. absence of symptoms at rest. Measurement of intracompartSupplementary symptoms may occur in gluteal or thigh mental pressures during patient training and the onset of pain compartment syndromes, including swelling and warmth of is the most valuable test. Imaging studies (plain radiographs, CT scan, or MRI) can be useful in ruling out other more the affected area. Some acute presentations may be misdiagnosed as but- common diagnoses. tock abscess or deep vein thrombosis causing a delay in management. More seriously, several patients will present a rhabdomyolysis that manifests as the following triad of 98.4 Treatment Options symptoms: myalgia, muscle weakness, and dark-tea-colored urine. In addition, clinicians need to look for the possibility Except for most chronic forms, conservative treatment of a more severe underlying medical condition such as mul- (dressing, splint, cast, and limb positioning at the level of the heart) is rarely considered for acute compartment tiple organ dysfunction. In the chronic form, the pain usually appears as a cloudy syndrome. Once the diagnosis of acute forms is made, the patient tender fullness that deteriorates and becomes strident with continuous physical activity but disappears when activity should undergo prompt fasciotomy. Many authors suggest

Further Reading

fasciotomy for pressures greater than 30 mmHg. The goal of surgery is to open all fascial sheaths of the involved muscles for limb salvage. The surgical approach for gluteal or thigh fasciotomy varies according to the muscle groups and subgroups involved. Often, primary closure may not be possible at the time of initial decompression due to edema and may need delayed primary closure in the next few days. However, wound complications are not rare. Rhabdomyolysis should be managed in the intensive care unit (fluid resuscitation, urine alkalinization, and so on) with hemodialysis sessions if needed. Hyperbaric oxygen therapy should be considered adjuvant therapy. Hyperbaric oxygen may decrease associated edema, save marginal hypoxic tissue, and increase granulation of the wound bed making easy wound closure or subsequent grafting. Physical therapy for sciatic nerve reinforcement should be started soon after surgery. Underlying causes should be controlled such as bleeding (hematoma), vascular lesions, mass lesions, or edematous and inflammatory etiologies. For patients who require prolonged bed rest, immobilization, or special long positioning, certain preventive measures are needed such as frequent and regular repositioning and keeping the lower extremities in a neutral position when possible to prevent such severe syndromes.

98.5 Outcomes and Prognosis Although patients with acute compartment syndrome have a high morbidity and mortality rate (especially related to Crush syndrome), most people with chronic exertional forms have an uncomplicated course with full functional recovery. The most important prognostic factor in cases with acute forms is the time to diagnosis and subsequent surgical fasciotomy. A mortality rate of up to 40% has been reported for acute compartment syndrome of the thigh. The extent of recovery depends on the severity of the initial injury or the underlying etiology. In people with a missed or late diagnosis of acute compartment syndrome, limb amputation may be necessary for survival. Despite the fasciotomy, some symptoms may be permanent depending on factors such as topographic compartment, the time until fasciotomy, and the extent of muscle necrosis. These may include muscle atrophy, muscle contracture, sciatic paralysis, foot drop, leg numbness, pain, scarring, and dystrophic calcification. The outcome for cases with chronic compartment syndrome is definitely more favorable.

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Iatrogenic-related forms can result in medico-legal claims.

Further Reading Alobaidi A, Backdash MM, El-Menyar A.  Thigh compartment syndrome complicated by sciatic nerve palsy, rhabdomyolysis, and acute renal failure. Clin Case Rep. 2015;4:107–10. https://doi. org/10.1002/ccr3.446. Broadhurst PK, Robinson LR. Compartment syndrome: neuromuscular complications and electrodiagnosis. Muscle Nerve. 2020;62:300–8. https://doi.org/10.1002/mus.26807. Ding A, Machin M, Onida S, Davies AH. A systematic review of fasciotomy in chronic exertional compartment syndrome. J Vasc Surg. 2020;72:1802–12. https://doi.org/10.1016/j.jvs.2020.05.030. Gleich J, Fürmetz J, Kamla C, Pedersen V, Böcker W, Keppler AM. Gluteal compartment syndrome after immobilization following opioid abuse. Unfallchirurg. 2020;123:496–500. https://doi. org/10.1007/s00113-­020-­00792-­9. Hatefi M, Pirabadi NR, Khajavikhan J, Jaafarpour M.  Claudication due to sciatic nerve palsy following Nicolau syndrome: a case report. J Clin Diagn Res. 2015;9:RD01–2. https://doi.org/10.7860/ JCDR/2015/14833.6596. Hayden G, Leung M, Leong J.  Gluteal compartment syndrome. ANZ J Surg. 2006;76:668–70. https://doi. org/10.1111/j.1445-­2197.2006.03797.x. Heyn J, Ladurner R, Ozimek A, Vogel T, Hallfeldt KK, Mussack T.  Gluteal compartment syndrome after prostatectomy caused by incorrect positioning. Eur J Med Res. 2006;11:170–3. Ji JW. Acute compartment syndrome which causes rhabdomyolysis by carbon monoxide poisoning and sciatic nerve injury associated with it: a case report. Hip Pelvis. 2017;29:204–9. https://doi.org/10.5371/ hp.2017.29.3.204. Katt BM, Mubin NF, Beredjiklian PK. Atraumatic posterior thigh compartment syndrome presenting as an acute sciatic nerve palsy. A case report. Arch Bone Jt Surg. 2021;9:361–6. https://doi.org/10.22038/ abjs.2020.43632.2195. Kuhlman GD, Gwathmey KG.  Gluteal compartment syndrome with neurologic impairment: report of 2 cases and review of the literature. Muscle Nerve. 2018;57:325–30. https://doi.org/10.1002/ mus.25630. Liu B, Barrazueta G, Ruchelsman DE. Chronic exertional compartment syndrome in athletes. J Hand Surg Am. 2017;42:917–23. https://doi. org/10.1016/j.jhsa.2017.09.009. McGoldrick NP, Green C, Connolly P. Gluteal compartment syndrome following bone marrow biopsy: a case report. Acta Orthop Belg. 2012;78:548–51. Mithöfer K, Lhowe DW, Vrahas MS, Altman DT, Altman GT. Clinical spectrum of acute compartment syndrome of the thigh and its relation to associated injuries. Clin Orthop Relat Res. 2004;425:223–9. https://doi.org/10.1097/00003086-­200408000-­00032. Owens BD, Garcia EJ, Alitz CJ. Fasciotomy for chronic exertional compartment syndrome of the leg. JBJS Essent Surg Tech. 2016;6:e1. https://doi.org/10.2106/JBJS.ST.N.00118. Schwartz JT Jr, Brumback RJ, Lakatos R, Poka A, Bathon GH, Burgess AR.  Acute compartment syndrome of the thigh. A spectrum of injury. J Bone Joint Surg Am. 1989;71:392–400. Shimada T, Tsunemi T, Hattori A, Nakazato-Taniguchi T, Yasuhara H, Ogaki K, Hattori N.  Bilateral thigh compartment syndromes from extended sitting with forward bending. J Clin Neurosci. 2019;64:35–7. https://doi.org/10.1016/j.jocn.2019.03.027. Spiliopoulos KC, Veltsista D, Theodoroula E, Soldatos T, Kelekis A, Chroni E. Long-term outcome of bilateral sciatic nerve palsy due

966 to unrecognized thigh compartment syndrome. Acta Neurol Belg. 2021; https://doi.org/10.1007/s13760-­021-­01669-­3. Viviani E, Giribono AM, Narese D, Ferrara D, Servillo G, Del Guercio L, et  al. Gluteal compartment syndrome following abdominal aortic aneurysm treatment: case report and review of the literature. Int J Low Extrem Wounds. 2016;15:354–9. https://doi. org/10.1177/1534734616663748. Wai K, Thompson PD, Kimber TE.  Fashion victim: rhabdomyolysis and bilateral peroneal and tibial neuropathies as a result of squatting in ‘skinny jeans’. J Neurol Neurosurg Psychiatry. 2016;87:782. https://doi.org/10.1136/jnnp-­2015-­310628.

98  Lower Limb Compartment Syndromes Yanagawa Y, Nishi K.  Case of gluteal compartment syndrome associated with bilateral sciatic nerve palsies. Brain Nerve. 2009;61:213–5. Young Cho J, Lee JW, Jung Cho E, Kim MG, Jo SK, Yong Cho W, et al. Bilateral gluteal compartment syndrome complicated by rhabdomyolysis and acute kidney injury in a patient with alcohol intoxication. Kidney Res Clin Pract. 2012;31:246–8. https://doi.org/10.1016/j. krcp.2012.07.005.

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Traumatic Sciatic Nerve Lesions

99.1 Generalities and Relevance Traumatic sciatic nerve mononeuropathy is a rare but severe condition sustained after acute (most frequent), chronic, or complex injuries. Trauma can be closed or open, accidental or iatrogenic. Due to its significant length, the sciatic nerve can be injured in different anatomical regions, from the sciatic notch to the knee. In addition, injuries in its peripheral divisions should be considered. Etiologies are varied and can lead to compression, stretching, or cutting of the sciatic nerve in the early period or late by scar or heterotopic ossification (mainly near the hip) enclosing the nerve. Clinical symptoms following such post-traumatic damage include neuropathic pain, paresthesia, and variable motor and/or sensory deficits. These symptoms can be similar to those caused by the most frequent etiologies of spinal sciatica (e.g., degenerative lumbosacral spinal disease). Practitioners should keep in mind that in some complex and open injuries, sciatic nerve injuries are usually accompanied by vascular compromise as well as bone and soft tissue damage. Furthermore, association with other peripheral nerve injuries is not rare (e.g., femoral, tibial, or peroneal nerves). A significant number of cases are related to an iatrogenic cause, particularly due to surgical intervention (mainly hip arthroplasty) and gluteal intramuscular injection. Most non-­ iatrogenic causes are secondary to hip/femoral fractures (mainly secondary to motor vehicular accidents) and gunshot wounds. Overall, the most known etiologies are summarized in Table 99.1. Damage may be minimal (neurapraxia) or may result in severe axonal and myelin degeneration (axonotmesis and neurotmesis) (Table  99.2 and Fig.  99.1). An incomplete injury is expected to eventually heal with a good return of neurologic function, although a complete return of function is not always predictable. Regarding penetrating wounds, military gunshot wounds (GSW) generate more massive tissue injuries than civilian ones. Whatever the lesion, the clini-

Table 99.1  The most known etiologies of traumatic sciatic nerve lesions Iatrogenic

Non-­ iatrogenic

Operative

• Faulty intraoperative positioning (prolonged or incorrect positions) • Orthopedic procedures (mainly hip replacement surgery or closed reduction) • Direct intraoperative damage (e.g., tumors or Baker cyst removal) •  Protruding material (hardware) •  Regional anesthetic technics Non-­ • Gluteal intramuscular injection operative (needle injury and/or neurotoxic injected agent) • External compression from orthotics and casts • Tourniquets Classic direct • Hip dislocation and acetabular trauma fractures •  Pelvic and femoral fractures Combat •  Gunshot wounds (GSW) injury •  Explosion and blast injuries

Table 99.2  Classification of peripheral nerve injury Seddon system Neurapraxia (Compression) Axonotmesis

Sunderland system Grade I Grade II

Grade III Grade IV Neurotmesis (Transection)

Grade V

Pathophysiologic description Focal demyelination damage Nerve still intact Axon disrupted Endoneurium, perineurium, and epineurium are intact Grade II with endoneurium disrupted Grade III with perineurium disrupted Grade IV with epineurium disrupted Complete transection with loss of continuity

cian should attempt to minimize the patient’s management time, which is the most important factor for the functional nervous prognosis.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_99

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99  Traumatic Sciatic Nerve Lesions

Fig. 99.1 Histological structures of a typical peripheral nerve

The global incidence of sciatic neuropathy secondary to traumatic lesions is unknown. However, sciatic nerve trauma could represent 5–10% of all traumatic peripheral nerve injuries. The sciatic nerve is the second most commonly injured peripheral nerve of the lower limb following the peroneal (fibular) nerve. Some nerve referral centers estimate that between 15% and 25% of the operated traumatic sciatic nerve lesions had been iatrogenic in nature. Additionally, the reported incidence of iatrogenic sciatic nerve injury following total hip arthroplasty is up to 1.9%. This rate reaches up to 7.6% of cases following hip revision surgery. A high incidence is seen in adult males in their fifth decade.

99.2 Clinical Presentations The initial evaluation should include a sufficient and detailed history and physical exam. Recent injury, presence of injection site scar, signs of trauma, or existence of wound along sciatic nerve course without lower back pain may help for the diagnosis (Figs. 99.2, 99.3, and 99.4). The onset of symptoms related to sciatic nerve injury may be instantaneous, acute, or delayed. Trauma may result in sciatic pain, paresthesia, numbness, and variable motor and sensory deficits. However, motor function is usually more severely impaired than sensory function. In some cases, symptoms may worsen more gradually and be exacerbated by secondary fibrosis. Habitually, transient benign forms have no neurologic deficits but the pain did not improve with traditional analgesics. Paralytic foot drop is a possible presentation (deficit of dorsiflexion and eversion) when peroneal nerve division is injured. Patients with tibial neuropathy may experience loss of foot plantar flexion, loss of toe flexion, and weakened inversion of the foot.

Fig. 99.2  Several penetrating wounds in the left gluteal region along the path of the sciatic nerve (arrows)

Fig. 99.3  A penetration wound with the entry point (arrow) is at the level of the left supero-lateral gluteal area but the path continues in depth and downwards (dotted line) toward the path of the sciatic nerve

99.2  Clinical Presentations Fig. 99.4  A penetrating wound of the right lateral leg (a) with the presence of two metallic foreign bodies on the lateral X-ray (b) (arrows)

Fig. 99.5  Right peroneal (fibular) nerve neuropathy secondary to a leg injury (a, b). The neurologic pain appeared several months after the initial trauma likely due to secondary scar fibrosis

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a

a

Some patients may present with symptoms of a complete sciatic nerve injury including motor weakness of the hamstring muscles and all the muscles below the knee leading to weak knee flexion and foot drop. All sensations below the knee (except the medial part of the leg and foot) are diminished. Classically, there is no tender area in the lumbosacral region. Neuropathic pain provocation extending on the course of the sciatic nerve (Tinel’s sign) is suggestive. Chronic forms

b

b

are more subtle (Fig.  99.5). Sometimes, there is ipsilateral atrophy (depending on the location and duration) in comparison to the contralateral side. In the context of trauma, peripheral nerve damage rarely exists in isolation but is often associated with other neurologic and/or non-neurologic symptoms linked with the main and/or secondary lesions. Sometimes, patients are multi-injured, and various medical specialties may be involved in their management.

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99.3 Paraclinic Features Electrodiagnostic studies, magnetic resonance (MR) imaging, and ultrasound enhance the clinical evaluation with functional and anatomic details that determine the extent and localization of the nerve injury. These investigations may help decisions regarding the timing of surgical intervention as well as the type of surgical procedures. Both nerve conduction studies and needle electromyography can define axonal damage in the nerve but may not be able to determine the exact location of the lesion. Like other types of traumatic peripheral nerve injury, the differentiation of neuropraxia from neurotmesis and axonotmesis is decisive. A repetitive surveillance program may be taken on to assess the possibility of reinnervation with time because the clinical–electrophysiological correlation is often unexploited or misinterpreted in the beginning. High-resolution MR imaging and especially MR neurography become useful techniques for the assessment of neurological structures. Depending on the severity of the injury, an altered signal intensity (especially high signal intensity on T2-weighted images) may be seen in the injured segment of the sciatic nerve. In addition, total loss of nerve continuity or secondary signs of denervation may be found in the muscles supplied by the affected nerve. MR imaging can also have a prognostic value regarding nerve injury. When there is a diffuse and moderate thickening of the nerve with signal alteration, recovery is usually complete. While if there is a formation of a neuroma-in-­ continuity, recovery is incomplete or poor. Unfortunately, no recovery is expected if there is end neuroma formation or complete transection of the nerve. Additional paraclinical investigations, such as computer tomography, ultrasonography, or angiographic studies, may be needed for specific cases in the search for concomitant traumatic lesions.

99.4 Treatment Options The goal of the treatment is pain control, eliminating the aggressive cause, restoring neural function, and sometimes repairing anatomical continuity of the nerve. However, the treating surgeon should consider some factors including but not limited to the causative agent, degree, and extension of nerve damage, clinical neurologic impairment, patient’s general condition, and further concomitant disorders. Many therapeutic tools, such as medication, conservative measures, surgery, and physical therapy, have been proposed. Surgically, three techniques are used in the treatment of the different damages including:

99  Traumatic Sciatic Nerve Lesions

(a) Neurolysis (after a positive nerve action potential testing) (b) Suture repair (c) Graft repair (autograft or human cadaver allograft) Tetanus prophylaxis should be considered for patients with penetrating wound injuries. In the vast majority of cases, especially those with grades I and II, a proper course of physical therapy and rehabilitation can restore normal nerve function within a few weeks. For patients with sharp transections of the sciatic nerve, a try was done to repair these lesions as soon as possible. Such conditions and procedures are known to have excellent results. Patients with severe deficits and no nerve action potential transmissions through their continuity lesions underwent resection and repair. Surgical exploration is recommended in cases who do not show spontaneous c­linical/electromyographic recovery after 3 months or more after the onset of the injury. For some authors, this period may be reached up to 6 months of observation (with serial clinical and electrophysiological monitoring) prior to nerve repair may be accepted, on the condition that there is no nerve discontinuity. When the sciatic nerve is continuous with a good intraoperative nerve action potential, neurolysis has a good outcome. In complete ruptures, a repair can be done either with direct suture or with grafting, depending on the size of the lesion and the loss of substance. Residual neuropathic pain is commonly treated with neuropathic pain medications, such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline) and some anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine). Physical therapy may be used to speed up the recovery of motor function. Any associated lesions will be treated appropriately. It is well known that military GSWs are associated with many regional and even general concomitant traumatic lesions.

99.5 Outcomes and Prognosis In patients with lesions in continuity and a positive nerve action potential recording, the best surgical results are obtained by neurolysis, followed by suture repair and graft repair, respectively. The best functional outcomes following surgery for gunshot injuries are in cases of partially injured nerves that undergo external neurolysis for decompression, or after direct microsurgical suture, especially in young adults. The best outcome is encountered in decreasing order with neurapraxia, axonotmesis, and neurotmesis.

Further Reading

Generally, traumatic lesions in the thigh had a better recovery than those in the buttock, as well as peroneal division injuries showed worse functional outcomes than those involving the tibial division. Usually, in the case of axonal loss, recovery follows over 6–12  months under an intensive rehabilitation program. Neurotmesis has a less favorable prognosis and may require surgical repair with either a nerve transfer or a tendon transfer. Denervated muscles do not improve after 18 months. Some preventive measures are to be remembered: • Special attention should be paid to positioning the patient in a lithotomic position, positioning the retractor blades, and avoiding extreme lateral extension of the transverse lower abdominal incisions. • The upper outer quadrant of the buttock safely avoids hitting sciatic nerve. • Surgical procedures (especially orthopedic) with a high rate of sciatic nerve complications need continuous intraoperative electro-physiologic monitoring to reduce the risk of sciatic nerve injury.

Further Reading Abdallah IE, Ayoub R, Sawaya R, Saba SC.  Iatrogenic sciatic nerve injury during liposuction and fat tissue grafting: a preventable surgical complication with devastating patient outcomes. Patient Saf Surg. 2020;14:40. https://doi.org/10.1186/s13037-­020-­00265-­3. Abou-Al-Shaar H, Yoon N, Mahan MA.  Surgical repair of sciatic nerve traumatic rupture: technical considerations and approaches. Neurosurg Focus. 2018;44:V3. https://doi.org/10.3171/2018.1.Foc usVid.17568. Caillaud M, Richard L, Vallat JM, Desmoulière A, Billet F.  Peripheral nerve regeneration and intraneural revascularization. Neural Regen Res. 2019;14:24–33. https://doi. org/10.4103/1673-­5374.243699. Dosani A, Giannoudis PV, Waseem M, Hinsche A, Smith RM. Unusual presentation of sciatica in a 14-year-old girl. Injury. 2004;35:1071– 2. https://doi.org/10.1016/S0020-­1383(03)00104-­9. Dubuisson A, Kaschten B, Steinmetz M, Gérardy F, Lombard A, Dewandre Q, et al. Iatrogenic nerve injuries: a potentially serious medical and medicolegal problem. About a series of 42 patients and review of the literature. Acta Neurol Belg. 2021;121:119–24. https://doi.org/10.1007/s13760-­020-­01424-­0. Flug JA, Burge A, Melisaratos D, Miller TT, Carrino JA. Post-operative extra-spinal etiologies of sciatic nerve impingement. Skelet Radiol. 2018;47:913–21. https://doi.org/10.1007/s00256-­018-­2879-­7. Geyik S, Geyik M, Yigiter R, Kuzudisli S, Saglam S, Elci MA, et al. Preventing sciatic nerve injury due to intramuscular injection: ten-year single-center experience and literature review. Turk Neurosurg. 2017;27:636–40. https://doi.org/10.5137/1019-­5149. JTN.16956-­16.1. Issack PS, Helfet DL.  Sciatic nerve injury associated with acetabular fractures. HSS J. 2009;5:12–8. https://doi.org/10.1007/ s11420-­008-­9099-­y. Jones PE, Meyer RM, Faillace WJ, Landau ME, Smith JK, McKay PL, et  al. Combat injury of the sciatic nerve—an institutional experi-

971 ence. Mil Med. 2018;183:e434–41. https://doi.org/10.1093/milmed/ usy030. Kim DH, Murovic JA, Tiel R, Kline DG.  Management and outcomes in 353 surgically treated sciatic nerve lesions. J Neurosurg. 2004;101:8–17. https://doi.org/10.3171/jns.2004.101.1.0008. Kline DG, Kim D, Midha R, Harsh C, Tiel R.  Management and results of sciatic nerve injuries: a 24-year experience. J Neurosurg. 1998;89:13–23. https://doi.org/10.3171/jns.1998.89.1.0013. Kouyoumdjian JA, Graça CR, Ferreira VFM. Peripheral nerve injuries: a retrospective survey of 1124 cases. Neurol India. 2017;65:551–5. https://doi.org/10.4103/neuroindia.NI_987_16. Kretschmer T, Heinen CW, Antoniadis G, Richter HP, König RW. Iatrogenic nerve injuries. Neurosurg Clin N Am. 2009;20:73– 90, vii. https://doi.org/10.1016/j.nec.2008.07.025. Macheras GA, Lepetsos P, Leonidou A, Anastasopoulos PP, Galanakos SP, Tsiridis E. Results from the surgical resection of severe heterotopic ossification of the hip: a case series of 26 patients. Eur J Orthop Surg Traumatol. 2017;27:1097–102. https://doi.org/10.1007/ s00590-­017-­1980-­2. Manidakis N, Kanakaris NK, Nikolaou VS, Giannoudis PV. Early palsy of the sciatic nerve due to heterotopic ossification after surgery for fracture of the posterior wall of the acetabulum. J Bone Joint Surg Br. 2009;91:253–7. https://doi.org/10.1302/0301-­620X.91B2.21183. Mathieu L, Goncalves M, Murison JC, Pfister G, Oberlin C, Belkheyar Z. Ballistic peripheral nerve injuries: basic concepts, controversies, and proposal for a management strategy. Eur J Trauma Emerg Surg. 2022; https://doi.org/10.1007/s00068-­022-­01929-­8. McQuarrie HG, Harris JW, Ellsworth HS, Stone RA, Anderson AE III.  Sciatic neuropathy complicating vaginal hysterectomy. Am J Obstet Gynecol. 1972;113:223–32. https://doi. org/10.1016/0002-­9378(72)90771-­5. Miller A, Stedman GH, Beisaw NE, Gross PT. Sciatica caused by an avulsion fracture of the ischial tuberosity. A case report. J Bone Joint Surg Am. 1987;69:143–5. Niempoog S, Chumchuen S.  Acute closed traumatic sciatic nerve injury: a complication of heterotopic ossification and prominence of the femoral nail: a case report. J Med Assoc Thail. 2014;97(Suppl 8):S213–6. Oldershaw JB, Salem A, Storrs BB, Milner B, Omer GE. Sciatic nerve entrapment in the upper thigh caused by an injury sustained during World War II at the battle of Anzio. Case report. J Neurosurg. 2004;100:295–7. https://doi.org/10.3171/spi.2004.100.3.0295. Plewnia C, Wallace C, Zochodne D.  Traumatic sciatic neuropathy: a novel cause, local experience, and a review of the literature. J Trauma. 1999;47:986–91. https://doi. org/10.1097/00005373-­199911000-­00036. Puranen J, Orava S. The hamstring syndrome. A new diagnosis of gluteal sciatic pain. Am J Sports Med. 1988;16:517–21. https://doi. org/10.1177/036354658801600515. Puranen J, Orava S. The hamstring syndrome—a new gluteal sciatica. Ann Chir Gynaecol. 1991;80:212–4. Seddon HJ. Three types of nerve injury. Brain. 1943;66:237–88. Sharp E, Roberts M, Żurada-Zielińska A, Zurada A, Gielecki J, Tubbs RS, et al. The most commonly injured nerves at surgery: a comprehensive review. Clin Anat. 2021;34:244–62. https://doi.org/10.1002/ ca.23696. Srinivasan J, Ryan MM, Escolar DM, Darras B, Jones HR.  Pediatric sciatic neuropathies: a 30-year prospective study. Neurology. 2011;76:976–80. https://doi.org/10.1212/ WNL.0b013e3182104394. Stavrakakis IM, Kritsotakis EI, Giannoudis PV, Kapsetakis P, Dimitriou R, Bastian JD, et al. Sciatic nerve injury after acetabular fractures: a meta-analysis of incidence and outcomes. Eur J Trauma Emerg Surg. 2022; https://doi.org/10.1007/s00068-­022-­01896-­0.

972 Sunderland S.  A classification of peripheral nerve injuries producing loss of function. Brain. 1951;74:491–516. https://doi.org/10.1093/ brain/74.4.491. Taha A, Taha J.  Results of suture of the sciatic nerve after missile injury. J Trauma. 1998;45:340–4. https://doi. org/10.1097/00005373-­199808000-­00022. Topuz K, Kutlay M, Simşek H, Atabey C, Demircan M, Senol Güney M. Early surgical treatment protocol for sciatic nerve injury due to injection—a retrospective study. Br J Neurosurg. 2011;25:509–15. https://doi.org/10.3109/02688697.2011.566380.

99  Traumatic Sciatic Nerve Lesions Yeremeyeva E, Kline DG, Kim DH. Iatrogenic sciatic nerve injuries at buttock and thigh levels: the Louisiana State University experience review. Neurosurgery. 2009;65:A63–6. https://doi.org/10.1227/01. NEU.0000346265.17661.1E. Yoon SJ, Park MS, Matsuda DK, Choi YH.  Endoscopic resection of acetabular screw tip to decompress sciatic nerve following total hip arthroplasty. BMC Musculoskelet Disord. 2018;19:184. https://doi. org/10.1186/s12891-­018-­2091-­x.

Heterotopic Ossification Around the Hip Joint

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100.1 Generalities and Relevance

Heterotopic ossification around the hip can induce sciatic nerve problems, given the particular anatomical arrangement Heterotopic ossification (HOS) [formerly known as para-­ of the trunk of the sciatic nerve near the hip joint. However, osteoarthropathy] is the formation of mature lamellar bone HOS in the hip region rarely affects the sciatic nerve. In 1971, within soft-tissue sites outside the skeleton. Classically, the the American orthopedist Scott Kleiman and his team reported development of HOS is extra-articular because it occurs out- the first case of late sciatic nerve palsy due to compression of side the joint capsule. There are two types of HOS: nonge- the nerve by ectopic bone a posterior fracture-­dislocation of netic (most frequent) and genetic (unusual). the hip. Since then, fewer than 30 cases have been described Nongenetic HOS is often designated by the tissue type it in the literature, often among the adult men population. involves, such as “myositis ossificans” when involving skelMany acquired etiologies are involved in sciatica secondetal muscle, or “fasciitis ossificans” when involving fascia. ary to hip heterotopic ossification whether they are surgical, Some rare genetic disorders can cause HOS such as fibrodys- traumatic, mechanical, neurogenic, general, or even idioplasia ossificans progressiva and progressive osseous het- pathic (Table 100.2). Muscle trauma and injury seem to be eroplasia. Myositis ossificans is much more prevalent than significant triggering events. However, the etiological diagthat of other subtypes of HOS. nosis of ossification is more difficult when there is no history Generally, HOS develops in the following sites in decreas- of injury or surgery. ing order: hip, knee, shoulder, and elbow. Ectopic bone ranges from small clinically insignificant clusters of ossification to large bone deposits that cause pain Table 100.2  Main acquired causes of HOS around the hip compressand limitation of function. The severity of heterotopic bone ing the sciatic nerve •  Extensive surgeries formation has been graded according to several systems. The Surgical •  Joint arthroplasty Brooker classification is one of the oldest containing four •  Persistence of bone debris grades. However, the Della Valle classification is a simpler •  Postoperative hematoma modified classification system (Table 100.1). The important •  Percutaneous fixation of pelvic fractures thing is whether the space between opposing bone surfaces is Traumatic • Penetrating injuries (gunshot, missile track, and so greater or smaller than 1 cm. on)

Table 100.1  The Della Valle classification of heterotopic bone formation around the hip region Grading Description A Absence of heterotopic ossification or island of bone smaller than 1 cm in length B Island of bone ≥1 in length or spurs leaving at least 1 cm between femur and pelvis C Bone spurs arising from the femur or pelvis smaller than 1 cm between opposing surfaces or apparent bone ankylosis

•  Posterior wall acetabulum fractures •  Posterior hip dislocations and burns Mechanical •  Long-term bed rest •  Prolonged immobilization • Sagittal balance disorders of the lumbopelvic complex Neurogenic •  Brain and spinal cord injuries • Strokes •  Guillain-Barré syndrome General •  Hypoxic conditions •  Mechanical ventilation •  Hypermetabolic status Idiopathic From unknown cause

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_100

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100  Heterotopic Ossification Around the Hip Joint

The pathophysiology of HOS is incompletely understood but most theories describe a cellular response to local tissue injury, which leads to the release of inflammatory mediators such as osteoblast-stimulating factors. These chemical mediators will then induce a process of osteoid formation that eventually leads to the mature heterotopic bone within extra-­ skeletal tissues. HOS is histologically indistinguishable from normal compact and cancellous bones. Sometimes, histopathological changes could mimic some tumors, such as osteochondroma, osteosarcoma, and chondrosarcoma.

Lower back pain and neurologic deficits are unusual findings. Many other concomitant symptoms related to underlying etiologies should be considered in clinical presentations. A neurophysiologic study is very useful especially if the clinical appearance is unclear. It may determine the localization and severity of sciatic nerve damage, including axonal loss, demyelination, or both. It will also help to define the occurrence of ongoing degenerative or regenerative changes.

100.3 Paraclinic Features

100.2 Clinical Presentations

The gold standard method for diagnosing HOS is principal with plain X-rays and computed tomography (CT) scans. On Clinical evaluation of patients with sciatica related to HOS plain radiography, there is typically a circumferential peri-­ around the hip region is often difficult particularly when articular ossification with a lucent center (Fig. 100.1). In the there is no history of injury or surgery. Symptoms are inac- majority of cases with sciatic nerve disorders, the new bone curate and may be mistaken with many other lumbosacral formation is frequently localized posterior and lateral to the spinal, pelvic, and especially peri-articular hip diseases. hip joint. For some authors, calcification may be shown In the early stage, signs and symptoms of hip HOS are 2 weeks earlier by ultrasonography when compared to plain non-specific including fever, soft tissue swelling, and devel- radiographs. opment of a painful, tender, enlarging mass located around CT scan provides a more precise 3D localization of the the hip region. Unilateral or bilateral, this condition may ossification and may reveal heterotopic bone that has not mimic cellulitis, thrombophlebitis, arthritis, osteomyelitis, been detected by plain radiography (Figs. 100.2 and 100.3). or tumor. There is often a history of an injury or other trau- CT scan is also important in staging the disease and for pre-­ matic event to the affected area from a few weeks to a few surgical planning. months earlier (often between 3 and 12  weeks). Later, a Magnetic resonance (MR) imaging is used in the assessdecreased range of motion of the hip joint may appear, and ment of a soft tissue mass. It will help to identify structures lastly, ankylosis of the joint may follow. that are encircled by the ossification particularly the trunk of Pain in the gluteal area, proximal thigh, and the postero-­ the sciatic nerve. The sciatic nerve is compressed and pushed lateral part of the leg radiating into the lateral and plantar away by the heterotopic bony mass. Neural enlargement, aspects of the foot are more evocative of sciatic neuropathy abnormal fascicular appearance, increased perifascicular and than radiculopathy. intraneural signal intensity on T2-weighted MR or short tau Additional palpation, compression, or percussion over the inversion recovery (STIR) sequences, and perifascicular fat sciatic nerve trunk may produce pain and paresthesias blurring are morphologic alterations that suggest neural extending on the course of the nerve (Valleix Phenomenon). damage. Fig. 100.1 Antero-posterior (a) and lateral (b) pelvic plain radiographs showing typically a circumferential peri-­ articular ossification of the hip joints (arrows). Note the new bone formation localized posterior and lateral to the hip joint. (Courtesy of Pr. Hafid Arabi)

a

b

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100.4  Treatment Options and Prognosis Fig. 100.2  Pelvic 3D CT scan (a, b) showing bilateral heterotopic ossification (new bone) around the hip joints. (Courtesy of Pr. Hafid Arabi)

a

a

b

b

Fig. 100.3  Heterotopic ossification around the hip joints (arrows) as seen on axial (a) and coronal reconstructions (b) pelvic CT scan. (Courtesy of Pr. Hafid Arabi)

In the beginning, laboratory values of serum alkaline phosphate levels remain normal. It gradually rises with the new osseous formation and reaches its highest value when the patient is clinically symptomatic. Though rarely associated with sciatic nerve disorders, some tumors and tumor-like conditions can mimic HOS in the hip area including malignant bony tumors, calcified nerve tumors, tumoral calcinosis, calcified tendinitis (especially calcific tendinitis of the gluteal maximus muscle), neuritis ossificans, osteomyelitis, calcified hematoma, calcification of the linea aspera, and other ectopic calcifications.

100.4 Treatment Options and Prognosis There is no clear guideline for treatment for HOS.  Firstline therapy comprises conservative measures including bed rest, oral non-steroidal anti-inflammatories agents (especially indomethacin), muscle relaxants, neuropathic drugs, bisphosphonates, ice therapy, and rehabilitation program. Aggressive hip physiotherapy is not recommended in the early phase of the disease to avoid the deterioration of symptoms. Progressively, a few days later, range-of-motion (ROM) exercise can be initiated if there is no pain on hip

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mobilization. Active ROM exercises are useful in patients with mature ectopic bone lesions to maintain joint function. If symptoms of HOS persist and are refractory to conservative management, surgical intervention will be performed with sciatic nerve neurolysis and extraction of the bony mass. Surgical procedures are advocated only after the ossified mass has fully matured, this may take sometimes several months after the beginning of the symptoms. All cases with sciatic involvement reported previously in the literature have undergone neurolysis with hip joint preservation. Surgical decompression of the entrapped sciatic nerve may improve the neurologic function partially or completely. However, sciatic nerve release may have better outcomes for sensory deficits than for motor deficits. Follow-up electromyogram studies have an important predictive value. Unfortunately, in some cases, sciatic nerve damage may be permanent. As a preventive measure, a single low dose of local radiation therapy, indomethacin with or without bisphosphonates, has been used against HOS, especially following hip surgery.

Further Reading Abayev B, Ha E, Cruise C. A sciatic nerve lesion secondary to compression by a heterotopic ossification in the hip and thigh region— an electrodiagnostic approach. Neurologist. 2005;11:184–6. https:// doi.org/10.1097/01.nrl.0000160557.86676.63. Ahuja V, Thapa D, Patial S, Chander A, Ahuja A. Chronic hip pain in adults: current knowledge and future prospective. J Anaesthesiol Clin Pharmacol. 2020;36:450–7. https://doi.org/10.4103/joacp. JOACP_170_19. Brooker AF, Bowerman JW, Robinson RA, Riley LH Jr. Ectopic ossification following total hip replacement. Incidence and a method of classification. J Bone Joint Surg Am. 1973;55:1629–32. Dashefsky JH. Calcific degeneration in the tendon of the long head of the biceps femoris. An unusual cause of sciatica. J Bone Joint Surg Am. 1973;55:211–2. de Charry C, Derkenne C, Morelon S. Sciatica due to hydroxyapatite deposition disease. Joint Bone Spine. 2018;85:499–500. https://doi. org/10.1016/j.jbspin.2017.11.004. Della Valle AG, Ruzo PS, Pavone V, Tolo E, Mintz DN, Salvati EA.  Heterotopic ossification after total hip arthroplasty: a critical analysis of the Brooker classification and proposal of a simplified rating system. J Arthroplast. 2002;17:870–5. https://doi. org/10.1054/arth.2002.34819. Denormandie P, de l’Escalopier N, Gatin L, Grelier A, Genêt F.  Resection of neurogenic heterotopic ossification (NHO) of the hip. Orthop Traumatol Surg Res. 2018;104:S121–7. https://doi. org/10.1016/j.otsr.2017.04.015. Douira L, Ismaili N, Raiss M, Bensaleh H, Senouci K, Hassam B, et al. Tumoral calcinosis. Ann Dermatol Venereol. 2007;134:464–7. https://doi.org/10.1016/s0151-­9638(07)89215-­5. Gokkus K, Sagtas E, Suslu FE, Aydin AT. Myositis ossificans circumscripta, secondary to high-velocity gunshot and fragment wound that causes sciatica. BMJ Case Rep. 2013;2013:bcr2013201362. https://doi.org/10.1136/bcr-­2013-­201362. Gong Y, Yang C, Jingyu W, Liu J, Qi X. Calcific tendinitis of the gluteus maximus tendon with sciatic pain. Eur J Radiol Extra. 2010;76:e59– 60. https://doi.org/10.1016/J.EJREX.2010.09.001. Jones BV, Ward MW. Myositis ossificans in the biceps femoris muscles causing sciatic nerve palsy.A case report. J Bone Joint Surg Br. 1980;62-­ B:506–7. https://doi.org/10.1302/0301-­620X.62B4.7430235.

100  Heterotopic Ossification Around the Hip Joint Kleiman SG, Stevens J, Kolb L, Pankovich A. Late sciatic-nerve palsy following posterior fracture-dislocation of the hip. A case report. J Bone Joint Surg Am. 1971;53:781–2. Koulouvaris P, Tsailas P, Tsiavos K, Soucacos PN.  Clinical observations on surgical details of resection of heterotopic ossification at the hip in traumatic brain-injured adult. J Surg Orthop Adv. 2010;19:177–80. Kpadonou GT, Biaou O, Fiossi-Kpadonou E, Hans-Moevi AA, Alagnide E, Odoulami H.  Hip paraosteoarthropathy after sciatica nerve injury by quinine intramuscular injection. Ann Readapt Med Phys. 2007;50:42–7. https://doi.org/10.1016/j.annrmp.2006.07.057. Laborde A, Hermier M, Cotton F.  Clinical Vignette. Sciatic nerve entrapment secondary to heterotopic ossification: imaging findings and potential effect of selective cox-2 inhibitors. Rheumatology (Oxford). 2005;44:110. https://doi.org/10.1093/rheumatology/ keh255. Low SBL, Toms AP.  Calcification of the linea aspera: a systematic narrative review. Eur J Radiol Open. 2019;6:101–5. https://doi. org/10.1016/j.ejro.2018.12.002. Macheras GA, Lepetsos P, Leonidou A, Anastasopoulos PP, Galanakos SP, Tsiridis E. Results from the surgical resection of severe heterotopic ossification of the hip: a case series of 26 patients. Eur J Orthop Surg Traumatol. 2017;27:1097–102. https://doi.org/10.1007/ s00590-­017-­1980-­2. Meyers C, Lisiecki J, Miller S, Levin A, Fayad L, Ding C, et  al. Heterotopic ossification: a comprehensive review. JBMR Plus. 2019;3:e10172. https://doi.org/10.1002/jbm4.10172. Niempoog S, Chumchuen S.  Acute closed traumatic sciatic nerve injury: a complication of heterotopic ossification and prominence of the femoral nail: a case report. J Med Assoc Thail. 2014;97(Suppl 8):S213–6. Pakos EE, Pitouli EJ, Tsekeris PG, Papathanasopoulou V, Stafilas K, Xenakis TH.  Prevention of heterotopic ossification in high-risk patients with total hip arthroplasty: the experience of a combined therapeutic protocol. Int Orthop. 2006;30:79–83. https://doi. org/10.1007/s00264-­005-­0054-­y. Panagiotopoulos EC, Syggelos SA, Plotas A, Tsigkas G, Dimopoulos P.  Sciatica due to extrapelvic heterotopic ossification: a case report. J Med Case Rep. 2008;2:298. https://doi. org/10.1186/1752-­1947-­2-­298. Reinstein L, Eckholdt JW.  Sciatic nerve compression by preexisting heterotopic ossification during general anesthesia in the dorsal lithotomy position. Arch Phys Med Rehabil. 1983;64:65–8. Riemenschneider PA, Ecker A. Sciatica caused by tumoral calcinosis; a case report. J Neurosurg. 1952;9:304–7. https://doi.org/10.3171/ jns.1952.9.3.0304. Safaz I, Alaca R, Bozlar U, Yaşar E. Bilateral sciatic nerve entrapment due to heterotopic ossification in a traumatic brain-injured patient. Am J Phys Med Rehabil. 2008;87:65–7. https://doi.org/10.1097/ PHM.0b013e31815b5b4d. Salga M, Jourdan C, Durand MC, Hangard C, Denormandie P, Carlier RY, et al. Sciatic nerve compression by neurogenic heterotopic ossification: use of CT to determine surgical indications. Skelet Radiol. 2015;44:233–40. https://doi.org/10.1007/s00256-­014-­2003-­6. Singh JR, Yip K. Gluteus maximus calcific tendonosis: a rare cause of sciatic pain. Am J Phys Med Rehabil. 2015;94:165–7. https://doi. org/10.1097/PHM.0000000000000190. Thakkar DH, Porter RW.  Heterotopic ossification enveloping the sciatic nerve following posterior fracture-dislocation of the hip: a case report. Injury. 1981;13:207–9. https://doi. org/10.1016/0020-­1383(81)90240-­0. Wu XB, Yang MH, Zhu SW, Cao QY, Wu HH, Wang MY, et  al. Surgical resection of severe heterotopic ossification after open reduction and internal fixation of acetabular fractures: a case series of 18 patients. Injury. 2014;45:1604–10. https://doi.org/10.1016/j. injury.2014.05.018.

Extrapelvic Musculoskeletal and Soft Tissues Tumors

101.1 Generalities and Relevance There are varying extrapelvic tumors associated with sciatic pain. These neoplasms may be originating from local or neighboring musculoskeletal or soft tissue structures along the course of the sciatic nerve from the sciatic notch to the knee (Table  101.1). Regardless of their cause and their aggressiveness, there are four main types of extrapelvic tumors related to sciatica (Table  101.2). This chapter will focus on tumors originating from adjacent musculoskeletal and soft tissue and causing compression, invasion, or infiltration of the sciatic nerve (Table 101.3). Intrinsic tumors growing within the sciatic nerve will be discussed in Chap. 102. Some tumors may extend further downstream below the knee (toward the leg) or upstream toward the intrapelvic space. Tumors within the sciatic notch can grow extremely great and develop wide dumbbell-shaped lesions. Although clinical manifestations vary with the type of tumors and organs, the majority of patients suffering from sciatica present with sciatic peripheral mononeuropathy. The

Table 101.2  The four main types of extrapelvic tumors related to sciatica Type Description A Intrinsic tumors of the sciatic nerve secondary to tumoral growth within the endoneurium or perineurium (c.f. Chap. 102) B Tumors originating from adjacent structures causing compression of the sciatic nerve (nerve compression without invasion) C Tumors originating from adjacent structures causing extrinsic invasion of the sciatic nerve D Tumors causing infiltration of the sciatic nerve

Table 101.3  Main sources and types of extrapelvic tumors involved in sciatic pain Tumors originating from Soft tissues structures adjacent structures causing nerve compression with or without invasion

Osteocartilaginous structures

Table 101.1  Anatomic structures involved in sciatica related to extrapelvic tumors Bones

Joints

Muscles

Neural structures Other soft tissues

Sacrum Iliac bone Femur Tibia Sacroiliac Hip Knee Superior tibio-fibular joint Muscles of the gluteal Thigh muscles Upper leg muscles Sciatic nerve and its branches Subcutaneous Adipose Lymph nodes Intermuscular

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Tumors causing infiltration of the sciatic nerve

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_101

Endoneural metastasis

Infiltrative hematological malignancies

Metastasis to muscle Sarcoma Lymphoma Lipoma Liposarcoma Myopericytoma Osteochondroma Chordoma Eosinophilic granuloma Osteoid osteoma Osteosarcoma Chondrosarcoma Chondromyxoid sarcoma Giant cell tumor Melanomas Breast tumors Lung tumors Gastric tumors Kidney tumors Acute lymphoblastic leukemia Lymphomatous involvement

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presence of a growing mass along the palpable course of the sciatic nerve is very helpful. Treatment is not well codified due to the rarity of this clinical condition. Many therapeutic options have been proposed depending on the underlying etiologies and the patients’ conditions. Early diagnosis and adequate therapeutic management of extrapelvic tumors inducing sciatic pain have an important impact on a patient’s functional outcome and even his/her survival. Although their prevalence is not well documented, extrapelvic extrinsic sciatic neuropathy is less frequent than intrinsic ones. It may be seen at all ages, from neonates to the elderly without gender predominance. Ten percent of pediatric sciatic neuropathies are associated with neoplasms.

101  Extrapelvic Musculoskeletal and Soft Tissues Tumors

Sometimes, the neurological condition is confused, and some clinical presentations may mimic symptoms of lumbosacral nerve roots or lumbosacral plexus diseases. Electrophysiologic studies including conduction explorations and electromyography play a key role in the assessment of a possible sciatic neuropathy. The electrophysiologic approach provides additional evidence to confirm localization and exclude disorders that can mimic sciatic neuropathy such as lumbosacral plexopathy and lumbosacral radiculopathy.

101.3 Paraclinic Features

Among all neuroimaging techniques, magnetic resonance (MR) imaging remains the best method to detect extrapelvic 101.2 Clinical Presentations tumors-related sciatica (Figs.  101.1, 101.2, 101.3, 101.4, 101.5, 101.6, 101.7, 101.8, and 101.9). The sciatic nerve Clinical evaluation of patients with sciatica related to extra- should be assessed within its extrapelvic course from the pelvic tumors is often difficult particularly when there is no greater sciatic foramen to below the knee. This should history of underlying malignancy or neurofibromatosis. include both T1-weighted images (with and without gadoSymptoms are inaccurate and may be comparable to those of linium agent), T2-weighted images, and a fluid-sensitive fat-­ the most frequent etiologies of spinal sciatica (mainly degen- suppressed sequence like short tau inversion recovery erative lumbosacral spinal disease) or mistaken with many (STIR). Furthermore, MR neurography becomes a useful other musculoskeletal lower limb diseases. technique for the assessment of neurological structures and Clinicians should consider the importance of having a their underlying causes. The subtle osseous lesion is better sufficient and detailed medical history. Cases with past seen on computed tomography (CT) scan, which is usually malignant disease are predisposed to have metastases until needed for the assessment of neoplasms involving bone. demonstrated otherwise. Patients who had an insidious onset Most of the malignant osseous neoplasms causing sciatof unilateral sciatic pain that becomes constant, progressive, ica are located in the proximal femur. They may be primitive unresponsive by positional change, worsening at night, and or secondary (bony metastasis). In addition to clearly analyzwithout low back pain should require special attention ing the bony lesion, computed tomography (CT) and magregarding a tumoral origin of their neurological pain. netic resonance imaging (MRI) also show in detail its relation Pain in the gluteal area, proximal thigh, and the postero-­ to the sciatic nerve. Often, histopathological examination is lateral part of the leg radiating into the lateral and plantar mandatory for a definitive diagnosis. aspects of the foot is more evocative of sciatic neuropathy Soft tissue lipoma and osteochondroma (exostosis) are than radiculopathy. the most frequent benign tumors causing sciatica. Meticulous examination of the entire palpable course of Osteochondroma can be either pedunculated or sessile and the entire extrapelvic sciatic nerve distal to the sciatic notch is seen in the metaphyseal region typically projecting away is mandatory. Indeed, diagnosis is much easier when the from the epiphysis. CT demonstrates medullary continuity treating physician can localize the pain or mass at a specific and the cartilage cap (Figs. 101.7 and 101.8). The cartilage point along the course of the sciatic nerve. Neuropathic pain cap of osteochondromas appears the same as cartilage elseprovocation extending on the course of the sciatic nerve where, with intermediate to low signal on T1- and high sig(Tinel’s sign) is suggestive. Sometimes, there is ipsilateral nal on T2 weighted images. Whether intramuscular or atrophy (depending on the location and duration) in compari- intermuscular, lipoma appears as a hyperechoic wellson to the contralateral side. defined mass with fine internal echoes or striated appearMost of the malignant tumors causing sciatica are located ance on ultrasound. On CT scan, there is a low-density in the proximal femur. The delay between initial pain and mass typically with Hounsfield measurements in the negaweakness or sensory loss may take weeks or months. In addi- tive range. On MR, the fat-containing mass has an iso sigtion, fatigue and weight loss should point toward nal appearance to subcutaneous fat in all sequences malignancy. sometimes with septae.

101.3  Paraclinic Features

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Fig. 101.1  Case 1. Large muscular sarcoma (stars) of the thigh as seen on coronal (a, b) and axial (c, d) MR imaging views. (Courtesy of Pr. Youssef Benyass)

Fig. 101.2  Case 2. Preoperative giant cell tumor of the right femur (stars). Coronal T1-weighted MRI (a) and angio-CT scan (b). (Courtesy of Pr. Youssef Benyass)

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Fig. 101.3  Case 2. Post-operative antero-posterior (a) and lateral (b) plain radiographs of this large distal femoral bone tumor. (Courtesy of Pr. Youssef Benyass)

The aspect of soft tissue metastasis and sarcoma is variable (Figs.  101.1, 101.2, 101.3, and 101.4). Often demonstrating low-attenuation mass in contrast CT-scan with heterogeneous contrast enhancement. Calcification within the mass may be noticeable. On MR imaging, there are both high and low signal appearances when compared with surrounding muscle tissues depending on the existence of inflammation, hemorrhage, lobulation, or necrosis. However, necrosis, peritumoral edema, and lobulation are less commonly seen in soft-tissue sarcomas than in metastatic lesions. A histopathological analysis is required for a definitive diagnosis. Lymphoma may compress the sciatic nerve via extranodal or intranodal involvement by enlarged lymph nodes. Mostly, the tumor appears as a heterogeneous low focal or diffuse density lesion on CT-scan and low signal on T1- and high signal on T2-weighted MRI. Contrast enhancement may be absent, ring-like, or uniform. More rarely, lymphoma can involve directly the sciatic nerve.

On imaging, some tumors can be easily confused with other diseases such as: • • • • • •

Ganglion cysts Hematomas Vascular lesions Lipomatosis Infectious collections (abscess) Intrinsic nerve tumors

Further imaging investigations, such as ultrasonography, bone scintigraphy (Fig. 101.4d), positron emission tomography (PET), and angiographic (Fig. 101.2b) studies, as well as biological investigations, may be indicated for specific cases in the search for the etiology. However, when paraclinical explorations are inconclusive, an image-guided percutaneous biopsy of the suspected lesion is needed.

101.3  Paraclinic Features

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Fig. 101.4  Case 3. Synovialosarcoma of the left knee (arrows) manifesting as sciatic pain. Antero-posterior X-ray (a), axial (b), and coronal (c) MR imaging as well as skeletal scintigraphy (bone scan) (d). (Courtesy of Pr. Youssef Benyass)

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Fig. 101.5  Case 4. Malignant muscular tumor of the lower thigh with distal femur involvement (arrows). Pre (a) and intraoperative (b, c) views. (Courtesy of Pr. Adil Arrob )

Fig. 101.6  Case 4. Specimen of the tumor resection. (Courtesy of Pr. Adil Arrob)

101.3  Paraclinic Features

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Fig. 101.7  Case 5. 3D bone reconstructions CT scan (a–c) showing a pedunculated osteochondroma (exostosis) (arrows) of the upper proximal part of the tibial bone with mass effect on the adjacent peroneal neck in a young patient with common peroneal nerve entrapment

Fig. 101.8  Case 5. Axial CT scan showing the bone tumor (arrows) on the right compared to the contralateral side

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Fig. 101.9  Axial pelvic post-gadolinium T1-weighted MRI (a) and post-contrast CT scan (b) in a 70-year-old patient with right-sided sciatic pain. There is a large intrapelvic lymphoma (triangle) with paraspi-

nal (circle), iliac bone, and extrapelvic extension (stars). Note the intra and extrapelvic tumoral involvement through the greater sciatic foramen (double arrow)

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101.4 Treatment Options The aim of treatment is tumor removal and nerve decompression. However, the treating surgeon should consider some factors including but not limited to tumor origin, size, grading, extension, degree of nerve involvement, patient’s general condition, and neurological disorders. Many therapeutic tools, such as medication, conservative measures, surgery, laser ablation, radiotherapy, and chemotherapy, have been proposed. In cases where surgical intervention has been planned, morphological and functional preservation of other neurovascular and osteoarticular anatomical structures must be integrated into the therapeutic planning. Sometimes, a multidisciplinary surgical team could be involved including vascular, orthopedic, and plastic surgeons. Nerve resection may require sural nerve grafting or end-to-end anastomosis. Some complications might necessitate further reconstructive surgeries. Most benign tumors may be directly dissected and completely removed respecting adjacent functional anatomic structures. Large tumors or double-shaped masses demand the need for combined operative approaches because of the tumor’s dimension and the difficult anatomical relationship between the tumors and other anatomical structures. When a malignant tumor is diagnosed, the aim of surgery is the complete removal of the mass with tumor-free borders. However, in large and complex tumors, it is difficult to achieve complete removal of the lesion with tumor-free borders without damaging the important adjacent structures. Sometimes joint and bone replacement procedures may be required. Unfortunately, some advanced cases need an amputation. Regarding their origins, malignancies should be correctly managed by chemotherapy, surgery, and/or radiation therapy. Residual neuropathic pain is commonly treated with neuropathic pain medications, such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline) and some anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine). Physical therapy may be used to accelerate neurological recovery.

101.5 Prognosis Overall, early diagnosis will result in less extensive surgery and may improve patient outcomes. The prognosis is variable depending on the tumor’s nature and aggressiveness, initial neurological disorders, treatment response, delay of treatment, and the patient’s general condition. Prognosis is better for patients with benign neoplasm as well as for those without neural infiltration or invasion.

101  Extrapelvic Musculoskeletal and Soft Tissues Tumors

Benign and small tumors are generally considered to have a favorable prognosis if they are completely removed with nerve preservation. Progressive clinical deterioration is common in patients with secondary malignancy with life-­ threatening consequences. Whatever the results, careful clinical and paraclinical follow-­up should be needed to diagnose any recurrence at an early stage.

Further Reading Ajala-Agbo T, Tang PT, Bat-Ulzii Davidson T.  Unilateral leg weakness and pain secondary to metastatic anal squamous cell carcinoma. BMJ Case Rep. 2019;12:e227563. https://doi.org/10.1136/ bcr-­2018-­227563. Akinyemi OA, Mabry LM, Dardenelle SI.  Buttock pain and sciatica caused by a femoral osteochondroma. J Orthop Sports Phys Ther. 2017;47:442. https://doi.org/10.2519/jospt.2017.6877. Aldashash F, Elraie M. Solitary osteochondroma of the proximal femur causing sciatic nerve compression. Ann Saudi Med. 2017;37:166–9. https://doi.org/10.5144/0256-­4947.2017.166. Arunachalam K. Refractory sciatica could be a sign of malignancy: a unique case presentation. R I Med J. 2013;2016(99):25–7. Botwin KP, Shah CP, Zak PJ.  Sciatic neuropathy secondary to infiltrating intermuscular lipoma of the thigh. Am J Phys Med Rehabil. 2001;80:754–8. https://doi. org/10.1097/00002060-­200110000-­00009. Brégeon C, Renier JC, Pidhorz L, François J, Cardi S, Mazé H.  An unusual cause of sciatica: soft tissue desmoid tumor. Apropos of 2 cases. Rev Rhum Mal Osteoartic. 1983;50:427–34. Burke NG, Muhammad Bilal M, Harrington P. Gluteal angiosarcoma presenting as sciatica: an unusual secondary cause. Joint Bone Spine. 2013;80:340. https://doi.org/10.1016/j.jbspin.2012.10.011. Cai ZJ, Salem AE, Wagner-Bartak NA, Elsayes KM, Negm AS, Rezvani M, et al. Sciatic foramen anatomy and common pathologies: a pictorial review. Abdom Radiol (NY). 2022;47:378–98. https://doi. org/10.1007/s00261-­021-­03265-­8. de Moraes FB, Silva P, do Amaral RA, Ramos FF, Silva RO, de Freitas DA.  Solitary ischial osteochondroma: an unusual cause of sciatic pain: case report. Rev Bras Ortop. 2014;49:313–6. https://doi. org/10.1016/j.rboe.2014.04.005. Drampalos E, Sadiq M, Thompson T, Lomax A, Paul A. Intrapiriformis lipoma: an unusual cause of piriformis syndrome. Eur Spine J. 2015;24(Suppl 4):S551–4. https://doi.org/10.1007/ s00586-­014-­3695-­y. Ergun T.  Bilateral sciatica secondary to mass lesions in the gluteal muscles. Intramuscular metastasis. J Clin Neurosci. 2008;15:1388, 1426. https://doi.org/10.1016/j.jocn.2007.10.008. Ersozlu S, Sahin O, Ozgur AF, Akkaya T.  Sciatic neuropathy from a giant hibernoma of the thigh: a case report. Am J Orthop (Belle Mead NJ). 2008;37:E103–6. Gökkuş K, Aydın AT, Sağtaş E.  Solitary osteochondroma of ischial ramus causing sciatic nerve compression. Eklem Hastalik Cerrahisi. 2013;24:49–52. https://doi.org/10.5606/ehc.2013.12. Guedes F, Brown RS, Lourenço Torrão-Júnior FJ, Siquara-de-Sousa AC, Pires Amorim RM. Nondiscogenic sciatica: what clinical examination and imaging can tell us? World Neurosurg. 2020;134:e1053– 61. https://doi.org/10.1016/j.wneu.2019.11.083. Halperin N, Gadoth N, Reif R, Axer A. Osteoid osteoma of the proximal femur simulating spinal root compression. Clin Orthop Relat Res. 1982;162:191–4.

Further Reading Hodzic R, Hodzic M, Piric N, Karasalihovic Z. Clinicopathologic features in a case of intermuscular myopericitoma of thigh. Acta Myol. 2019;38:41–4. Hunt JA, Thompson JF.  Giant infiltrating lipoma of the thigh causing sciatica. Aust N Z J Surg. 1997;67:225–6. https://doi. org/10.1111/j.1445-­2197.1997.tb01949.x. Kim JY, Koo HJ, Park GY, Choi Y. Lipoma compressing the sciatic nerve in a patient with suspicious central post-stroke pain. Ann Rehabil Med. 2017;41:488–92. https://doi.org/10.5535/arm.2017.41.3.488. Mavrogenis AF, Rossi G, Rimondi E, Calabrò T, Papagelopoulos PJ, Ruggieri P.  Palliative embolization for osteosarcoma. Eur J Orthop Surg Traumatol. 2014;24:1351–6. https://doi.org/10.1007/ s00590-­013-­1312-­0. McMillan HJ, Srinivasan J, Darras BT, Ryan MM, Davis J, Lidov HG, et al. Pediatric sciatic neuropathy associated with neoplasms. Muscle Nerve. 2011;43:183–8. https://doi.org/10.1002/mus.21867. Moore KR, Tsuruda JS, Dailey AT. The value of MR neurography for evaluating extraspinal neuropathic leg pain: a pictorial essay. AJNR Am J Neuroradiol. 2001;22:786–94. Nishikawa T, Iguchi T, Honda H, Harada T, Kurosaka M, Mizuno K.  Primary bone tumors of the femur presenting with spinal symptoms: a report of two cases and review of the literature. J Spinal Disord. 2000;13:360–4. https://doi. org/10.1097/00002517-­200008000-­00015. O’Brien AL, West JM, Zewdu A, Grignol VP, Scharschmidt TJ, Moore AM.  Nerve transfers to restore femoral nerve function following oncologic nerve resection. J Surg Oncol. 2021;124:33–40. https:// doi.org/10.1002/jso.26487. Odell RT, Key JA. Lumbar disk syndrome caused by malignant tumors of bone. J Am Med Assoc. 1955;157:213–6. https://doi.org/10.1001/ jama.1955.02950200011003. Paone G, Itti E, Capacchione D, Ortonne N, Brugières P, Evangelista E, et al. Image of the month. Diagnosis of endoneural sciatic nerve

985 invasion by uterine cervical epidermoid cancer using [18F]FDG-­ PET/CT.  Eur J Nucl Med Mol Imaging. 2007;34:1711–2. https:// doi.org/10.1007/s00259-­007-­0510-­6. Shah SS, Consuegra JM, Subhawong TK, Urakov TM, Manzano GR.  Epidemiology and etiology of secondary piriformis syndrome: a single-institution retrospective study. J Clin Neurosci. 2019;59:209–12. https://doi.org/10.1016/j.jocn.2018.10.069. Sim FH, Dahlin DC, Stauffer RN, Laws E. Primary bone tumors simulating lumbar disc syndrome. Spine. 1977;2:65–74. Sugawara S, Ehara S, Hitachi S, Okada K.  Patterns of soft-tissue tumor extension in and out of the pelvis. AJR Am J Roentgenol. 2010;194:746–53. https://doi.org/10.2214/AJR.09.2585. Turan Ilica A, Yasar E, Tuba Sanal H, Duran C, Guvenc I. Sciatic nerve compression due to femoral neck osteochondroma: MDCT and MR findings. Clin Rheumatol. 2008;27:403–4. https://doi.org/10.1007/ s10067-­007-­0761-­4. Wadhwa V, Thakkar RS, Maragakis N, Höke A, Sumner CJ, Lloyd TE, et  al. Sciatic nerve tumor and tumor-like lesions—uncommon pathologies. Skelet Radiol. 2012;41:763–74. https://doi. org/10.1007/s00256-­012-­1384-­7. Woertler K.  Tumors and tumor-like lesions of peripheral nerves. Semin Musculoskelet Radiol. 2010;14:547–58. https://doi. org/10.1055/s-­0030-­1268073. Yablon CM, Hammer MR, Morag Y, Brandon CJ, Fessell DP, Jacobson JA. US of the peripheral nerves of the lower extremity: a landmark approach. Radiographics. 2016;36:464–78. https://doi.org/10.1148/ rg.2016150120. Ye BS, Sunwoo IN, Suh BC, Park JP, Shim DS, Kim SM. Diffuse large B-cell lymphoma presenting as piriformis syndrome. Muscle Nerve. 2010;41:419–22. https://doi.org/10.1002/mus.21538. Yu K, Meehan JP, Fritz A, Jamali AA. Osteochondroma of the femoral neck: a rare cause of sciatic nerve compression. Orthopedics. 2010;33. https://doi.org/10.3928/01477447-­20100625-­26.

Intrinsic Tumors of the Sciatic Nerve

102.1 Generalities and Relevance There are varying extrapelvic tumors associated with sciatic pain. These neoplasms may be originating from local or neighboring musculoskeletal or soft tissue structures along the course of the sciatic nerve (c.f. Chap. 101). Intrinsic tumors growing within the sciatic nerve constitute a specific group of neoplasms-inducing sciatica largely dominated by two benign neurogenic tumors: schwannomas and neurofibromas. The remaining tumors are rarer and have problems with histological diagnosis (Table 102.1). Whether they are neurogenic or not, most patients with intrinsic sciatic tumors present with symptoms of unilateral peripheral mononeuropathy much more than symptoms of pure L5/S1 radiculopathy or lumbosacral plexopathy. The presence of a growing mass along the palpable course of the sciatic nerve is very useful for the diagnosis. Some tumors may extend further downstream below the knee (toward the leg) or upstream toward the intrapelvic space. Tumors within the sciatic notch have the possibility to grow extremely great and develop wide dumbbell-shaped lesions.

Table 102.1  The main tumors of the sciatic nerve reported in the literature Schwannoma Neurofibroma Perineurioma Neurofibromatosis Malignant peripheral sheath tumors Neurofibrosarcoma Lymphoma Lipoma Neuromuscular choriostoma Malignant granular cell tumor Glomus tumor Chloroma Neural metastasis

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Schwannoma (AKA neurinoma or neurilemmoma) originates from Schwann cells of the neural sheath; therefore, the tumor is eccentric and it does not penetrate the nerve fascicles. On the opposite, neurofibromas deeply affects the nerve that is central and disorganized by the mass. In contrast to schwannomas, most neurofibromas are not encapsulated. Schwannoma accounts for 5% of all benign soft tissue tumors and is most commonly detected as a solitary lesion between 20 and 50 years of age. An association with neurofibromatosis type 1 (NF-1) is relatively rare. Some “ancient” tumors are somewhat large and may contain degenerative changes, such as cyst formation, calcification, hyalinization, or bleeding. There are two subtypes of neurofibroma: localized (90%) and plexiform (10%). In contrast to plexiform neurofibroma, localized one is not associated with NF-1 if found as a solitary lesion. Localized neurofibroma represents about 5% of all benign soft tissue tumors. This tumor is commonly observed in younger persons between 20 and 30 years of age. Plexiform neurofibroma is pathognomonic of NF-1. The lesions are usually detected during childhood and can appear before any cutaneous neurofibromas. The risk for malignant transformation can extend to 10%. Malignant peripheral nerve sheath tumors (MPNSTs) represent 5–10% of all soft tissue sarcomas and are rarer than benign nerve sheath tumors. MPNSTs develop most often in cases with NF-1, especially following radiation therapy, and are usually detected in individuals between 20 and 50 years of age. Other primary malignancies that can directly occur in the sciatic nerve include lymphoma (especially grade B cell lymphomas) and chloroma (granulocytic sarcoma). Intraneural metastases from systemic malignancies are very rare, often from melanomas and lung tumors. Intraneural perineurioma (AKA localized hypertrophic neuropathy) is a benign neurogenic tumor composed entirely of whorls of perineurial cells surrounding nerve fibers. The lesion typically occurs in children and young adults without gender predilection.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_102

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The remaining tumors involving the sciatic nerve are exceptionally described. As other extrapelvic tumors induce sciatic pain, early diagnosis and adequate therapeutic management have an important impact on a patient’s functional outcome and even his/her survival.

102.2 Clinical Presentations Clinical evaluation of patients with intrinsic tumors of the sciatic nerve trunk is often difficult particularly when there is no history of underlying malignancy or neurofibromatosis. Symptoms are unspecific and may be similar to those of the most frequent etiologies of spinal sciatica (e.g., discogenic lumbosacral disease) or mistaken with many other musculoskeletal and articular lower limb diseases. The clinical appearance of an endoneural sciatic tumor is usually that of a soft tissue slow-growing mass that might be associated with symptoms and signs related to the involved neural structures. However, unless it is large, it is very difficult to examine the lesion clinically because it is often located deep within the lower extremity. Benign nerve tumors are more frequent than malignant ones. Overall, schwannoma and neurofibroma represent the most common true neoplasms of intrinsic tumors of the sciatic nerve. Clinicians should consider the importance of having a sufficient and detailed medical history. Cases with past malignant disease are predisposed to have metastases until demonstrated otherwise. Patients who had an insidious onset of unilateral sciatic pain that becomes constant, progressive, unresponsive by positional change, worsening at night, and without low back pain should require special attention regarding a tumoral origin of their neurological pain. Careful palpation of the entire course of the entire sciatic nerve is mandatory. Indeed, diagnosis is much easier when the treating physician is able to localize the pain or mass at a specific point along the pathway of the sciatic nerve. Neuropathic pain provocation extending on the course of the sciatic nerve (i.e., Tinel’s sign) is suggestive. Sometimes, there is ipsilateral atrophy (depending on the location and duration) in comparison to the contralateral side. Patients with suspected neurogenic tumors should be investigated for possible association with neurofibromatosis. A deep neurocutaneous examination will be needed. Perineuriomas typically present with painless, slowly progressive weakness, unlike other neurogenic tumors of the sciatic nerve where the pain is often a presenting complaint. On the other hand, MPNSTs are most commonly located in the proximal portion of the lower limb, and clinical presentations are more potentially painful with rapid progression. However, the delay between initial pain and weakness or

102  Intrinsic Tumors of the Sciatic Nerve

sensory loss may take weeks or months. In addition, fatigue and weight loss should point toward malignancy. Sometimes, the neurological condition is confused, and some clinical presentations may mimic symptoms of lumbosacral nerve roots or lumbosacral plexus diseases. Electrophysiologic studies including conduction explorations and electromyography play a key role in the assessment of a possible sciatic neuropathy. The electrophysiologic approach provides additional evidence to confirm localization and exclude disorders that can mimic sciatic neuropathy such as lumbosacral plexopathy and lumbosacral radiculopathy.

102.3 Paraclinic Features Among all neuroimaging techniques, high-resolution magnetic resonance (MR) imaging remains the best method to detect intraneural tumor-related sciatic pain. The sciatic nerve should be assessed within its extrapelvic course from the greater sciatic foramen to below the knee. This should include both T1-weighted images (with and without gadolinium enhancement), T2-weighted images, and a fluid-­ sensitive fat-suppressed sequence like short tau inversion recovery (STIR). Furthermore, MR neurography becomes a useful technique for the assessment of neurological structures and their underlying causes. MR imaging is also a useful tool for depicting regionally associated lesions and muscle denervation changes. Additional paraclinical investigations, such as computer tomography, ultrasonography, positron emission tomography (PET), angiographic studies, as well as biological examinations, may be needed for specific cases in the search for the tumoral lesion. However, when paraclinical explorations are inconclusive, a minimally invasive approach may be needed for performing percutaneous biopsies guidance of the suspected mass. Both schwannomas and solitary neurofibromas are often indistinguishable from neuroimaging. Both tumors have a similar density on computed tomography (CT) scans to that of adjacent muscles with various degrees of contrast enhancement. The majority of benign neurogenic tumors are homogeneous and iso-hypointense with muscle on T1 and hyperintense on T2-weighted MR images. Interestingly, a central area of a low-intensity signal associated with peripheral high-intensity signal on T2-weighted images termed the “target sign,” is more frequently seen in neurofibromas. Furthermore, schwannomas are encapsulated while neurofibromas have rarely a true capsule. Plexiform neurofibromas are associated with NF-1. In such cases, neurofibromas are multiple with progressive diffuse involvement from the proximal to the distal part of the sciatic nerve trunk.

102.3  Paraclinic Features

Some characteristics are evocative of the diagnosis of perineurioma such as the localized cylindrical or fusiform shape of the lesion on MRI outside the traditional entrapment sites in the lower limb, clear perineurial fat limitations, uniform prominent fascicles, uniform enhancement, young age of the patient, clinical presentation of peripheral mononeuropathy with slow weakness, and absence of a history of neurofibromatosis. The imaging features of malignant neural tumors overlap those of their benign counterparts, making differentiation between the two challenges. Findings that favor a malignant neural tumor include large dimensions of the mass, irregular margins, heterogeneity, peripheral enhancement, and perilesional edema (Fig. 102.1). Neurolymphomatous tumors present as diffuse peripheral nerve enlargement with multifocal nodularities on MR imaging. There is usually interspersed, minimal heterogeneous hypointensity (dark spots) inside the tumor on T2-weighted images. On post-gadolinium T1-weighted images, there is a homogenous or heterogeneous enhancement of the mass. The MR imaging appearance of the metastasis within and around the involved nerve is usually unspecific, and signal

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intensities vary depending on the nature of its tissue of origin. Findings that differentiate a secondary from a primary tumor of the nerve are the presence of multiple lesions with infiltrative margins, enlargement of contiguous lymph nodes, concomitant osteolytic lesions, and advanced age of the patient. A histopathological analysis is sometimes required for a definitive diagnosis. On neuroimaging, some intrinsic tumors can be easily confused with other diseases such as: • • • • • • • • • • •

Ganglion cysts Hematomas Vascular lesions Endometriosis Extrinsic musculoskeletal and soft tissue nerve tumors Paradoxical neural hypertrophy Post-traumatic neuroma Amyloidosis Fibromatosis Inflammatory and systemic peripheral neuropathies Neuritis ossificans (rare)

Fig. 102.1  Gluteal MRI in case 2. A Coronal MRI shows a fusiform tumor in the femoral region (arrow) (a). T2-weighted axial MRI shows a mixed low- and high-­ intensity signal (arrow) (b). (Reproduced from Zhao L, Wei J, Wan C, Han S, Sun H. The diagnostic pitfalls of lumbar disc herniation— malignant sciatic nerve tumour: two case reports and literature review. BMC Musculoskelet Disord. 2021;22:848. https://doi. org/10.1186/s12891-­021-­ 04728-­1; Creative Commons CC BY 4.0; http:// creativecommons.org/ licenses/by/4.0/)

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102.4 Treatment Options The aim of the treatment of intrinsic sciatic nerve tumors is tumor removal and nerve decompression. However, the treating surgeon should consider some factors including but not limited to tumor origin, size, grading, extension, degree of nerve involvement, patient’s general condition, and neurological disorders. Many therapeutic tools, such as medication, conservative measures, surgery, laser ablation, radiotherapy, and chemotherapy, have been proposed. The treatment of choice for a benign schwannoma is usually aggressive resection because of the high frequency of recurrence. Such surgical resection, better known as enucleation, is often possible because schwannoma is an encapsulated tumor somewhat eccentric relative to the affected nerve trunk. However, large tumors and most neurofibromas deeply affect the nerve, and thus, complete surgical removal may be challenging without iatrogenic neurological damage. Sometimes, some procedures are needed to repair nerve damage and/or resection: (a) Short neural gap after resection of the tumor requires neural end-to-end suture anastomosis without tension. (b) Long neural gaps need nerve grafts (e.g., sural nerve autograft) interposed between the prepared proximal and distal nerve stumps. When a malignant tumor is diagnosed, the aim of surgery is the complete removal of the mass with tumor-free borders. However, in large and complex tumors, it is difficult to achieve complete removal of the lesion with tumor-free margins without damaging the important adjacent structures. Sometimes joint and bone replacement procedures may be required. Unfortunately, some advanced cases need an amputation. Regarding their origins, malignancy should be correctly managed by chemotherapy, surgery, and/or radiation therapy (e.g., treatment of neurolymphomatosis consists of either chemotherapy alone or combined with radiotherapy). Residual neuropathic pain is commonly treated with neuropathic pain medications, such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline) and some anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine). Physical therapy may be used to speed up the recovery of motor function.

102.5 Prognosis The prognosis is variable depending on the tumor’s nature and aggressiveness, initial neurological disorders, delay of treatment, treatment response, and the patient’s general condition. The prognosis is better for patients with benign and

102  Intrinsic Tumors of the Sciatic Nerve

small neoplasms with mild or without motor weakness. Benign neurogenic tumors (schwannoma and neurofibroma) are generally considered to have a favorable prognosis if they are completely removed with nerve preservation. Progressive neurological deterioration is common in patients with sciatic mononeuropathy secondary to malignancy with life-­ threatening consequences. For example, in cases of MPNST, pulmonary metastasis is the main reason for death. Recovery from neurologic pain generally precedes the reappearance of muscle strength. Improvement is usually monophasic, slow, and incomplete. In advanced cases with delayed management, complete recovery of motor function is rare, even after total surgical removal of the lesion. Fibrosis during the healing process is likely to induce permanent nerve damage. Whatever the results, careful clinical and paraclinical follow-up should be needed in order to diagnose any recurrence at an early stage.

Further Reading Advani P, Paulus A, Murray P, Jiang L, Goff R, Pooley R, Jain M, Garner H, Foran J. A rare case of primary high-grade large B-cell lymphoma of the sciatic nerve. Clin Lymphoma Myeloma Leuk. 2015;15:e117–20. https://doi.org/10.1016/j.clml.2014.12.001. Bang JS, Adsul N, Lim JH, Jang IT. Extra-osseous Ewing sarcoma of sciatic nerve masquerading as benign nerve sheath tumor and presented as lumbar radiculopathy: case report and review of literature. World Neurosurg. 2018;115:89–93. https://doi.org/10.1016/j. wneu.2018.04.045. Benzel EC, Morris DM, Fowler MR. Nerve sheath tumors of the sciatic nerve and sacral plexus. J Surg Oncol. 1988;39:8–16. https://doi. org/10.1002/jso.2930390103. Bindra V, Nori M, Reddy R, Reddy R, Satpathy G, Reddy CA. Sciatic nerve endometriosis—the correct approach matters: a case report. Case Rep Womens Health. 2023;38:e00515. https://doi. org/10.1016/j.crwh.2023.e00515. Brand C, Pedro MT, Pala A, Heinen C, Scheuerle A, Braun M, et al. Perineurioma: a rare entity of peripheral nerve sheath tumors. J Neurol Surg A Cent Eur Neurosurg. 2022;83:1–5. https://doi. org/10.1055/s-­0041-­1726110. Chew DCY, Zhao DBH, Sittampalam K, Kumar SK. Malignant transformation in a sciatic plexiform neurofibroma in Neurofibromatosis Type 1—imaging features that aid diagnosis. J Radiol Case Rep. 2020;14:1–13. https://doi.org/10.3941/jrcr.v14i12.4028. D’Ancona G, Merlot B, Verrelli L, Boulos S, Dennis T, Roman H. Robotic management of isolated endometriosis of sciatic nerve: a reproducible approach which can guide in the labyrinth of pelvic neuroanatomy. Fertil Steril. 2023;120(3 Pt 2):703–5. https://doi. org/10.1016/j.fertnstert.2023.06.008. Descamps MJ, Barrett L, Groves M, Yung L, Birch R, Murray NM, et  al. Primary sciatic nerve lymphoma: a case report and review of the literature. J Neurol Neurosurg Psychiatry. 2006;77:1087–9. https://doi.org/10.1136/jnnp.2006.087577. Erdoğan F, Say F, Barış YS. Schwannomatosis of the sciatic nerve: a case report. Br J Neurosurg. 2021;37:100. https://doi.org/10.1080/ 02688697.2021.1950628. Feinberg J, Sethi S.  Sciatic neuropathy: case report and discussion of the literature on postoperative sciatic neuropathy and sciatic nerve tumors. HSS J. 2006;2:181–7. https://doi.org/10.1007/ s11420-­006-­9018-­z.

Further Reading Ghaly RF. A posterior tibial nerve neurilemoma unrecognized for 10 years: case report. Neurosurgery. 2001;48:668–72. https://doi. org/10.1097/00006123-­200103000-­00045. He W, Wang W, Gustas C, Malysz J, Kaur D. Isolated sciatic neuropathy as an initial manifestation of a high grade B-cell lymphoma: a case report and literature review. Clin Neurol Neurosurg. 2016;149:147– 53. https://doi.org/10.1016/j.clineuro.2016.07.029. Hibbard J, Schreiber JR.  Footdrop due to sciatic nerve endometriosis. Am J Obstet Gynecol. 1984;149:800–1. https://doi. org/10.1016/0002-­9378(84)90128-­5. Hurrell MA, McLean C, Desmond P, Tress BM, Kaye A. Malignant granular cell tumour of the sciatic nerve. Australas Radiol. 1995;39:86– 9. https://doi.org/10.1111/j.1440-­1673.1995.tb00242.x. Kim KT, Kim SI, Do YR, Jung HR, Cho JH. Sciatic nerve neurolymphomatosis as the initial presentation of primary diffuse large B-cell lymphoma: a rare cause of leg weakness. Yeungnam Univ J Med. 2021;38:258–63. https://doi.org/10.12701/yujm.2021.00983. Kumar R, Vu L, Madewell JE, Herzog CE, Bird JE. Glomangiomatosis of the sciatic nerve: a case report and review of the literature. Skelet Radiol. 2017;46:807–15. https://doi.org/10.1007/ s00256-­017-­2594-­9. Lam S, Grandhi R, Wong R, Hamilton R, Greene S.  Neuromuscular hamartoma of the sciatic nerve: case report and review of the literature. Surg Neurol Int. 2013;4:8. https://doi. org/10.4103/2152-­7806.106266. Liu HC, Hung GY, Yen HJ, Hsieh MY, Chiou TJ.  Acute sciatica: an unusual presentation of extramedullary relapse of acute lymphoblastic leukemia. Int J Hematol. 2007;86:163–5. https://doi. org/10.1532/IJH97.A10703. Maher CO, Spinner RJ, Giannini C, Scheithauer BW, Crum BA.  Neuromuscular choristoma of the sciatic nerve. Case report. J Neurosurg. 2002;96:1123–6. https://doi.org/10.3171/ jns.2002.96.6.1123. McMillan HJ, Srinivasan J, Darras BT, Ryan MM, Davis J, Lidov HG, et  al. Pediatric sciatic neuropathy associated with neoplasms. Muscle Nerve. 2011;43:183–8. https://doi.org/10.1002/ mus.21867. Mezian K, Záhora R, Vacek J, Kozák J, Navrátil L.  Sciatic nerve schwannoma in the gluteal region mimicking sciatica. Am J Phys Med Rehabil. 2017;96:e139–40. https://doi.org/10.1097/ PHM.0000000000000673. Moore KR, Tsuruda JS, Dailey AT. The value of MR neurography for evaluating extraspinal neuropathic leg pain: a pictorial essay. AJNR Am J Neuroradiol. 2001;22:786–94. O’Brien AL, West JM, Zewdu A, Grignol VP, Scharschmidt TJ, Moore AM.  Nerve transfers to restore femoral nerve function following oncologic nerve resection. J Surg Oncol. 2021;124:33–40. https:// doi.org/10.1002/jso.26487. Park JE. Long-term natural history of a neuromuscular choristoma of the sciatic nerve: a case report and literature review. Clin Imaging. 2019;55:18–22. https://doi.org/10.1016/j.clinimag.2019.01.003. Patel DK, Gwathmey KG.  Neoplastic nerve lesions. Neurol Sci. 2022;43:3019–38. https://doi.org/10.1007/s10072-­022-­05951-­x.

991 Peters PA, Kaszuba MC, Raghunathan A, Puffer RC, Spinner RJ. Synchronous development of multicentric malignant peripheral nerve sheath tumors: institutional review. World Neurosurg. 2018; https://doi.org/10.1016/j.wneu.2018.12.088. Quiñones-Hinojosa A, Friedlander RM, Boyer PJ, Batchelor TT, Chiocca EA.  Solitary sciatic nerve lymphoma as an initial manifestation of diffuse neurolymphomatosis. Case report and review of the literature. J Neurosurg. 2000;92:165–9. https://doi.org/10.3171/ jns.2000.92.1.0165. Roncaroli F, Poppi M, Riccioni L, Frank F.  Primary non-­ Hodgkin’s lymphoma of the sciatic nerve followed by localization in the central nervous system: case report and review of the literature. Neurosurgery. 1997;40:618–21. https://doi. org/10.1097/00006123-­199703000-­00038. Scheithauer BW, Rodriguez FJ, Spinner RJ, Dyck PJ, Salem A, Edelman FL, et al. Glomus tumor and glomangioma of the nerve. Report of two cases. J Neurosurg. 2008;108:348–56. https://doi.org/10.3171/ JNS/2008/108/2/0348. Shariatzadeh H, Amiri S, Joudi S, Bahrabadi M. Multiple schwannomas in sciatic nerve: a rare case report. Arch Bone Jt Surg. 2021;9:601– 4. https://doi.org/10.22038/abjs.2021.53165.2638. Sharma RR, Pawar SJ, Mahapatra AK, Doctor M, Musa MM. Sciatica due to malignant nerve sheath tumour of sciatic nerve in the thigh. Neurol India. 2001;49:188–90. Sintzoff SA Jr, Bank WO, Gevenois PA, Matos C, Noterman J, Flament-­ Durand J, et al. Simultaneous neurofibroma and schwannoma of the sciatic nerve. AJNR Am J Neuroradiol. 1992;13:1249–52. Strobel K, Fischer K, Hany TF, Poryazova R, Jung HH. Sciatic nerve neurolymphomatosis—extent and therapy response assessment with PET/CT.  Clin Nucl Med. 2007;32:646–8. https://doi.org/10.1097/ RLU.0b013e3180a1ac74. Thomas JE, Piepgras DG, Scheithauer B, Onofrio BM, Shives TC.  Neurogenic tumors of the sciatic nerve. A clinicopathologic study of 35 cases. Mayo Clin Proc. 1983;58:640–7. Wadhwa V, Thakkar RS, Maragakis N, Höke A, Sumner CJ, Lloyd TE, et  al. Sciatic nerve tumor and tumor-like lesions—uncommon pathologies. Skelet Radiol. 2012;41:763–74. https://doi. org/10.1007/s00256-­012-­1384-­7. Woertler K.  Tumors and tumor-like lesions of peripheral nerves. Semin Musculoskelet Radiol. 2010;14:547–58. https://doi. org/10.1055/s-­0030-­1268073. Yablon CM, Hammer MR, Morag Y, Brandon CJ, Fessell DP, Jacobson JA. US of the peripheral nerves of the lower extremity: a landmark approach. Radiographics. 2016;36:464–78. https://doi.org/10.1148/ rg.2016150120. Yuga ACQ, Pascual JSG, Valparaiso AP, Khu KJO.  Extensive neuritis ossificans of the sciatic nerve: systematic review and illustrative case. J Clin Neurosci. 2022;98:224–8. https://doi.org/10.1016/j. jocn.2022.02.021. Zhao L, Wei J, Wan C, Han S, Sun H. The diagnostic pitfalls of lumbar disc herniation—malignant sciatic nerve tumour: two case reports and literature review. BMC Musculoskelet Disord. 2021;22:848. https://doi.org/10.1186/s12891-­021-­04728-­1.

Extrapelvic Ganglion and Synovial Cysts

103.1 Generalities and Relevance Ganglion and synovial cysts are nonneoplastic synovial or gelatinous cystic lesions that originate within the soft tissue near a joint. These cysts may be unilocular or multilocular mostly located in the periarticular regions of the wrists, knees, and feet. Ganglion and synovial cysts are similar clinically and in imaging appearance. Sometimes, these terms are used synonymously. However, ganglion cysts are lined with dense connective tissue, whereas synovial cysts have a synovial-cell lining. Throughout this chapter, both cysts will be called ganglionic cysts. In the lower limbs, most ganglionic cysts occur in the periarticular areas around the hip and the knee. Often unilateral and asymptomatic, only a few cases of ganglionic cysts with sciatica are reported in the literature, particularly those developed: • Near the superior tibiofibular joint neck and compressing the peroneal nerve (the most common). • Near the posteromedial aspect of the hip and compressing the sciatic nerve. These cysts may be classified as intraneural or extraneural; however, the majority of cysts are intraneural (AKA endoneural). Most ganglion cysts remain asymptomatic but occasionally, some large juxta-articular cysts can compress neurovascular structures, especially the sciatic nerve or its branches, causing neurologic symptoms. It is necessary to mention that some authors distinguish a third group of juxta-articular cysts around the hip named “paralabral cysts.” These cysts occur specifically near the acetabular labrum secondary to a labral tear. However, paralabral cysts are rarely involved in sciatic pain. The majority of ganglionic cysts develop locally, while some may extend up and down along the sciatic nerve or its branches. Some cysts originating from the dorsal aspect of

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the hip joint can even spread up to the intrapelvic space along the lumbosacral plexus via the sciatic notch. Although the first case of an intraneural ganglionic cyst (INGC) was described by Hartwell in 1901 in a patient with median nerve involvement, the mechanism underlying their formation has been controversial. Various hypotheses have been proposed, including: (a) Intraneural hemorrhage (b) Recurrent trauma (c) Degenerative changes, especially mucoid degeneration of the nerve sheath (d) Intraneural entrapment of embryonic synovial remnants (de novo formation from hamartomatous cell rests) (e) Ingrowth of an articular cyst into the nerve (articular origin) Nowadays, the articular theory first described by Spinner et al. is most generally accepted. According to their theory, the origin of the cyst is the articular joint. Through a capsular weakness (traumatic) or deficiency (degenerative), synovial fluid contents reach the main nerve trunk via a small articular branch nerve. In other words, the articular branch nerve constitutes a connecting bridge between the synovial joint and the sciatic nerve or its branches.

103.2 Clinical Presentations The clinical manifestations depend on the volume of the cyst, its site, and its relationship to the surrounding bony, joint, neural, and vascular structures. Symptoms may be insidious, fluctuating, or, less usually, acute in nature, most often triggered by a previous traumatic episode in the area. Classically, there is a combined presentation of symptoms attributable to intrinsic joint disease (local pain and decreased articular function) and peripheral neuropathy without back pain. Neurologic symptoms and signs include pain, numb-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_103

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ness, tingling, paresthesias, motor weakness, and sensory abnormalities along the distribution of the affected nerve. Muscle denervation and atrophy have also been described. These findings can be confirmed by neurophysiological studies (electromyography and/or nerve conduction explorations). Rarely, some patients may present with a painless foot drop. At the hip, the cysts are deep and not palpable; however, a mass may be palpated along the anterolateral aspect of the knee in proximity to the fibular head (corresponding to the superior tibiofibular joint). Tinel’s sign may also be present. However, many cases will remain asymptomatic and the cyst will be found only incidentally.

103.3 Imaging Features Ultrasonography and magnetic resonance imaging (MRI) are useful tools for the diagnostic process. On musculoskeletal ultrasonography, an endoneural ganglion cyst appears as a large well-circumscribed hypoechogenic lesion. However, it fails to provide a clear definition of the surrounding tissue. Ultrasonography may be useful when guided percutaneous aspiration is decided. While on MRI, the cyst appears multilobulated with low signal intensity on T1-weighted images and high signal on T2-weighted images, oriented longitudinally along the course of the involved nerve or its branches. Furthermore, muscle denervation edema can be seen as T2 hyperintensity. Muscle atrophy is also characterized as T1 hyperintensity. MRI neurography is a modified MRI approach to visualize the nervous system. This imaging modality is a useful technique for determining morphological nervous abnormalities, especially in the lumbosacral plexus within the intrapelvic space. MRI features are important for differentiating between intraneural and extraneural ganglionic cysts. Unlike INGC, an extraneural cyst does not have an articular connection. In addition, in extraneural forms, the nerve is seen separately from the cyst with an intervening preserved fat plane. An intramuscular extension is unusual. Sometimes, joint connections are difficult to detect on an MRI for INGC. On the computed tomography (CT) scan, the ganglionic cyst appears as a round, uni, or multiloculated mass with a thin and well-defined wall that does not enhance after contrast injection. The relationship between the cyst and the nerve may be best evaluated with a high-resolution CT scan. Articular degenerative changes are not mandatory. Occasionally, imaging appearances are atypical and may be confused with other possible cystic lesions in the hip or knee regions, such as: • Cystic peripheral nerve sheath tumors • Baker’s cysts (knee)

103  Extrapelvic Ganglion and Synovial Cysts

• • • • • •

Paralabral cysts (hip) Myxomas Synovial sarcomas Atypical vascular or lymphatic malformations Abscess collections Hydatidosis

Some authors have proposed aggressive radiological work-up regimes, such as arthrography, arthro-CT scan, and even arthro-MRI, especially in cases of recurrence, to reveal a potential connection to the joint space.

103.4 Treatment Options and Prognosis The classic treatment for symptomatic ganglionic cysts is surgical excision of the cystic lesions and nerve decompression. The standard surgical procedure can be summarized in three main steps: • Removing the entire ganglionic cyst and its wall. • Destroying any potential connection to the adjacent articular space to avoid any recurrence. • Preserving morphologically and functionally the remaining neurological fascicles. Surgical resection is considered a more definitive treatment, but it may be accompanied by certain complications related to nerve damage, muscle atrophy, and infection. Percutaneous aspiration of the cyst under ultrasound guidance, with or without corticosteroid injection, is an alternative “minimally invasive” treatment. However, these methods have potentially high relapse rates. Direct decompression of INGC within the pelvis (involving the lumbosacral plexus) is more technically difficult and may result in more residual postoperative pain. The risk of (postoperative) relapse of ganglionic cysts after simple percutaneous aspiration is between 10% and 30%, especially for INGC. The identification of a potential joint connection in cases of INGC is crucial as failure to recognize and treat the joint connection might lead to recurrence. The best results were accomplished in relation to pain control because the recovery of motor function is less predictable and more variable. In general, delayed diagnosis and the existence of motor weakness are associated with poorer outcomes. Neuropathic residual pain is commonly treated with neuropathic pain medications, such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline) and some anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine). Physical therapy may be used if needed.

Further Reading

Further Reading Briem T, Haemmerle G, Kramers-de Quervain I, Leunig M. Synovial ganglion of the hip as a rare cause of L5 radiculopathy: a case report. JBJS Case Connect. 2016;6:e59. https://doi.org/10.2106/ JBJS.CC.15.00234. Colombo EV, Howe BM, Amrami KK, Spinner RJ. Elaborating upon the descent phase of fibular and tibial intraneural ganglion cysts after cross-over in the sciatic nerve. Clin Anat. 2014;27:1133–6. https://doi.org/10.1002/ca.22466. García García FJ, Pescador Hernández D, Rendon Díaz D, Blanco Blanco J.  Intraneural ganglion cyst of the external popliteal sciatic nerve: a possible cause of foot drop. Neurologia (Engl Ed). 2018;33:486–9. https://doi.org/10.1016/j.nrl.2017.02.006. Hartwell AS. Cystic tumor of median nerve, operation: restoration of function. Boston Med Surg J. 1901;144:582–3. Juglard G, Le Nen D, Lefevre C, Leroy JP, Le Henaff B.  Synovial cyst of the hip with revealing neurologic symptoms. J Chir (Paris). 1991;128:424–7. Kim JL, Do JG, Yoon YC, Lim SJ, Sung DH. Intraneural ganglion cyst of the sciatic nerve treated using arthroscopic hip surgery: a case report. PM R. 2019;11:895–9. https://doi.org/10.1002/pmrj.12090. Kim SW, Yoon YC, Sung DH.  Intraneural ganglion cysts originating from the hip joint: a single-center experience. Muscle Nerve. 2022;66:339. https://doi.org/10.1002/mus.27535. Lakhotia D, Prashant K, Shon WY. Ganglion cyst of the hip mimicking lumbar disk herniation—a case report. J Clin Orthop Trauma. 2017;8:153–5. https://doi.org/10.1016/j.jcot.2016.07.001. Lang CJ, Neubauer U, Qaiyumi S, Fahlbusch R.  Intraneural ganglion of the sciatic nerve: detection by ultrasound. J Neurol Neurosurg Psychiatry. 1994;57:870–1. https://doi.org/10.1136/ jnnp.57.7.870-­a. Lee JG, Peo H, Cho JH, Kim DH. Intraneural ganglion cyst of the lumbosacral plexus mimicking L5 radiculopathy: a case report. World J Clin Cases. 2021;9:4433–40. https://doi.org/10.12998/wjcc. v9.i17.4433. Maury F, Migaud H, Cotten A, Hurtevent JF, Flipo RM.  Intraneural myxoid cyst of the common peroneal nerve. A rare cause of sciatic paralysis. Rev Rhum Engl Ed. 1995;62:534–6. Mayer SL, Grewal JS, Gloe T, Khasho CA, Harder S. A rare case of tibial intraneural ganglion cyst arising from the tibiofibular joint. Cureus. 2021;13:e13570. https://doi.org/10.7759/cureus.13570. Panwar J, Mathew A, Thomas BP. Cystic lesions of peripheral nerves: are we missing the diagnosis of the intraneural ganglion cyst? World J Radiol. 2017;9:230–44. https://doi.org/10.4329/wjr.v9.i5.230. Park JH, Jeong HJ, Shin HK, Park SJ, Lee JH, Kim E. Piriformis ganglion: an uncommon cause of sciatica. Orthop Traumatol Surg Res. 2016;102:257–60. https://doi.org/10.1016/j.otsr.2015.11.018. Park SH, Do HK, Jo GY. Compressive peroneal neuropathy by an intraneural ganglion cyst combined with L5 radiculopathy: a case report.

995 Medicine (Baltimore). 2019;98:e17865. https://doi.org/10.1097/ MD.0000000000017865. Rendon D, Pescador D, Cano C, Blanco J. Intraneural ganglion cyst on the external popliteal nerve. BMJ Case Rep. 2014;2014:bcr2013201970. https://doi.org/10.1136/bcr-­2013-­201970. Robertson CM, Robertson RF, Strazerri JC.  Proximal dissection of a popliteal cyst with sciatic nerve compression. Orthopedics. 2003;26:1231–2. https://doi.org/10.3928/0147-­7447-­20031201-­16. Roger J, Chauvin F, Bertani A, Rongieras F, Vitry T, Le Moigne F, et al. Synovial cyst of the knee: a rare case of acute sciatic neuropathy. Ann Phys Rehabil Med. 2017;60:274–6. https://doi.org/10.1016/j. rehab.2016.05.005. Salunke AA, Panchal R.  A paralabral cyst of the hip joint causing sciatica: case report and review of literature. Malays J Med Sci. 2014;21:57–60. Sherman PM, Matchette MW, Sanders TG, Parsons TW.  Acetabular paralabral cyst: an uncommon cause of sciatica. Skelet Radiol. 2003;32:90–4. https://doi.org/10.1007/s00256-­002-­0543-­7. Spinner RJ, Desy NM, Rock MG, Amrami KK.  Peroneal intraneural ganglia. Part I. Techniques for successful diagnosis and treatment. Neurosurg Focus. 2007a;22:E16. Spinner RJ, Desy NM, Rock MG, Amrami KK.  Peroneal intraneural ganglia. Part II. Lessons learned and pitfalls to avoid for successful diagnosis and treatment. Neurosurg Focus. 2007b;22(6):E27. Spinner RJ, Desy NM, Amrami KK. Intraneural ganglion cysts at the hip: the next celestial frontier. Muscle Nerve. 2022;66:236. https:// doi.org/10.1002/mus.27643. Stack RE, Bianco AJ Jr, Maccarty CS.  Compression of the common peroneal nerve by ganglion cysts: report of nine cases. J Bone Joint Surg Am. 1965;47:773–8. Stamiris S, Stamiris D, Sarridimitriou A, Anestiadou E, Karampalis C, Vrangalas V.  Acute complete foot drop caused by intraneural ganglion cyst without a prior traumatic event. Case Rep Orthop. 2020;2020:1904595. https://doi.org/10.1155/2020/1904595. Swartz KR, Wilson D, Boland M, Fee DB. Proximal sciatic nerve intraneural ganglion cyst. Case Rep Med. 2009;2009:810973. https:// doi.org/10.1155/2009/810973. Tehli O, Celikmez RC, Birgili B, Solmaz I, Celik E.  Pure peroneal intraneural ganglion cyst ascending along the sciatic nerve. Turk Neurosurg. 2011;21:254–8. https://doi.org/10.5137/1019-­5149. JTN.2660-­09.1. Wang J, Shao J, Qiu C, Chen Y, Liu B. Synovial cysts of the hip joint: a single-center experience. BMC Surg. 2018;18:113. https://doi. org/10.1186/s12893-­018-­0450-­z. Wu KW, Hu MH, Huang SC, Kuo KN, Yang SH.  Giant ganglionic cyst of the hip as a rare cause of sciatica. J Neurosurg Spine. 2011;14:484–7. https://doi.org/10.3171/2010.12.SPINE10498. Zhang Y, Wei Z, Zhang G, Wang D. Sciatic nerve schwannoma in the lower limb mimicking ganglion cyst. Am J Phys Med Rehabil. 2022;101:e143. https://doi.org/10.1097/PHM.0000000000002013.

Extrapelvic Vascular Lesions

104.1 Generalities and Relevance Extrapelvic vascular causes of sciatic pain represent a rare, heterogeneous group of pathologies that are occasionally confused with traditional spinal causes. However, most patients present a deep gluteal syndrome with sciatic peripheral neuropathy much more than a pure L5/S1 radiculopathy. Besides neurologic pain and symptoms, they may produce a variety of symptoms related to thromboembolic complications. These vascular lesions are variable. Regardless of their origin (arterial, venous, arteriovenous, or capillary), they frequently develop from the gluteal vessels or their branches. The basic mechanism of vascular lesions-related sciatica may be multifactorial depending on their origin, size, and progression (acute, subacute, or chronic). However, most lesions develop progressively, finally leading to the development of symptoms and complications with time. Pathologic, structural, and hemodynamic changes may lead to: (a) Compression and mass effect on the sciatic trunk (until even flattening of the nerve) (b) Local destruction and demyelination of the nerve (c) Diversion of blood flow from the nerve (ischemia due to vascular steal) (d) Venous hypertension These vascular lesions can be congenital, acquired, or idiopathic. Acquired causes are, above all, post-traumatic, including both penetrating and blunt. Trauma also includes iatrogenic injury because of the increase in minimally invasive needle biopsies and interventional surgical procedures. Table 104.1 represents the most frequent extrapelvic vascular etiologies that contribute to sciatic pain previously published in the literature. Although rare, aneurysms arising from persistent sciatic arteries are the most frequent extrapelvic vascular lesions related to sciatica. True and false aneurysms from the gluteal

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Table 104.1  The most frequent extrapelvic vascular etiologies-related sciatica Arterial

Aneurysm

Pseudo-aneurysm

Arteriovenous Arteriovenous fistula

Capillary Venous

Superior gluteal artery Inferior gluteal artery Persistent sciatic artery Superior gluteal artery Inferior gluteal artery Inferior gluteal vessels

Arteriovenous malformation Angioma Venous varix (inferior gluteal venous varicosity, popliteal fossa) Persistent sciatic vein (Klippel-Trenaunay syndrome) Venous malformation (Klippel-Trenaunay syndrome) Angioma

arteries are less common, followed by gluteal venous varicosities. The rest of the lesions are extremely rare. Because of the rarity of these diseases, preoperative diagnosis is often not successful.

104.1.1 Persistent Sciatic Artery Aneurysm Persistent sciatic artery (PSA) is a rare congenital anomaly of blood circulation in which the internal iliac artery and the embryonic axial artery continue to provide the major blood supply to the lower limb after birth. This pathology affects approximately 0.04% of people of both genders equally, with a mean average age of 66 years old, and up to 50% of cases develop an aneurysm. PSA was first described by Green in 1832  in a post-mortem case. There are two types of PSA: complete and incomplete forms. The complete, in which the PSA is the main arterial blood supply of the lower limb, and the incomplete, in which the lower extremity obtains blood flow predominantly from the femoropopliteal artery.

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Classically, the artery extends along and close to the sciatic nerve in the back of the thigh and is crossed obliquely and posteriorly by the long head of the biceps femoris muscle. The most frequent complication of a PSA appears to be aneurysm formation, with a higher risk of thromboembolic complications. Aneurysm formation is probably correlated to the chronic compression of the sciatic artery against the sacrospinal ligament and the repeated flexion of the hip joint.

104.1.2 Gluteal Artery Aneurysms and Pseudoaneurysms Aneurysms of the gluteal artery (GArt) represent less than 1% of all aneurysms. They can be true or false aneurysms (AKA pseudoaneurysms). About 200 cases of gluteal artery aneurysms and pseudoaneurysms have been reported in the literature, commonly from the superior GArt rather than the inferior one. Pseudoaneurysms are mostly secondary to blunt trauma, pelvic fractures, or perforating injuries. In recent years, there has also been an increasing number of cases related to iatrogenic origin. True GArt aneurysms are rather secondary to polyarteritis nodosa, infection (mycotic aneurysm), or atherosclerosis. The earliest case of gluteal artery aneurysm in the literature was reported by Hunter in the 1700s and was treated by proximal arterial ligation. Surgical treatment of gluteal artery aneurysms was introduced by Battle in 1898.

104.1.3 Gluteal Venous Varicosities In 2003,  Bendszus et al. described the first case of sciatic nerve compression from varicotic gluteal veins. Less than 20 cases have been reported in the literature so far. Congenital or post-traumatic, all reported cases arise from the inferior gluteal vein. Some authors hypothesized that gluteal varicosities are the result of piriformis muscle inflammation and repetitive trauma occasioning sciatic pain.

104.2 Clinical Presentations

104  Extrapelvic Vascular Lesions

related sciatica. Indeed, most sciatic pain presents in a gradual subacute mode without low back pain. The majority of patients present with a combination of sciatic pain, progressive numbness and weakness, and sensory loss in the leg. Sphincter dysfunctions are unusual. Occasionally, obturator neuralgia, lower limb weakness, or foot drop has been reported. Neurological presentations are often unilateral, but some lesions manifest bilaterally. Severe pain in the leg and buttocks was provoked by sitting rather than standing and walking. As for other causes of the deep gluteal syndrome, the majority of cases have positive straight-leg raising tests and Freiberg’s sign. Gluteus muscle atrophy may be found in late clinical forms. Clinically, these vascular malformations can be easily confused with soft-tissue neoplasms and infectious collections. Remarkably, patients with PSA or GArt aneurysms present a pulsatile gluteal mass specifically located in the second third of the buttock. This vascular mass is firm and non-­ tender, with a pulsation or thrill on palpation and a bruit on auscultation. However, unless it is large, it is very difficult to examine it clinically because it is located deep within the buttock. Cowie’s sign is considered to be pathognomic for a PSA, but it is known to be inconstant. This sign consists of a diminished or absent femoral pulse in combination with a palpable popliteal pulse. Further symptoms can coexist related to distal thromboembolism, including claudication, rest pain, and ischemia. Patients with gluteal venous varicosities present symptoms that are somewhat similar to those encountered in the piriformis syndrome. Among them, there is severe pain in the buttock and leg that could be induced by sitting or lying on the affected leg and rapidly relieved by standing and walking. Sciatica evolves insidiously with time, and in some cases, it may present edema of the legs. There is also tenderness along the piriformis fossa. Motor and sensory deficits in the affected limb are rare but possible presentations.

104.3 Paraclinic Features

Traditional lumbar computed tomography (CT) and magnetic resonance (MR) imaging are shown to be insufficient. The primary assessment should include a detailed past medi- Most extrapelvic vascular anomalies are diagnosed with cal history and careful neurological and vascular examina- Doppler ultrasound or, more easily, with CT angiography tion. History would include questions about recent injuries, (CTA) and/or MR angiography (MRA). infections, medical procedures, surgeries in the pelvic region, Formal digital subtraction arteriography can also be used. medications, or any underlying health problems. It determines whether there was a traumatic pseudoaneuTypically, sciatic pain caused by traumatic injury or vas- rysm, arteriovenous malformation, arteriovenous fistula, or cular etiologies presents acutely. Nevertheless, there can be a blush from a well-vascularized tumor. In addition, the venous significant delay between the initial trauma or iatrogenic phase of the arteriogram is helpful in demonstrating the procedure and the onset of symptoms in extrapelvic vascular-­ abnormal venous lesion. Arteriography provides information

104.4  Treatment Options

about the classification and outflow of the potential lesions, which is important concerning treatment. While CTA or MRA may delineate the true extent of the lesion, its precise topographic localization, and the involvement of adjacent structures such as the sciatic nerve. Regarding PSA aneurysm, radiological diagnosis should be done with aortography and the whole arterial axis of the low extremity and not just with femoral angiographies because the origin of the vascular anomaly is before the femoral artery and the lesion might be undiagnosed. Classically, the aneurysm had a large neck, and the pseudoaneurysm had a tight one. Sometimes, there is a thrombus formation within the aneurysm. On MR imaging, patients with varicotic gluteal veins present a flow void on gradient echo, and two-dimensional time-of-flight images confirmed the vascular nature of the lesion. There is a hyperintense tubular structure (focal varicosity or varix node) immediately adjacent to the sciatic nerve on T1 and T2 images of the painful area. Sometimes, there is a relative prominence of the inferior gluteal vein. When there is a hematoma, its appearance is variable on a CT-scan and MRI depending on the chronicity of the bleeding due to hemoglobin degradation products. Hyperacute hematoma can present as an isodense collection that is difficult to identify on a CT scan. Contrast enhancement is unusual but depends on the age of the hematoma. On MRI, acute hematoma (1–4 days) is hypointense in all sequences with surrounded edema. Early bleeding (2–7  days) and late (1–3  weeks) subacute periods, hematoma shows high signal intensity on the T1-weighted images secondary to its methemoglobin accumulation. On the T2-weighted images, the signal is hypointense during the early subacute period but hyperintense in the late subacute period. The wall of a chronic hematoma has a hypointense signal on both sequences due to hemosiderin content (c.f. Chap. 105 about Extrapelvic Hematomas). Results of neurophysiologic examinations were mostly normal for age or showed a minor and nonspecific decrease of compound muscle action potentials, F-wave persistence, or sensory action potentials of leg nerves. However, electrodiagnostic investigations can be useful in distinguishing peripheral neuropathies from lumbosacral radiculopathies. Diagnosis of gluteal vessel affection should be suspected principally if there is evidence of compression of the superior gluteal nerve (weakness of gluteus maximus), the pudendal nerve (peroneal sensory loss including the scrotum or labia majora), and the posterior cutaneous nerve of the thigh. Supplementary paraclinical and biological investigations may be used for specific cases in the search for an underlying etiology.

999

104.4 Treatment Options Treatment choice should take into account the lesion size, angioarchitecture, hemodynamics, involvement of other vascular segments, unilaterality or bilaterality of the lesion, compression symptoms, as well as the patient’s comorbidities and general conditions. Generally, asymptomatic, small, or mildly symptomatic lesions should not be treated. While treatment of symptomatic lesions is often challenging. There are different ways to treat these vascular lesions, such as endovascular procedures, surgical repair, percutaneous angioplasty, thrombolysis, or a combination of some of them. Nowadays, endovascular techniques are increasingly used and preferred procedures because of fewer technical risks and complications. Surgical options include the exclusion of the aneurysm with simple ligation or embolization for an incomplete PSA and a complex bypass procedure for a complete PSA. Recently, the repair of a PSA aneurysm may be due to using a traditional or self-expanding stent graft through a minimally invasive endovascular approach. Associated thromboembolic complications can be treated by percutaneous angioplasty, chemical thrombolysis, or anticoagulation. Unfortunately, up to 8% of patients may require amputation. Treatment of GArt aneurysm is indicated by the presence of symptoms that arise from the displacement of adjacent structures if there is a risk of damage to the sciatic nerve and a risk of rupture. In such cases, the goals of surgery are to evacuate the hematoma, ligate the neck of the aneurysm or the parent artery, and release any neural tissues that are compressed by adhesive fibrotic tissues. Sometimes, transperitoneal or retroperitoneal control of the internal iliac artery is mandatory because if bleeding occurs, it is almost impossible to control the feeding artery from extrapelvic access only. Then, the aneurysm can be explored via the posterior approach. Also, the temporary occlusion of the iliac arteries by a percutaneous balloon catheter can be chosen. Regarding gluteal varicosities, when conservative treatment is ineffective (including oral analgesics and muscle relaxants, physical therapy, local analgesic, and corticosteroid injections), decompression surgery is performed to ligate the varicotic portion of the gluteal vein, to resect the varix node, and to release the piriformis muscle. The surgical approach of external and limited internal neurolysis was shown to improve pain in venous angioma, arteriovenous malformation, Klippel-Trenaunay syndrome, and capillary hemangioma. If possible, embolization may n be required for some arteriovenous malformations.

1000

Precautions should be taken for certain large vascular lesions because of the possiblity of severe bleeding when they are treated surgically. Sometimes, preoperative angiography and embolization may be essential.

104.5 Outcome and Prognosis The prognosis is variable depending on the type of vascular lesions, treatment response, and delay of treatment. The prognosis is better for patients with venous or arteriovenous lesions. Traumatic arterial lesions are generally considered to have a less favorable prognosis. Whatever the method of arterial reconstruction or endovascular management, the outcomes were considered satisfactory. However, endovascular procedures are known to have less risk of complications. Indeed, treating physicians should be aware of iatrogenic sciatic nerve damage in patients operated on for sciatic aneurysms. If pressure symptoms are predominant, endovascular treatment compared to the open surgical method takes more time to resolve symptoms. In general, delayed diagnosis of vascular lesions and lack of response to initial traditional therapies are associated with poor prognosis.

Further Reading Agarwal M, Giannoudis PV, Syed AA, Hinsche AF, Matthews SJ, Smith RM.  Pseudoaneurysm of the inferior gluteal artery following polytrauma: diverse presentation of a dangerous complication: a report of two cases. J Orthop Trauma. 2003;17:70–4. https://doi. org/10.1097/00005131-­200301000-­00013. Battle WH.  Case of traumatic gluteal artery aneurysm. Br Med J. 1898;2:1415. Bendszus M, Rieckmann P, Perez J, Koltzenburg M, Reiners K, Solymosi L. Painful vascular compression syndrome of the sciatic nerve caused by gluteal varicosities. Neurology. 2003;61:985–7. https://doi.org/10.1212/wnl.61.7.985. Benevenia J, Zimmerman MG, O’Neil M, Choudhri A. Aneurysm of a congenitally persistent sciatic artery presenting as a soft-tissue mass of the buttock. A case report. J Bone Joint Surg Am. 1995;77:1724– 8. https://doi.org/10.2106/00004623-­199511000-­00013. Charisis N, Giannopoulos S, Tzavellas G, Tassiopoulos A, Koullias G.  Endovascular treatment of persistent sciatic artery aneurysms with primary stenting: a systematic review of the literature. Vasc Endovasc Surg. 2020;54:264–71. https://doi. org/10.1177/1538574419899034. Fukuda H, Onitsuka S, Yoshida S, Hirata Y, Hiromatsu S, Tanaka H.  Endovascular stent-graft repair of a persistent sciatic artery aneurysm. Ann Vasc Dis. 2017;10:246–9. https://doi.org/10.3400/ avd.cr.17-­00021. Green PH.  On a new variety of the femoral artery: with observations. Lancet. 1832;17:730–1. https://doi.org/10.1016/ S0140-­6736(02)83351-­7. Kuwabara M, Onitsuka T, Nakamura K, Nakashima S, Araki K, Yano Y, et al. Persistent sciatic artery aneurysm with ruptured internal iliac artery aneurysm. J Cardiovasc Surg. 1997;38:169–72.

104  Extrapelvic Vascular Lesions Lowenthal RM, Taylor BV, Jones R, Beasley A. Severe persistent sciatic pain and weakness due to a gluteal artery pseudoaneurysm as a complication of bone marrow biopsy. J Clin Neurosci. 2006;13:384–5. https://doi.org/10.1016/j.jocn.2005.03.027. Maniker A, Thurmond J, Padberg FT Jr, Blacksin M, Vingan R.  Traumatic venous varix causing sciatic neuropathy: case report. Neurosurgery. 2004;55:1224. https://doi.org/10.1227/01. neu.0000142354.54603.35. Mariani E, Andreone A, Perini P, Azzarone M, Ucci A, Freyrie A.  Endovascular treatment of persistent sciatic artery occlusion: case report and literature review. Ann Vasc Surg. 2021;74:526.e13– 23. https://doi.org/10.1016/j.avsg.2021.03.022. Mazet N, Soulier-Guerin K, Ruivard M, Garcier JM, Boyer L. Bilateral persistent sciatic artery aneurysm discovered by atypical sciatica: a case report. Cardiovasc Intervent Radiol. 2006;29:1107–10. https:// doi.org/10.1007/s00270-­005-­0140-­y. Modugno P, Amatuzio M, De Filippo CM, Centritto EM, Pierro A, Inglese L. Endovascular treatment of persistent sciatic artery aneurysm with the multilayer stent. J Endovasc Ther. 2014;21:410–3. https://doi.org/10.1583/13-­4568R.1. Nuño-Escobar C, Pérez-Durán MA, Ramos-López R, Hernández Chávez G, Llamas-Macías F, Baltazar-Flores M, et  al. Persistent sciatic artery aneurysm. Ann Vasc Surg. 2013;27(1182):e13–6. https://doi.org/10.1016/j.avsg.2013.04.003. Pacult MA, Henderson FC Jr, Wooster MD, Varma AK. Sciatica caused by venous varix compression of the sciatic nerve. World Neurosurg. 2018;117:242–5. https://doi.org/10.1016/j.wneu.2018.06.058. Papadopoulos SM, McGillicuddy JE, Messina LM.  Pseudoaneurysm of the inferior gluteal artery presenting as sciatic nerve compression. Neurosurgery. 1989;24:926–8. https://doi. org/10.1227/00006123-­198906000-­00025. Proschek R, Fowles JV, Bruneau L. A case of post-traumatic false aneurysm of the superior gluteal artery with compression of the sciatic nerve. Can J Surg. 1983;26:554–5. Rinaldi I, Fitzer PM, Whitley DF, Peach WF Jr, Umstott CE, Graham WH, et  al. Aneurysm of the inferior gluteal artery causing sciatic pain. Case report. J Neurosurg. 1976;44:100–4. https://doi. org/10.3171/jns.1976.44.1.0100. Rovira OJ, Repollet-Otero C, Rodriguez LE, Martinez-Trabal JL.  Symptomatic, unilateral, isolated, complete persistent sciatic vein. J Vasc Surg Venous Lymphat Disord. 2018;6:104–6. https:// doi.org/10.1016/j.jvsv.2017.09.002. Schorn B, Reitmeier F, Falk V, Oestmann JW, Dalichau H, Mohr FW. True aneurysm of the superior gluteal artery: case report and review of the literature. J Vasc Surg. 1995;21:851–4. https://doi. org/10.1016/s0741-­5214(05)80017-­5. Van Gompel JJ, Griessenauer CJ, Scheithauer BW, Amrami KK, Spinner RJ.  Vascular malformations, rare causes of sciatic neuropathy: a case series. Neurosurgery. 2010;67:1133–42. https://doi. org/10.1227/NEU.0b013e3181ecc84e. van Hooft IM, Zeebregts CJ, van Sterkenburg SM, de Vries WR, Reijnen MM.  The persistent sciatic artery. Eur J Vasc Endovasc Surg. 2009;37:585–91. https://doi.org/10.1016/j.ejvs.2009.01.014. Yamamoto H, Yamamoto F, Ishibashi K, Yamaura G, Shiroto K, Motokawa M, et al. Intermediate and long-term outcomes after treating symptomatic persistent sciatic artery using different techniques. Ann Vasc Surg. 2011;25(837):e9–15. https://doi.org/10.1016/j. avsg.2011.02.017. Zafarghandi MR, Akhlaghi H, Shojaiefard A, Farshidfar F.  Sciatic nerve compression resulting from posttraumatic pseudoaneurysm of the superior gluteal artery: a case report and literature review. J Trauma. 2009;66:1731–4. https://doi.org/10.1097/01. ta.0000242215.42642.01. Zhang Z, Zhang X, Yang C, Wen X.  Refractory sciatica caused by gluteal varicosities. Orthopade. 2017;46:781–4. https://doi. org/10.1007/s00132-­017-­3451-­1.

Extrapelvic Hematomas

105.1 Generalities and Relevance Extrapelvic hematomas causing sciatic pain represent a rare, heterogeneous group of pathologies that are occasionally confused with the traditional spinal causes of sciatica. However, most patients with this condition present with sciatic peripheral mononeuropathy, much more than an isolated L5/S1 radiculopathy or pure lumbosacral neuropathy. Extrapelvic localizing bleeding can be acquired, congenital, or idiopathic. Acquired causes are the most frequent, especially following interventional surgical procedures (e.g., hip surgery). Table 105.1 represents the most frequent extrapelvic hematoma etiologies that contribute to sciatic pain previously published in the literature. Whatever the causes, the majority of patients complain, after a variable period of time, of unexpected local pain and swelling, as well as signs of sciatic nerve irritation. Associated sciatic nerve palsy is not rare. There are two main types of circumscribed collection of blood encountered along the sciatic nerve trunk: extraneural (the most common type) and intraneural (within the nerve). Symptomatic extraneural hematoma is often large and causes direct nerve compression. However, the intraneural one is smaller and tends to dissipate along the subepineurial space. Hematoma may develop acutely, subacutely, or chronically, finally leading to the development of symptoms and complications. Pathologic, structural, and hemodynamic changes may lead to: (a) Direct compression and mass effect on the sciatic trunk (increased pressure on the nerve). (b) Local destruction and demyelination of the nerve. (c) Occlusion of the vascular supply of the nerve (vasa nervorum) inducing anoxic ischemia and then infarction. This rare condition may be seen in all ages and genders; however, of the 40 cases reported in the literature, most patients are adult males.

105

Table 105.1  The most frequent extrapelvic hematoma causes-related sciatica Iatrogenic

•  Postoperative complication (mainly hip surgery) • Loco-regional anesthesia procedure (e.g. sciatic nerve block) •  Bone graft donor site (e.g. iliac bone) •  Transvaginal needle biopsy •  Injection targeting sciatic nerve Traumatic • Fall •  Sport injury Vascular •  Aneurysm (e.g. gluteal artery) •  Pseudoaneurysm (traumatic or iatrogenic) Coagulopathy •  Anticoagulant medication •  Inherited bleeding disorder Idiopathic From unknown cause

105.2 Clinical Presentations The initial evaluation should include a detailed past medical history and a careful neurological and vascular examination. History would include questions about recent injuries, medical procedures, surgeries in the pelvic region or lower limb, medications, or any underlying diseases. The clinical presentation may be acute, subacute, or chronic. Most patients complain of unilateral sciatic peripheral mononeuropathy without low back pain or sphincter dysfunction. However, depending on the exact location and size of the hematoma, a deep gluteal syndrome is not uncommon when the bleeding occurs in the buttock area. The dreaded “compartment syndrome” is rare but previously reported. Typically, sciatic pain caused by traumatic injury or vascular etiologies presents acutely. Nevertheless, there can be a significant delay between the initial trauma or iatrogenic procedure and the onset of symptoms in extrapelvic hematoma-­related sciatica. Following a variable interval of time, patients may present mild-to-severe pain of acute or subacute onset in the distribution of the sciatic nerve followed by signs of motor weakness, variable loss of sensa-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_105

1001

105  Extrapelvic Hematomas

1002

tion, and decreased appropriate reflexes in comparison to the contralateral side. Chronic presentations are more subtle. Careful palpation of the buttocks and abdomen should always be part of the workup. Marked local swelling in the region of the sciatic nerve helps guide the diagnosis. Clinical pulsation, thrill on palpation, and a bruit on auscultation suggest the presence of vascular malformation. A previous case had even presented with a chronic expanding hematoma over gluteal muscles mimicking a tumoral lesion. Sometimes, patients may present an additional lumbosacral plexopathy when there is an extension of the hematoma toward the pelvic cavity. Many other concomitant symptoms related to underlying etiologies should be considered in clinical presentations. Neurophysiologic investigations can be very useful, especially if the clinical appearance is imprecise. It may determine the localization and severity of sciatic nerve damage, including axonal loss, demyelination, or both.

105.3 Paraclinic Features Extrapelvic hematomas can be assessed with computer tomography (CT), magnetic resonance (MR) imaging, ultrasonographic and Doppler examinations, and angiographic studies, including CT angiography and/or MR angiography. Biological exploration can be useful in the search for any disorder of hemostasis. Supplementary paraclinical and biological investigations may be used for specific cases in the search for a potential underlying etiology. The appearance of the hematoma itself has variable CT and MRI features depending on the chronicity of the bleeding due to hemoglobin degradation products. Hyperacute hematoma can present as an isodense collection that is difficult to identify on a CT scan. Contrast enhancement is unusual but depends on the age of the hematoma. On MRI, acute hematoma (1–4 days) is hypointense in all sequences with surrounding edema. Early bleeding (2–7 days) and late (1–3 weeks) subacute periods, hematoma shows high signal intensity on the T1-weighted images secondary to its methemoglobin accumulation. On the T2-weighted images, the signal is hypointense during the early subacute period but hyperintense in the late subacute period. The wall of a chronic hematoma has a hypointense signal on both sequences due to hemosiderin content (Table 105.2). A mass that appears following trauma and whose signal changes and size decreases over time is highly suggestive of hematoma. The adjacent affected muscles show more edema, fatty infiltration, and muscular atrophy. The sciatic nerve should be clearly identified. Depending on the severity of the dam-

Table 105.2  MRI findings of hematomas according to their stages of formation Stage Hyperacute

Timing 21 days Slightly hypointense

Hyperintense Hypointense

age, T2-weighted MRI may show hyperintensity in the nerve fibers, abnormal fascicular appearance, nerve enlargement, or deformation. The size and extent of the neural lesion will be better seen on short tau inversion recovery (STIR) sequences. MR neurography is a promising imaging tool for the assessment of peripheral nerve damage. In addition, MR imaging may help identify the potential underlying lesions, such as vascular malformations or tumors. When needed, MR angiography, CT scan angiography, or digital subtraction angiography will be used for identifying potential vascular abnormalities and for assessment of the hemorrhagic source. On imaging, some hematomas can be easily confused with soft-tissue neoplasms (e.g., sarcoma, schwannoma), ganglion cysts, and infectious collections (abscesses).

105.4 Treatment Options No further treatment is needed if the patient has asymptomatic, small, or mildly symptomatic lesions. However, causative and underlying diseases and patient general conditions should always be taken into account. Prompt decompressive surgery, hematoma evacuation, and bleeding control must be considered if the patient complains of unexpected sciatic pain, shows sciatic nerve dysfunction, and/or signs of vascular failure of the lower extremity due to the mass effect of the collection of blood. Combined endovascular embolization and open fasciotomy have been described in some cases for the management of acute compartment syndrome. Management of some arterial lesions may be challenging and some patients require blood transfusions. There are different ways to treat aneurysms or pseudoaneurysms including endovascular procedures, surgical repair, percutaneous angioplasty, or a combination of some of them. Nowadays, endovascular techniques are increasingly used and preferred procedures because of fewer technical risks and complications. Any blood clotting disturbances or subsequent medical complications should be managed adequately.

Further Reading

Physical therapy for sciatic nerve reinforcement should be started as soon as possible to speed up neurological recovery.

105.5 Outcome and Prognosis The prognosis is variable depending on the type of causative factor, delay in management, and treatment response. As so often, missed and delayed diagnoses may negatively affect the prognosis. Indeed, patients’ inadequate management will show little or no neurological recovery. Sometimes, there are life-threatening and debilitating consequences, especially with the associated acute compartment syndrome or the coexistence of multiple serious injuries. Clinicians should be aware of this rare condition. The sooner the patients are diagnosed and treated (nerve decompression), the better the chance is to reverse their symptoms and prevent further neural damage. Iatrogenic-related forms can result in medico-legal claims.

Further Reading Abou-Al-Shaar H, Mahan MA.  Sciatic nerve intraneural hematoma. World Neurosurg. 2019;129:170–1. https://doi.org/10.1016/j. wneu.2019.05.256. Augustin P, Daluzeau N, Dujardin M, Clement O, Denis P. Hematoma of the pyramidal muscle. A complication of anticoagulant treatment. Rev Neurol (Paris). 1984;140:443–5. Braswell MJ, Anderson A, Donohue M, DiVito MC, White PW, Wagner SC.  Delayed presentation of gluteal compartment syndrome due to pseudoaneurysm rupture: a case report. JBJS Case Connect. 2019;9:e0346. https://doi.org/10.2106/JBJS.CC.18.00346. Butt AJ, McCarthy T, Kelly IP, Glynn T, McCoy G.  Sciatic nerve palsy secondary to postoperative haematoma in primary total hip replacement. J Bone Joint Surg Br. 2005;87:1465–7. https://doi. org/10.1302/0301-­620X.87B11.16736. Farrell CM, Springer BD, Haidukewych GJ, Morrey BF. Motor nerve palsy following primary total hip arthroplasty. J Bone Joint Surg Am. 2005;87:2619–25. https://doi.org/10.2106/JBJS.C.01564. Fleming RE Jr, Michelsen CB, Stinchfield FE. Sciatic paralysis. A complication of bleeding following hip surgery. J Bone Joint Surg Am. 1979;61:37–9. Guillemin F, Czorny A, Pourel J. Sciatic nerve compression by hematoma. Case report of a late complication of Harrington’s operation. Spine (Phila Pa 1976). 1991;16:237–9. Katati MJ, Vilchez R, Piñar L, Abdulha O, Horcajadas A, Ros B, et al. Haematoma of the piriformis muscle simulating a giant presacral tumour: unusual case of lumbosacral radiculopathy. Acta Neurochir. 1998;140:403–4. https://doi.org/10.1007/s007010050115. Khattar NK, Parry PV, Agarwal N, George HK, Kretz ES, Larkin TM, et  al. Total hip arthroplasty complicated by a gluteal hematoma

1003 resulting in acute foot drop. Orthopedics. 2016;39:e374–6. https:// doi.org/10.3928/01477447-­20160307-­04. Kitagawa Y, Yokoyama M, Tamai K, Takai S. Chronic expanding hematoma extending over multiple gluteal muscles associated with piriformis syndrome. J Nippon Med Scheme. 2012;79:478–83. https:// doi.org/10.1272/jnms.79.478. K-Reddy VP, Rangasami R, Vignesh G.  Sciatic nerve hematoma—case report. Neurol India. 2021;69:1043–4. https://doi. org/10.4103/0028-­3886.325299. Kuwabara M, Onitsuka T, Nakamura K, Nakashima S, Araki K, Yano Y, et al. Persistent sciatic artery aneurysm with ruptured internal iliac artery aneurysm. J Cardiovasc Surg. 1997;38:169–72. López Domínguez JM, Rodríguez Arce A, Pamiés Andreu E, Gil Néciga E. Compression neuropathy of the sciatic nerve during anticoagulant treatment. Med Clin (Barc). 1993;101:557. Macdonald J, McMahon SE, O’Longain D, Acton JD.  Delayed sciatic nerve compression following hamstring injury. Eur J Orthop Surg Traumatol. 2018;28:305–8. https://doi.org/10.1007/ s00590-­017-­2029-­2. Poivert C, Malinovsky JM. Thigh haematoma after sciatic nerve block and fondaparinux. Ann Fr Anesth Reanim. 2012;31:484–5. https:// doi.org/10.1016/j.annfar.2011.12.015. Richardson RR, Hahn YS, Siqueira EB. Intraneural hematoma of the sciatic nerve. Case report. J Neurosurg. 1978;49:298–300. https:// doi.org/10.3171/jns.1978.49.2.0298. Rog D, Basmajian HG. A rare presentation of sciatic palsy due to hematoma after use of the Kocher-Langenbeck approach to the acetabulum. JBJS Case Connect. 2015;5:e24. https://doi.org/10.2106/JBJS. CC.N.00114. Roth JS, Newman EC.  Gluteal compartment syndrome and sciatica after bone marrow biopsy: a case report and review of the literature. Am Surg. 2002;68:791–4. Saraf SK, Singh OP, Singh VP.  Peripheral nerve complications in hemophilia. J Assoc Physicians India. 2003;51:167–9. Schmalzried TP, Eckardt JJ. Spontaneous gluteal artery rupture resulting in compartment syndrome and sciatic neuropathy. Report of a case in Ehlers-Danlos syndrome. Clin Orthop Relat Res. 1992;275:253–7. Sorensen JV, Christensen KS. Wound hematoma induced sciatic nerve palsy after total hip arthroplasty. J Arthroplast. 1992;7:551. https:// doi.org/10.1016/s0883-­5403(06)80078-­1. Stevens KJ, Banuls M. Sciatic nerve palsy caused by haematoma from iliac bone graft donor site. Eur Spine J. 1994;3:291–3. https://doi. org/10.1007/BF02226583. Wallach HW, Oren ME.  Sciatic nerve compression during anticoagulation therapy. Computerized tomography aids in diagnosis. Arch Neurol. 1979;36:448. https://doi.org/10.1001/ archneur.1979.00500430078016. Ward TRW, Garala K, Dos Remedios I, Lim J.  Piriformis syndrome as a result of intramuscular haematoma mimicking cauda equina effectively treated with piriformis tendon release. BMJ Case Rep. 2022;15:e247988. https://doi.org/10.1136/bcr-­2021-­247988. Weil Y, Mattan Y, Goldman V, Liebergall M. Sciatic nerve palsy due to hematoma after thrombolysis therapy for acute pulmonary embolism after total hip arthroplasty. J Arthroplast. 2006;21:456–9. https://doi.org/10.1016/j.arth.2005.03.042. Yurtseven T, Zileli M, Göker EN, Tavmergen E, Hoşcoşkun C, Parildar M. Gluteal artery pseudoaneurysm, a rare cause of sciatic pain: case report and literature review. J Spinal Disord Tech. 2002;15:330–3. https://doi.org/10.1097/00024720-­200208000-­00013.

Common Peroneal Nerve Entrapment

106.1 Generalities and Relevance Common peroneal nerve entrapment (CPNE) occurs because of the compression of this nerve, typically at the fibular tunnel where the nerve is most vulnerable. Due to its superficial nature, the common peroneal nerve can be easily damaged by various etiologies involving the nerve in the fibular head region. This condition may occur in both acute and chronic forms and can produce symptoms of common peroneal peripheral nerve neuropathy, which is a partial clinical presentation of traditional sciatic neuropathy. However, the most evident manifestation of peroneal neuropathy is a “foot drop.” The common peroneal (AKA fibular) nerve receives innervation from L4 to S1 (mainly L5) nerve roots through the sciatic nerve. In the posterior thigh, the sciatic nerve contains two separate nerves within a common sheath: the common peroneal (AKA fibular or lateral popliteal) nerve and the tibial posterior (AKA medial popliteal) nerve. At a variable level in the thigh, the common peroneal nerve separates completely as an independent nerve before reaching the popliteal fossa and passing around the fibular neck and through the fibular tunnel (Fig. 106.1a). The fibular tunnel, a potential site of nerve entrapment, is composed of the arch formed by: • The peroneus longus muscle • The soleus tendon • The bone of the proximal fibula

106

Below the fibular head, the nerve divides into superficial (AKA musculocutaneous nerve) and deep branches (AKA anterior tibial nerve). • The superficial branch supplies sensation to the dorsal foot and lower two-thirds of the lateral leg as well as motor innervation to the lateral compartment muscles [Foot evertors]. • The deep branch of the peroneal nerve supplies sensation to the dorsal web space between the first (great) and second toes and motor innervation to the muscles of the anterior compartment [Foot and toe extensors]. Common peroneal neuropathy is the most common compressive mononeuropathy of the lower limb and the third most common focal neuropathy overall (after median and ulnar neuropathies). This entity can be encountered at any age and both genders are involved. Most cases are unilateral, but bilateral cases have also been reported. The various causes described can be classified into different categories, such as traumatic or atraumatic causes, acute or chronic, intrinsic or extrinsic compression, and following iatrogenic or non-iatrogenic immobilizations. The most known etiologies that produce CPNE are summarized in Table 106.1. The management of patients with CPNE varies between purely conservative treatment and early surgery. However, when indicated, early surgical decompression leads to good neurological results.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_106

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106  Common Peroneal Nerve Entrapment

1006 Fig. 106.1  Posterior view of the lower limb showing the course of the sciatic nerve in the right side. Note the division of the sciatic nerve into its two terminal branches: the tibial nerve and the common peroneal nerve (a). Anterior view of the right leg showing the cutaneous (sensory) distribution of superficial (pink) and deep (green) peroneal nerves (b)

a

Table 106.1  Most etiologies involved in common peroneal nerve entrapment •  Weight loss (malnutrition) • Prolonged immobilization (surgical procedures, anesthesia, long bed rest, lengthy hospitalization) • Extrinsic compression: leg crossing, prolonged squatting, leg cast, or orthoses • Compression secondary to a space-occupying lesion (e.g., schwannoma, osteochondroma, ganglion cyst) • Traumatic injuries at the fibular head/neck or the knee (knee dislocations and fibular fractures) •  Post-traumatic compartment syndrome •  Chronic exertional compartment syndrome in runners • Surgical procedures (posterolateral corner reconstruction of the knee, high tibial osteotomy, knee arthroplasty) •  Hematoma and vascular lesion (aneurysm) •  Synovial cyst from proximal tibiofibular joint

106.2 Clinical Presentations The initial evaluation of patients with CPNE should include a sufficient and detailed history and physical exam. A recent injury, the presence of signs of trauma, or the existence of scar/wound along the sciatic nerve course without lower back pain may help with the diagnosis. Symptoms can

b

develop acutely or gradually over the course of several weeks, varying in severity. Clinical evaluation is sometimes difficult since symptoms are inaccurate and may be mistaken for many other neurologic, musculoskeletal, or even vascular diseases, especially in chronic and non-traumatic forms. Patients with CPNE may present pain at the site of compression radiating along the anterolateral aspect of the leg from just below the nerve tunnel to the dorsal aspect of the foot. There are also sensory impairments such as burning, tingling, or numbness. The gait may appear unaffected, with weakness noted only when the patient is asked to walk on his or her heels. Motor testing will reveal a weakness in the ankle dorsiflexor, evertor, and toe extensor muscles. The examination may reveal Tinel’s sign over the fibular head or neck. In serious cases, patients complain of difficulty walking with a steppage gait. A classic “foot drop” or a foot slap can be found on examination. A sensory loss could also be observed over the deep and superficial fibular nerve distributions (Fig. 106.1b). Muscle atrophy can be seen in advanced cases. However, treating clinicians should consider some diagnostic differentiation that may be confused with common

106.3  Paraclinic Features

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peroneal nerve neuropathy, such as sciatic neuropathy or L5 radiculopathy. Weakness of foot inversion, decreased Achilles reflex, or sensory deficit in the sole of the foot and lateral knee region should suspect a sciatic nerve cause. Additional weakness in hip abduction or sensory disturbances in the thigh with low back pain may indicate L5 radiculopathy. Many other concomitant signs/symptoms related to underlying etiologies should be considered in clinical presentations. Furthermore, consultations with clinical experts, such as orthopedists, rheumatologists, or neurologists, can aid in the correct diagnosis.

106.3 Paraclinic Features Plain radiography, computed tomography, ultrasonography, angiography, and magnetic resonance (MR) imaging of the knee and contiguous area are helping to elucidate a potential mass lesion compressing the nerve. Depending on the severity of the damage, T2-weighted MR imaging may show hyperintensity in the nerve fibers, abnormal fascicular appearance, nerve enlargement or deformation, and loss of nerve continuity. The size and extent of the lesion will be

a

b

better seen on short tau inversion recovery (STIR) sequences. In addition, affected muscles showed more edema, fatty infiltration, and even muscular atrophy. MR neurography is a promising imaging tool for the assessment of peripheral nerve damage. Besides clinical examination, electrodiagnostic studies are recommended to confirm the diagnosis of peroneal neuropathy, rule out other diagnoses, and guide the prognosis. If there is an abnormality in the peroneal nerve motor innervation, other muscles supplied by the L5 nerve root must be examined to rule out radiculopathy, lumbosacral plexopathy, or sciatic neuropathy. Comparison with the contralateral side is important in quantifying the degree of nerve damage, particularly axon loss. Significant axon damage on nerve conduction studies and electromyography also predict poor outcomes with conservative management. Some specific patients should be assessed with appropriate biologic and imaging tools to exclude hip, sacroiliac joint, and lumbar spine disorders (Figs. 106.2 and 106.3). Sometimes local perineural injection tests of the common peroneal nerve with corticosteroid and local anesthetic under ultrasound guidance can be used for diagnostic and even therapeutic purposes.

c

Fig. 106.2  Case 1. 3D bone reconstructions CT scan (a–c) showing a pedunculated osteochondroma (exostosis) (arrows) of the upper proximal part of the tibial bone with mass effect on the adjacent peroneal neck in a young patient with common peroneal nerve entrapment

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106  Common Peroneal Nerve Entrapment

Fig. 106.3  Case 1. Axial CT scan showing the bone tumor (arrows) on the right compared to the contralateral side

106.4 Treatment Options and Prognosis First-line treatment usually includes removing any reversible etiology that may cause external compression, providing stability to any unstable articulations that may put tension on the common peroneal nerve, and decreasing local inflammation. In addition, some conservative measures include oral anti-inflammatory agents, bed rest, neuropathic drugs, muscle relaxants, and physical therapy. Surgical exploration, decompression, and repair are usually considered in cases of traumatic damage, any sudden clinical worsening, or when there is no improvement within 3  months. When the peroneal nerve is continuous with a good intraoperative nerve action potential, neurolysis has a good outcome. In complete ruptures (a rare occurrence), a repair can be done either with a direct suture or grafting, depending on the size of the lesion and the loss of substance. Any associated lesions will be treated appropriately. Residual neuropathic pain is commonly treated with corresponding medications such as tricyclic antidepressants (e.g., amitriptyline or nortriptyline) and some anticonvulsants (e.g., gabapentin, pregabalin, or carbamazepine). Physical therapy should be started as soon as possible to speed up the recovery of motor function. Overall, CPNE is associated with a good prognosis. Indeed, most patients experience a full return of peroneal nerve function after conservative and/or surgical treatment. Predictors of poorer results consist of evidence of denervation injury on electromyography, severe initial motor deficit, and advanced age of patients. For patients who require prolonged bed rest, prevention comprises frequent and regular repositioning and keeping the lower extremities in a neutral position. In some particular physical activities and positioning, the lateral knee region should be protected to prevent such injuries and decrease the

effect of long-term neuropathies. Furthermore, patient education is important to remove some inciting factors as well as to avoid certain positions, habits, and sports activities. Regarding iatrogenic complications related to knee surgery, some authors use nerve pre-release procedures for common peroneal nerve protection. Iatrogenic-related forms can result in medico-legal claims.

Further Reading Aymen F, Jacem S, Youssef O, Issam A, Abderrazek A. Peroneal nerve palsy caused by a synovial cyst of the proximal tibiofibular joint: a report of two cases and review of the literature. Pan Afr Med J. 2019;34:115. https://doi.org/10.11604/pamj.2019.34.115.18339. Bowley MP, Doughty CT.  Entrapment neuropathies of the lower extremity. Med Clin North Am. 2019;103:371–82. https://doi. org/10.1016/j.mcna.2018.10.013. Broekx S, Van Der Straeten R, D’Haen B, Vandevenne J, Ernon L, Weyns F. Intraneural ganglion cyst of the common peroneal nerve causing foot drop in a 12-year old child. Clin Neurol Neurosurg. 2021;209:106915. https://doi.org/10.1016/j.clineuro.2021.106915. Chahla J, Murray IR, Robinson J, Lagae K, Margheritini F, Fritsch B, et al. Posterolateral corner of the knee: an expert consensus statement on diagnosis, classification, treatment, and rehabilitation. Knee Surg Sports Traumatol Arthrosc. 2019;27:2520–9. https://doi. org/10.1007/s00167-­018-­5260-­4. Consales A, Pacetti M, Imperato A, Valle M, Cama A.  Intraneural ganglia of the common peroneal nerve in children: case report and review of the literature. World Neurosurg. 2016;86(510):e11–7. https://doi.org/10.1016/j.wneu.2015.10.023. Costales JR, Socolovsky M, Sánchez Lázaro JA, Costales DR. Peripheral nerve injuries in the pediatric population: a review of the literature. Part II: Entrapment neuropathies. Childs Nerv Syst. 2019;35:37–45. https://doi.org/10.1007/s00381-­018-­3975-­7. Craig A.  Entrapment neuropathies of the lower extremity. PM R. 2013;5:S31–40. https://doi.org/10.1016/j.pmrj.2013.03.029. Dallari D, Pellacani A, Marinelli A, Verni E, Giunti A. Deep peroneal nerve paresis in a runner caused by ganglion at capitulum peronei. Case report and review of the literature. J Sports Med Phys Fitness. 2004;44:436–40.

Further Reading Distad BJ, Weiss MD.  Clinical and electrodiagnostic features of sciatic neuropathies. Phys Med Rehabil Clin N Am. 2013;24:107–20. https://doi.org/10.1016/j.pmr.2012.08.023. Dy CJ, Inclan PM, Matava MJ, Mackinnon SE, Johnson JE.  Current concepts review: common peroneal nerve palsy after knee dislocations. Foot Ankle Int. 2021;42:658–68. https://doi. org/10.1177/1071100721995421. Fortier LM, Markel M, Thomas BG, Sherman WF, Thomas BH, Kaye AD. An update on peroneal nerve entrapment and neuropathy. Orthop Rev (Pavia). 2021;13:24937. https://doi.org/10.52965/001c.24937. Fridman V, David WS. Electrodiagnostic evaluation of lower extremity mononeuropathies. Neurol Clin. 2012;30:505–28. https://doi. org/10.1016/j.ncl.2011.12.004. Goitz RJ, Tomaino MM.  Management of peroneal nerve injuries associated with knee dislocations. Am J Orthop (Belle Mead NJ). 2003;32:14–6. Heilbrun ME, Tsuruda JS, Townsend JJ, Heilbrun MP. Intraneural perineurioma of the common peroneal nerve. Case report and review of the literature. J Neurosurg. 2001;94:811–5. https://doi.org/10.3171/ jns.2001.94.5.0811. Hobson-Webb LD, Juel VC.  Common entrapment neuropathies. Continuum (Minneap Minn). 2017;23:487–511. https://doi. org/10.1212/CON.0000000000000452. Johnson DB Jr, Marfo KA, Zochowski CG, Berend KR, Lombardi AV Jr. Acute common peroneal nerve decompression after total knee arthroplasty. Orthopedics. 2021;44:e556–62. https://doi. org/10.3928/01477447-­20210618-­17. Jones HR Jr, Felice KJ, Gross PT.  Pediatric peroneal mononeuropathy: a clinical and electromyographic study. Muscle Nerve. 1993;16:1167–73. https://doi.org/10.1002/mus.880161105. Kokkalis ZT, Kalavrytinos D, Kokkineli S, Kouzelis A, Sioutis S, Mavrogenis AF, et  al. Intraneural ganglion cysts of the peroneal nerve. Eur J Orthop Surg Traumatol. 2021;31:1639–45. https://doi. org/10.1007/s00590-­021-­02903-­7. Kokubo R, Kim K, Morimoto D, Isu T, Morita A. Paralysis immediately after surgical decompression for common peroneal nerve entrapment. J Nippon Med Scheme. 2022;90:237. https://doi.org/10.1272/ jnms.JNMS.2023_90-­201. Mackay MJ, Ayres JM, Harmon IP, Tarakemeh A, Brubacher J, Vopat BG. Traumatic peroneal nerve injuries: a systematic review. JBJS Rev. 2022;10. https://doi.org/10.2106/JBJS.RVW.20.00256. Madani S, Doughty C.  Lower extremity entrapment neuropathies. Best Pract Res Clin Rheumatol. 2020;34:101565. https://doi. org/10.1016/j.berh.2020.101565.

1009 Malek E, Salameh JS.  Common entrapment neuropathies. Semin Neurol. 2019;39:549–59. https://doi.org/10.1055/s-­0039-­1693004. Margulis M, Ben Zvi L, Bernfeld B. Bilateral common peroneal nerve entrapment after excessive weight loss: case report and review of the literature. J Foot Ankle Surg. 2018;57:632–4. https://doi. org/10.1053/j.jfas.2017.10.035. Myers RJ, Murdock EE, Farooqi M, Van Ness G, Crawford DC.  A unique case of common peroneal nerve entrapment. Orthopedics. 2015;38:e644–6. https://doi.org/10.3928/01477447-­20150701-­91. Nercessian OA, Ugwonali OF, Park S. Peroneal nerve palsy after total knee arthroplasty. J Arthroplast. 2005;20:1068–73. https://doi. org/10.1016/j.arth.2005.02.010. Oh MW, Gu MS, Kong HH. Bilateral common peroneal neuropathy due to rapid and marked weight loss after biliary surgery: a case report. World J Clin Cases. 2021;9:1909–15. https://doi.org/10.12998/ wjcc.v9.i8.1909. Oosterbos C, Decramer T, Rummens S, Weyns F, Dubuisson A, Ceuppens J, et al. Evidence in peroneal nerve entrapment: a scoping review. Eur J Neurol. 2022;29:665–79. https://doi.org/10.1111/ ene.15145. Power FR, Mohan K, Bergin D, Shannon F. Intra-articular entrapment of an avulsed common peroneal nerve following atypical knee fracture-dislocation. BMJ Case Rep. 2021;14:e242575. https://doi. org/10.1136/bcr-­2021-­242575. Rodriguez-Merchan EC.  Peripheral nerve injuries in haemophilia. Blood Transfus. 2014;12(Suppl 1):s313–8. https://doi. org/10.2450/2012.0111-­12. Szwedowski D, Ambroży J, Grabowski R, Dallo I, Mobasheri A. Diagnosis and treatment of the most common neuropathies following knee injuries and reconstructive surgery—a narrative review. Heliyon. 2021;7:e08032. https://doi.org/10.1016/j.heliyon.2021. e08032. Wai K, Thompson PD, Kimber TE.  Fashion victim: rhabdomyolysis and bilateral peroneal and tibial neuropathies as a result of squatting in ‘skinny jeans’. J Neurol Neurosurg Psychiatry. 2016;87:782. https://doi.org/10.1136/jnnp-­2015-­310628. Wang T, Zhao J, Yuan D.  Successful surgical management of a ruptured popliteal artery aneurysm with acute common peroneal nerve neuropathy: a rare case. Vascular. 2021;29:256–9. https://doi. org/10.1177/1708538120950870.

Herpes Zoster Virus (Shingles) Infection

107.1 Generalities and Relevance Herpes simplex virus (HSV) and varicella-zoster virus (VZV) are both DNA viruses that are closely linked. Initial infection with VZV can cause acute illness (chickenpox), generally in children and young adults. It presents as a highly contagious rash associated with clusters of vesicles on the skin and mucous membranes. Herpes simplex virus infection is a reactivation of the latent VZV within the dorsal root ganglion, which can lead to a large incidence, especially in the elderly and patients with compromised immune function. However, many patients with HSV do not remember previous primary infections (chicken pox). Following its reactivation, HSV subsequently spreads (axoplasmic transport) from the dorsal ganglion down to the affected nerve and then to the skin to produce neuralgic pain and a characteristically segmentally grouped vesicular rash. The anterograde velocity for the HSV is about 5.55 mm/h. The majority of cases of HSV infection involve the thoracic dermatome (56%), the head (20%), and the cervical dermatomes (17%). Infrequently (10%) the virus affects lower nerve divisions and causes symptoms of pain, burning, and dysesthesia. Lumbosacral territories are more rarely involved (less than 5%) and the symptoms may mimic discogenic sciatica. Sciatica related to HSV infection may be associated with a wide variety of neurological manifestations depending on topographic involvement: meningo-radiculopathy, peripheral neuropathy, polyneuropathy, and even lumbosacral plexopathy. Serious forms may be associated with motor deficits known as “segmental zoster paresis,” foot drop, cauda equina syndrome, sphincter disturbances, and post-­ herpetic neuralgia. Nearly one in three people in the United States population will develop an HSV infection over their lifetime, with a rate of 4/1000 case-years annually. This incidence increases to

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Table 107.1  The most common causes of viral reactivation leading to sciatic pain •  Recent trauma (exogenous or iatrogenic) •  Malignant tumors •  Leukemia (acute or chronic) •  Corticosteroids (possibly) • Chronic immunosuppressive disease (e.g., Wegener’s granulomatosis) •  Immunosuppressive drug therapy • Other infectious diseases (e.g., HIV and cytomegalovirus infection) • Postoperative (especially, following orthopedic surgery or spinal surgery) • Ageing •  Chronic lung disease, renal failure, or liver disease

1/100 person-years annually among people greater than 60 years. Herpes zoster is most commonly found in middle-­ aged to elderly patients, with female predominance. There is no exact incidence of lumbosacral herpes zoster stated in the literature. However, less than a hundred cases would have been published. Classically, herpes zoster infection is categorized as spontaneous/primary (70%) and symptomatic/secondary (30%) depending on whether or not there is a predisposing factor. According to a hundred cases already published, the most common causes of viral reactivation leading to sciatic pain are summarized in Table 107.1.

107.2 Clinical Presentations Classically, sciatica related to HSV infection produces neuralgic pain and a segmentally painful vesicular eruption (painful skin rash with blisters) along the sciatic nerve territory (Figs.  107.1 and 107.2). The practitioner should look for a history of recent injuries, infections, surgeries, medications, or possible systemic illness.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_107

1011

1012

107  Herpes Zoster Virus (Shingles) Infection

a

b

c

Fig. 107.1  Painful grouped erythematous plaques with vesicles found along the right L5/S1 dermatomes in a 62-year-old man, about 1 week after the start of right-sided sciatic symptoms (a–c). (Courtesy of Pr. Hatim Belfquih)

Fig. 107.2  Painful low back and buttock pain associated with an adjacent vesicular eruption in a diabetic woman (a, b)

a

b

107.4  Treatment Options and Prognosis

Zooster-induced sciatica is characterized by its acute unilateral burning pain that generally develops 4–7 days before the rash and tenderness. Sensory alterations (e.g., dysesthesia) also arise before the rash. The incidence of segmental muscle weakness and motor paralysis has been reported in up to 30% of cases. Pain is usually independent of the position. Sacral zoster can cause detrusor paralysis, producing urinary retention. Occasionally, the disease may pose a diagnostic challenge, especially before the rash (shingles) starts to develop. In addition, skin rash can be easily mistaken for various other forms of vesicular rash and infections. Physicians should be aware of concomitant skin lesions; in case of doubt, they must refer for a dermatologic evaluation. Rarely, sciatic neuropathy can occur without skin lesions at all (zoster sine herpete). Clinically, Achilles and hamstring reflexes are depressed or absent on the involved side. The Lasègue test may ­sometimes be positive, but sciatic pain rarely arises following back motion or the Valsalva maneuver. The majority of cases have located and limited sciatic neuropathy, unlike disseminated viral infection, which occurs in the context of a patchy or multifocal segmental neuropathic process. Forms with meningo-radicular involvement (meningoradiculitis) can be associated with the meningeal syndrome.

1013

In case of doubt or lacking skin rash (zoster sine herpete), some laboratory diagnostics may be helpful: the VZV DNA polymerase chain reaction (PCR) and the detection of VZV in cell cultures are well-established methods. Furthermore, multinucleated giant cells and epithelial cells containing acidophilic intranuclear inclusion bodies may be seen in the Tzanck smear test. MR imaging might be normal or show rarely minor modifications such as asymmetric nerve enlargement/swelling, increased T2 signal, or mild Gadolinium enhancement at the dorsal root ganglion of the involved side. In patients with electrodiagnostically defined postganglionic lesions, two-­ thirds might show alteration of the plexus or nerves in the MR imaging of the plexus or nerves. However, MR imaging’s utility lies mainly in ruling out other anatomical etiologies for neurological symptoms. Interestingly, MR neurography is a promising imaging tool for the assessment of peripheral nerve damage. It may provide an early diagnosis of axonal neuropathy in its acute stage before electroneuromyography alterations become evident. It also provides a reliable anatomic-pathological localization, which has a good correlation with electrodiagnostic results.

107.4 Treatment Options and Prognosis

The hallmarks of herpes zoster treatment combine rest, anti107.3 Paraclinic Features viral drugs, and pain control. Pain treatment may be performed according to the WHO analgesic ladder and A thorough analysis of the past medical history, accurate co-analgesics, such as amitryptiline. However, most patients neurological tests, and exploration of the skin lesion would did not respond to traditional analgesic drugs. be essential for the final diagnosis. The combined use of Some authors have already reported the efficacy of electrophysiologic exploration and magnetic resonance selective nerve root block and epidural infiltration with ste(MR) imaging may help to diagnose and localize the affected roids. However, these procedures remain controversial site. because of the potential risk of viral reactivation with Normally, electrodiagnostic studies are not required but corticosteroids. can be generally used to evaluate the extent of herpes-zoster-­ Antiviral drugs should be started as soon as possible, at associated neuropathy. The typical electrodiagnostic find- best within the first 3  days after the onset of symptoms. ings in segmental HSV motor weakness are similar to those Antiviral therapy should be given for at least 7 days and can encountered with radiculopathy due to root compression be conducted orally or intravenously. A common antiviral with one important exception: sensory conduction explora- agent is acyclovir. Simple cases of herpes zoster can be mantions in the affected lower limb are nearly constantly abnor- aged as outpatients with oral antivirals and appropriate folmal. Multiple motor action potentials may also be absent or low-­up for resolution and complications. However, patients of reduced amplitude. Unusually, motor nerve conduction who do not improve under oral therapy may require hospitalreduction may be seen. Furthermore, needle examination is ization for intravenous therapy for 7–10  days. In addition, an important means for localizing the lesion: whether is spi- skin eruptions need local wet dressings of post-grouped nal/radicular, within the lumbosacral plexus, or peripheral vesicles. neuropathic. About half of patients with motor symptoms have a good Classically, there are no biological signs of systemic recovery and a third have a fair to good recovery. Some inflammation. Cerebrospinal fluid examination recovered by authors suggest poorer recovery when motor neuropathy prelumbar puncture may provide valuable orientation by show- cedes the rash than when motor neuropathy follows the rash. ing a lymphocytic and mononuclear reaction with mild pro- Furthermore, the outcome seems to be correlated with the tein elevation indicative of meningoradiculitis. severity of the initial electromyographic alterations.

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Postherpetic neuralgia is a painful, numb, itching, tingling sensation that lasts long after the rash has cleared and the skin has healed. The use of medication during the early stages of the disease may help prevent this complication. Again, the sooner treatment is started, the better the outcome.

Further Reading Ablin J, Symon Z, Mevorach D. Sacral herpes-zoster infection presenting as sciatic pain. J Clin Rheumatol. 1996;2:167–9. https://doi. org/10.1097/00124743-­199606000-­00012. Bagaphou TC, Santonastaso D, Gargaglia E, Norgiolini L, Tiburzi C, Cristallini S, et  al. Ultrasound guided continuous sciatic nerve block for acute herpetic neuralgia. Case Rep Anesthesiol. 2019;2019:7948282. https://doi.org/10.1155/2019/7948282. Burkman KA, Gaines RW Jr, Kashani SR, Smith RD. Herpes zoster: a consideration in the differential diagnosis of radiculopathy. Arch Phys Med Rehabil. 1988;69:132–4. Clavel M. Symptomatic herpes zoster and sciatica. A case report. Acta Neurochir. 1981;58:259–63. https://doi.org/10.1007/BF01407132. Hackenberg RK, von den Driesch A, König DP.  Lower back pain with sciatic disorder following L5 dermatome caused by herpes zoster infection. Orthop Rev (Pavia). 2015;7:6046. https://doi. org/10.4081/or.2015.6046. Hung MH, Kuo JR, Huang KF, Wang WC.  Sacral herpes zoster presenting as sciatica. CMAJ. 2010;182:E534. https://doi.org/10.1503/ cmaj.091534. Jain M, Tripathy PR, Mohanty CR.  Post-total knee arthroplasty herpes zoster activation. BMJ Case Rep. 2019;12:e228639. https://doi. org/10.1136/bcr-­2018-­228639. Jensen PK, Andersen EB, Boesen F, Dissing I, Vestergaard BF.  The incidence of herniated disc and varicella zoster virus infection in lumboradicular syndrome. Acta Neurol Scand. 1989;80:142–4. https://doi.org/10.1111/j.1600-­0404.1989.tb03856.x. Ke DS, Hsu CY, Lin CL, Hsu CY, Kao CH. Herpes zoster in patients with sciatica. BMC Musculoskelet Disord. 2020;21:813. https://doi. org/10.1186/s12891-­020-­03847-­5.

107  Herpes Zoster Virus (Shingles) Infection Koda M, Mannoji C, Oikawa M, Murakami M, Okamoto Y, Kon T, et  al. Herpes zoster sciatica mimicking lumbar canal stenosis: a case report. BMC Res Notes. 2015;8:320. https://doi.org/10.1186/ s13104-­015-­1272-­z. Kulcu DG, Naderi S.  Differential diagnosis of intraspinal and extraspinal non-discogenic sciatica. J Clin Neurosci. 2008;15:1246–52. https://doi.org/10.1016/j.jocn.2008.01.017. Leo AM, Kasper DA, Saxena A. Atypical herpes zoster infection preceded by sciatica and foot drop. Arch Dermatol. 2009;145:954–5. https://doi.org/10.1001/archdermatol.2009.168. Merchut MP, Gruener G.  Segmental zoster paresis of limbs. Electromyogr Clin Neurophysiol. 1996;36:369–75. Muché JA, Raghavendra M. Post-surgical herpes zoster of the plantar aspect of the foot. J Pain Symptom Manag. 2003;26:788–90. https:// doi.org/10.1016/s0885-­3924(03)00282-­3. Park KS, Yoon TR, Kim SK, Park HW, Song EK. Acute postoperative herpes zoster with a sciatic nerve distribution after total joint arthroplasty of the ipsilateral hip and contralateral knee. J Arthroplast. 2010;25(497):e11–5. https://doi.org/10.1016/j.arth.2008.10.007. Rota E, Morelli N, Belloni E, Scagnelli P. Early diagnosis of Varicella-­ zoster virus sciatic neuropathy by MRI neurography. Neurol India. 2016;64:1088–9. https://doi.org/10.4103/0028-­3886.190235. Tannous R, Grose C.  Calculation of the anterograde velocity of varicella-­zoster virions in a human sciatic nerve during shingles. J Infect Dis. 2011;203:324–6. https://doi.org/10.1093/infdis/jiq068. Ter Meulen BC, Rath JJ.  Motor radiculopathy caused by varicella zoster virus without skin lesions (‘zoster sine herpete’). Clin Neurol Neurosurg. 2010;112:933. https://doi.org/10.1016/j. clineuro.2010.06.013. Wei FL, Li T, Song Y, Bai LY, Yuan Y, Zhou C, et  al. Sciatic herpes zoster suspected of lumbar disc herniation: an infrequent case report and literature review. Front Surg. 2021;8:663740. https://doi. org/10.3389/fsurg.2021.663740. Wendling D, Langlois S, Lohse A, Toussirot E, Michel F. Herpes zoster sciatica with paresis preceding the skin lesions. Three case-reports. Joint Bone Spine. 2004;71:588–91. https://doi.org/10.1016/j. jbspin.2003.12.002.

108

Decompression Sickness

108.1 Generalities and Relevance Sciatic radicular pain can be the consequence of “decompression sickness” (DS): a condition that results when quick decompression causes nitrogen (less often helium) bubbles to form in the tissues of the body. This complication occurs mainly from underwater diving decompression (Fig. 108.1). Other conditions may be encountered, such as flying in an unpressurized aircraft, working in a caisson, and extra-­ vehicular activity from spacecraft. The gas is thought to arise when a diver ascends too rapidly and the air enlarges quickly, which damages the surrounding tissue and leads to temporary or permanent neurologic disability. Many facets of neurologic decompression sickness are poorly understood, including the pathogenic mechanisms involved in the development of the neurologic disease. Overall, peripheral mononeuropathies occur only rarely in association with decompression illness. Regarding the sciatic nerve and its branches, less than a dozen cases of decompression illness have been reported in the literature. In this particular condition, the presumed mechanisms of sciatic nerve damage include:

Decompression

Isopression

(a) Direct nerve compression in an enclosed space by gas bubbles. (b) A gas bubble causing blood flow obstruction (gas embolism) within the vasa nervorum. (c) Vascular spasm.

Fig. 108.1  Illustration explaining underwater diving decompression. The gas is thought to arise when a diver ascends too rapidly and air enlarges quickly, which damages the surrounding tissue and leads to temporary or permanent neurologic disability

This phenomenon would cause sciatic neuropathy from hypoxia or even ischemic infarct. There are some specific causative factors recognized to the possible increased risk of decompression illness (Fig. 108.2):

• • • •

• Dehydration • Patent foramen oval • Previous injury

The incidence is rare and depends on the length and depth of the dive. The risk for decompression sickness seems higher in men (72%) than in women (28%).

Heavy exercise Cold ambient temperature High body fat content Recent alcohol ingestion

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Fig. 108.2  Main causative factors that can increase the risk of developing decompression sickness

108.2 Clinical Presentations

108.3 Paraclinic Features

The initial evaluation of a patient suspected of decompression sickness should include a detailed history and physical exam. The patient should have an ear examination to look for barotrauma. The disease generally occurs rapidly; most patients with sciatica become symptomatic during ascent or within 10 min of returning to 1 atm of pressure. More rarely, the onset of symptoms is delayed for more than 1 h. Sciatica can be associated with lower limb muscle cramps, numbness, and even peripheral paralysis. Some cases may imitate symptoms of demyelinating disease, particularly multiple sclerosis or traditional discogenic sciatica. Possible concomitant systemic complications of DS should be taken into consideration, especially joint pain, other mild neurologic and visual manifestations, cardiac, pulmonary, or dermatologic disturbances. More serious central nervous system lesions in the spine and brain may occur.

Computed tomography scans can occasionally identify bubbles in DS, but they are not good at determining the correct. Magnetic resonance imaging can be used to rule out a concomitant lumbosacral degenerative disease. DS is ultimately a clinical diagnosis. The goal for treating all patients with symptomatic DS is hyperbaric oxygen therapy without delay in treatment for additional paraclinical examination. However, a chest X-ray is needed, as untreated pneumothorax is an absolute contraindication for hyperbaric oxygen. Later, electromyography can define axonal damage in the nerve, but may not be able to determine the exact location of the lesion.

108.4 Treatment Options and Prognosis All decompression sickness patients should have preliminary treatment with 100% oxygen until hyperbaric oxygen therapy is available. Prompt recompression in a hyperbaric

Further Reading

a

1017

b

Fig. 108.3  Multiplace hyperbaric oxygen chamber (a, b)

chamber (Fig.  108.3) remains the main treatment and can greatly influence the patient’s outcome. Mononeuropathies associated with DS improved after two to eight sessions in the hyperbaric oxygen chamber. Further methods are used, such as rehydration, steroids, acupuncture, and physical therapy. The presence of initial motor weakness or the aggravation of symptoms is predictive of a poor prognosis. Indeed, the prognosis is severity-dependent. In addition, the recovery depends on the time to recompression, availability and time to surface oxygen, and supportive care. Patients who have had previous decompression sickness may have an increased risk for upcoming comparable events.

Further Reading Blatteau JE, Lambrechts K, Ruffez J. Factors influencing the severity of long-term sequelae in fishermen-divers with neurological decompression sickness. Diving Hyperb Med. 2020;50:9–16. https://doi. org/10.28920/dhm50.1.9-­16. Butler WP.  Epidemic decompression sickness: case report, literature review, and clinical commentary. Aviat Space Environ Med. 2002;73:798–804. Decavel P, Bonniaud V, Joassin R, Pérennou D.  Neurogenic bladder dysfunction a main disability of decompression sickness: a case report. Ann Readapt Med Phys. 2007;50:174–8. https://doi. org/10.1016/j.annrmp.2006.12.003. Gempp E, Blatteau JE.  Risk factors and treatment outcome in scuba divers with spinal cord decompression sickness. J Crit Care. 2010;25:236–42. https://doi.org/10.1016/j.jcrc.2009.05.011.

Jan MH, Jankosky CJ.  Multiple sclerosis presenting as neurological decompression sickness in a U.S. navy diver. Aviat Space Environ Med. 2003;74:184–6. Kamtchum Tatuene J, Pignel R, Pollak P, Lovblad KO, Kleinschmidt A, Vargas MI.  Neuroimaging of diving-related decompression illness: current knowledge and perspectives. AJNR Am J Neuroradiol. 2014;35:2039–44. https://doi.org/10.3174/ajnr.A4005. Livingstone DM, Smith KA, Lange B. Scuba diving and otology: a systematic review with recommendations on diagnosis, treatment and post-operative care. Diving Hyperb Med. 2017;47:97–109. https:// doi.org/10.28920/dhm47.2.97-­109. Magriço M, Faustino P, Pereira Coutinho M, Ramos J, Viana-Baptista M.  Decompression sickness or something else? Eur J Neurol. 2021;28:555. https://doi.org/10.1111/ene.14975. Mastaglia FL, McCallum RI, Walder DN. Myelopathy associated with decompression sickness: a report of six cases. Clin Exp Neurol. 1983;19:54–9. Sander HW. Mononeuropathy of the medial branch of the deep peroneal nerve in a scuba diver. J Peripher Nerv Syst. 1999;4:134–7. Stevens DM, Caras BG, Flynn ET, Dutka AJ, Thorp JW, Thalmann ED. Management of herniated intervertebral disks during saturation dives: a case report. Undersea Biomed Res. 1992;19:191–8. Sun Q, Gao G. Decompression sickness. N Engl J Med. 2017;377:1568. https://doi.org/10.1056/NEJMicm1615505. Sykes JJ. Spinal cord decompression sickness: a review of the pathology and some new findings. J R Nav Med Serv. 1985;71:139–43. Yoshiyama M, Asamoto S, Kobayashi N, Sugiyama H, Doi H, Sakagawa H, et al. Spinal cord decompression sickness associated with scuba diving: correlation of immediate and delayed magnetic resonance imaging findings with severity of neurologic impairment—a report on 3 cases. Surg Neurol. 2007;67:283–7. https://doi.org/10.1016/j. surneu.2006.06.036.

Sciatic Double Crush Syndrome Involving Different Sites

109

“One train can hide another” (That is the French standard safety warning at railway crossings)

109.1 Generalities and Relevance The classic definition of the double crush syndrome (DCS) describes a clinical entity of two (or rarely more) sites of compression along a single peripheral nerve. It was first described in 1973 by two Canadian neurologists Adrian Upton and Alan McComas, who postulated that a proximal lesion in a nerve would make that same nerve more vulnerable to additional distal lesions. Furthermore, a poor result obtained after treatment at one site may be the consequence of persistent damage at another site along the peripheral nerve. This unusual condition is often little known and can present an important diagnostic and management problem for physicians. Many of the studies investigating the possibility of DCS involve lesions in the upper extremity. The most usually considered association is between low cervical radiculopathies and carpal tunnel syndrome. On the contrary, very few cases of DCS are documented in the lower extremity. Until now, no more than 30 cases have been described in the surgical literature. Among them, those who presented with sciatic pain are rare. The original definition of DCS, although based on comprehensive pathophysiologic processes, may be limited in scope because many studies have found that “compressive” pathology is not the only contributor to nerve damage. Indeed, a double crush is also more likely in settings where the overall health of the nerve is compromised. The list of such underlying problems is long and comprises endocrine (especially diabetes mellitus), nutritional, metabolic,

genetic, iatrogenic, anatomical, infectious, and systemic pathologies. For some authors, “multifocal neuropathy” is a more appropriate term describing the multiple etiologies of the DCS. For others, these underlying disorders can act as the first “crush” on the nerve rather than spinal nerve compression. Diverse factors may play a role in the development of this syndrome. The most plausible mechanisms are: (a) Disturbance of axonal transport. (b) Deregulation of ion channel. (c) Immune-response inflammation in the dorsal root ganglions. (d) Formation of neuroma-in-continuity. (e) Other factors may also be involved, such as dynamic factors (e.g., altered movement of the nerve and loss of elasticity), underlying abnormalities of the connective tissue, direct neural pressure (neural edema and/or ischemic change), and psychological or psychosocial aspects. (f) Combined mechanisms as a summation of two or more above-mentioned mechanisms. Anatomically, there are two different types of involvement: • DCS may implicate one anatomic level whether it be funicular, radicular, plexopathic, or neuropathic (e.g., both intraspinal and far-lateral root compression). • DCS caused by a remote lesion involving different anatomic levels (e.g., lumbar radiculopathy and sciatic nerve neuropathy).

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1020 Table 109.1  Common proximal and distal sites of compression of DCS in the lower limbs Proximal site Lumbosacral root(s)

Distal site Extraforaminal far lateral lumbosacral roots Sciatic nerve Peroneal nerve at the fibular head Tibial nerve at the popliteal fossa Tibial nerve in the ankle (tarsal tunnel syndrome) Femoral nerve Tibial nerve in the leg Tibial nerve at foot/tarsal tunnel Sciatic nerve Peroneal nerve at the neck of the fibula (proximal)

There are various ways a nerve can be trapped from the lumbosacral spine to the toes. Fortunately, many of these are unusual. The most common DCS of the lower limb involves the proximal sciatic nerve with the common peroneal nerve at the fibular head and L5 radiculopathy with the common peroneal nerve at the head of the fibula/near the knee. The other common situations are summarized in Table 109.1. Many etiologies are involved in sciatica DCS including those: • Degenerative (disc herniation, spinal stenosis, osteophytosis). • Traumatic (direct injury). • Iatrogenic (postoperative). • Vascular (deep venous thrombosis, agenesis of the inferior vena cava). • Congenital (lumbosacral transitional vertebra). • Tumoral (epidermoid cyst). • Ganglion cyst. • Idiopathic. Because there are no standardized or validated criteria to define or diagnose DCS, no true consensus exists regarding its prevalence or general epidemiology. However, the lower limbs are much less affected than the upper limbs.

109.2 Clinical Presentations Clinical symptoms of DCS are greatly variable and generally dependent on several factors, including which particular parts of the nerve are affected, how and when they are affected, the manner in which they are affected (compression vs. stretch), and contributing underlying comorbidities. However, most cases are less obvious and difficult to diagnose because two or more underlying etiologies can become increasingly difficult to elucidate. The treating physician should distinguish between lumbosacral radiculopathies from sacral plexopathies, sciatic peripheral neuropathies, peroneal, and tibial neuropathies. Sciatic neuropathies caused by traumatic injury, acute com-

109  Sciatic Double Crush Syndrome Involving Different Sites

pression, or vascular etiologies present acutely. Apart from that, most sciatic neuropathies present in a gradual, subacute, or chronic manner. Clinical history is important to consider to direct the diagnosis towards a second or more cause. Also, underlying conditions are useful to know. A full physical examination, including gait analysis and appropriate laboratory studies to rule out metabolic, endocrine, or rheumatologic abnormalities should be performed. A work-up of low-back pain, beginning with palpation, active and passive range of motion, and the straight leg raise test, should be performed. Additional palpation, compression, or percussion over the sciatic nerve trunk may produce pain and paresthesias extending along the course of the nerve (Valleix phenomenon). The two or more involved causes may be revealed simultaneously or remotely (step by step) generally after the failure of a first medical and/or surgical treatment. DCS may also mask the typical signs and symptoms of common discogenic sciatica. Many other concomitant symptoms related to underlying etiologies or systemic diseases should be considered in clinical presentations.

109.3 Paraclinic Features Paraclinic studies may determine the level of the nerve lesion and assist the treating physician in the creation of a therapeutic plan. The diagnosis can be suspected on a clinical basis and may be confirmed or supported with electrodiagnostic tests such as nerve conduction explorations and electromyography. Imaging studies such as magnetic resonance imaging (MRI) and ultrasound might show  denervation changes in the involved muscles, help to localize the site of sciatic nerve damage, and provide evidence for the etiology. When needed, the additional measurements may be performed based on data from the history and physical exam. The electrodiagnostic study may be critical in differentiating between a true unifocal compressive neuropathy or a double lesion, specifying the anatomic level of the nerve lesion, as well as defining the relative severity of the two causative etiologies. Also, neurophysiology evaluations have a prognostic value by predicting the prognosis or follow-up course of recovery. MRI is useful for detailing anatomical sites of compression in the lumbosacral spine. However, results should be considered in perspective with other clinical results because they produce somewhat high proportions of false positives in paucisymptomatic patients. Recently, ultrasonography has been utilized in combination with other techniques to improve electrodiagnostic testing for the diagnosis of peripheral nerve conditions, including double crush syndrome.

Further Reading

Sometimes, a subsequent anesthetic block may be helpful for determining the main site of neural dysfunction, especially in patients with imprecise initial clinical and paraclinical results. Computer tomography, ultrasonographic, and angiographic studies, as well as biological explorations, can be useful in the search for any underlying problems.

109.4 Treatment Options and Prognosis The vast majority of DCS cases need an initial provisional of conservative, nonsurgical management. Multimodal therapy may be necessary in order to adequately treat all locations and primary causes of DCS. When two or more distinct locations of damage are present on the nerve, the clinician is tasked with developing a treatment plan involving the correct steps and in the proper order. Anyway, it is important to recognize both problems, as treating only one site can result in residual symptoms from the uncorrected second location of impingement. When one of the two entrapments is more predominant on electrodiagnostic testing, the surgeon can recommend a twostaged approach that starts by treating the more obvious lesion. If significant residual symptoms remain after the first stage, the second part can then be treated (decompressed) as well. Sometimes one site can improve with the conservative method. In this situation, surgery can be restricted to the second area of the crush syndrome. Potential underlying diseases should be evaluated and managed in cooperation with other corresponding specialists (internists, endocrinologists, and other primary care providers and consultants). Overall, when surgery is needed, bimodal decompression for the double crush syndrome is more effective than unimodal surgery. Surgical outcomes for the treatment of DCS are difficult to study due to the rarity of the condition in the lower limbs. However, most patients reported a satisfactory (fair or better) functional outcome. Some patients had residual neurological sequelae that alternated between slight paresthesia and severe foot drop. As found in the upper limbs, it seems that patients with DCS are less responsive to surgical treatment than patients with single lesions.

Further Reading Albert FK, Oldenkott P, Bieker G, Danz B. Lumbar intervertebral disk herniation with a concomitant nerve root neurinoma at the same site. Case report and review of the literature. Neurochirurgia (Stuttg). 1988;31:222–5. https://doi.org/10.1055/s-­2008-­1053942.

1021 Ang CL, Foo LS. Multiple locations of nerve compression: an unusual cause of persistent lower limb paresthesia. J Foot Ankle Surg. 2014;53:763–7. https://doi.org/10.1053/j.jfas.2014.06.013. Augustijn P, Vanneste J. The tarsal tunnel syndrome after a proximal lesion. J Neurol Neurosurg Psychiatry. 1992;55:65–7. https://doi. org/10.1136/jnnp.55.1.65. Bhatia R, Jaunmuktane Z, Zrinzo A, Zrinzo L. Caught between a disc and a tumour: lumbar radiculopathy secondary to disc herniation and filum paraganglioma. Acta Neurochir. 2013;155:315–7. https:// doi.org/10.1007/s00701-­012-­1537-­4. Borgia AV, Hruska JK, Braun K. Double crush syndrome in the lower extremity: a case report. J Am Podiatr Med Assoc. 2012;102:330–3. https://doi.org/10.7547/1020330. Cohen BH, Gaspar MP, Daniels AH, Akelman E, Kane PM. Multifocal neuropathy: expanding the scope of double crush syndrome. J Hand Surg Am. 2016;41:1171–5. https://doi.org/10.1016/j. jhsa.2016.09.009. Dahlin LB, Nordborg C, Lundborg G.  Morphologic changes in nerve cell bodies induced by experimental graded nerve compression. Exp Neurol. 1987;95:611–21. https://doi. org/10.1016/0014-­4886(87)90303-­7. Dellon AL, Mackinnon SE. Chronic nerve compression model for the double crush hypothesis. Ann Plast Surg. 1991;26:259–64. https:// doi.org/10.1097/00000637-­199103000-­00008. Dupeyron A, Lecocq J, Jaulhac B, Isner-Horobeti ME, Vautravers P, Cohen-Solal J, et al. Sciatica, disk herniation, and neuroborreliosis. A report of four cases. Joint Bone Spine. 2004;71:433–7. https:// doi.org/10.1016/j.jbspin.2003.09.002. Fassler PR, Swiontkowski MF, Kilroy AW, Routt ML Jr. Injury of the sciatic nerve associated with acetabular fracture. J Bone Joint Surg Am. 1993;75:1157–66. https://doi. org/10.2106/00004623-­199308000-­00005. Giannoudis PV, Da Costa AA, Raman R, Mohamed AK, Smith RM.  Double-crush syndrome after acetabular fractures. A sign of poor prognosis. J Bone Joint Surg Br. 2005;87:401–7. https://doi. org/10.1302/0301-­620x.87b3.15253. Golovchinsky V.  Double crush syndrome in lower extremities. Electromyogr Clin Neurophysiol. 1998;38:115–20. Kane PM, Daniels AH, Akelman E.  Double crush syndrome. J Am Acad Orthop Surg. 2015;23:558–62. https://doi.org/10.5435/ JAAOS-­D-­14-­00176. Kara M, Ozçakar L, Eken G, Ozen G, Kiraz S.  Deep venous thrombosis and inferior vena cava agenesis causing double crush sciatic neuropathy in Behçet’s disease. Joint Bone Spine. 2008;75:734–6. https://doi.org/10.1016/j.jbspin.2007.12.010. Lakhotia D, Prashant K, Shon WY. Ganglion cyst of the hip mimicking lumbar disk herniation—a case report. J Clin Orthop Trauma. 2017;8:153–5. https://doi.org/10.1016/j.jcot.2016.07.001. Maejima R, Aoyama M, Hara M, Miyachi S. Double crush syndrome of the lower limb in L5 radiculopathy and peroneal neuropathy: a case report. NMC Case Rep J. 2021;8:851–5. https://doi.org/10.2176/ nmccrj.cr.2021-­0169. Nishimura Y, Hara M, Awaya T, Ando R, Eguchi K, Nagashima Y, et al. Possible double crush syndrome caused by iatrogenic acquired lumbosacral epidermoid tumor and concomitant sacral Tarlov cyst. NMC Case Rep J. 2020;7:195–9. https://doi.org/10.2176/nmccrj. cr.2019-­0236. Ochoa-Cacique D, Córdoba-Mosqueda ME, Aguilar-Calderón JR, García-González U, Ibarra-De la Torre A, Reyes-Rodríguez VA, et  al. Double crush syndrome: epidemiology, diagnosis, and treatment results. Neurochirurgie. 2021;67:165–9. https://doi. org/10.1016/j.neuchi.2020.09.011. Pan J, Wang Y, Huang Y.  Coexistence of intervertebral disc herniation with intradural schwannoma in a lumbar segment: a case report. World J Surg Oncol. 2016;14:113. https://doi.org/10.1186/ s12957-­016-­0864-­y.

1022 Park SH, Do HK, Jo GY. Compressive peroneal neuropathy by an intraneural ganglion cyst combined with L5 radiculopathy: a case report. Medicine (Baltimore). 2019;98:e17865. https://doi.org/10.1097/ MD.0000000000017865. Sonkodi B, Bardoni R, Hangody L, Radák Z, Berkes I. Does compression sensory axonopathy in the proximal tibia contribute to noncontact anterior cruciate ligament injury in a causative way?—a new theory for the injury mechanism. Life (Basel). 2021;11:443. https:// doi.org/10.3390/life11050443. Upton AR, McComas AJ.  The double crush in nerve entrapment syndromes. Lancet. 1973;2:359–62. https://doi.org/10.1016/ s0140-­6736(73)93196-­6.

109  Sciatic Double Crush Syndrome Involving Different Sites Wessel LE, Fufa DT, Canham RB, La Bore A, Boyer MI, Calfee RP. Outcomes following peripheral nerve decompression with and without associated double crush syndrome: a case control study. Plast Reconstr Surg. 2017;139:119–27. https://doi.org/10.1097/ PRS.0000000000002863. Wilbourn AJ, Gilliatt RW. Double-crush syndrome: a critical analysis. Neurology. 1997;49:21–9. https://doi.org/10.1212/wnl.49.1.21. Zahir KS, Zahir FS, Thomas JG, Dudrick SJ.  The double-crush phenomenon—an unusual presentation and literature review. Conn Med. 1999;63:535–8.

Phantom Sciatic Pain

110.1 Generalities and Relevance Phantom limb pain (PLP) is a well-known consequence following the amputation of the upper or lower limb, occurring in up to 80% of amputee patients. This condition was first described in 1552 by the French surgeon Ambroise Paré (1510–1590) who clearly differentiated between PLP, phantom sensation, and stump pain (Table 110.1). The American physician Silas Weir Mitchell (1829–1914) created the term “phantom limb” later in 1871. Central neural mechanisms seem to be the major factor in PLP; however, peripheral and psychological mechanisms may also be involved. PLP may be intermittent or continuous, sometimes worsened by emotional stress, anxiety, weather changes, or pressure on the stump. Generally, the pain remains unchanged or improves progressively within a few years even without treatment. However, many patients present obvious physical and psychological disorders. Interestingly, a small percentage of amputee patients experience phantom lumbosacral radiculopathy with sciatic pain caused by degenerative spinal diseases mainly as a lumbar disc herniation (80%) or lumbar spinal stenosis. Less than 20 cases have been previously reported in the literature. In the majority of these patients, the cause of sciatic pain was

110

Table 110.1  The distinction between different forms of perception in the amputated limb Designation Phantom limb pain Phantom limb sensation Stump pain

Characteristics •  Pain perception in the amputated limb • Burning, aching, or cramping pain (classified as neuropathic pain) Perception of still having the amputated limb, but with non-painful residual phenomena • Pain located at the amputation site (residual located limb pain) •  Pressing, throbbing, burning, or squeezing pain • Various causes: infection, wound healing problems, heterotopic ossification, terminal bone overgrowth, soft tissue inflammation, or neuromas

diagnosed late due to the coexistence of an ipsilateral stump or phantom pain (Fig. 110.1). The increased risk of degenerative spine diseases in lowerextremity amputees may be secondary to their atypical position while walking and standing. The pathophysiology of phantom lumbosacral radiculopathy/sciatic pain and its relation to the primary phantom pain are not fully understood but must certainly combine the central and peripheral nervous systems. Phantom sciatica more often develops among adult men between their fourth and sixth decades without recognized risk factors.

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110  Phantom Sciatic Pain

Fig. 110.1  Perception of Phantom leg pain in lower limb amputees

110.2 Clinical Presentations Clinical evaluation of patients with phantom sciatica is often difficult and delayed (from 7 months up to 27 years following the amputation) since symptoms are inaccurate and may be mistaken for classic PLP or stump pain. It is important to differentiate between post-amputation pains and pains not directly related to amputation. Among the 20 cases described, amputations (below or above the knee) are commonly unilateral, and a consequence of traumatic injury and neoplasm. Treated clinicians should be aware of the type of lower limb pain because most patients presented with new-onset radicular pain superimposed on a previous phantom limb or stump pain (Fig. 110.1). The pain was perceived in the corresponding distribution of the sciatic nerve and even distal to the site of the resection of the nerve trunk. Concomitant lower back pain (in 70% of cases) is similar to those encountered in patients with traditional discogenic sciatica.

Closer attention should be paid to spinal and stump examinations to rule out any complications at the local amputation site, including infection, inflammation, heterotopic bone formation, terminal osseous overgrowth, and neuroma. In addition, the gluteal, hip, and retro-trochanteric regions, as well as the course of the sciatic nerve, should be carefully examined to exclude other mimicking or associated pathologies. However, in almost all cases, identifying the nature of the condition by examining the symptoms is often impossible without imaging exploration.

110.3 Imaging Features Magnetic resonance (MR) imaging is the diagnostic procedure of choice for assessing lumbosacral radicular pain and may significantly influence the management of these patients.

Further Reading

For a long time, patients were diagnosed using myelo-­ radiculography. Nevertheless, since 1997, MR imaging was almost the only diagnostic tool used in the literature. In one case, MR imaging was not conclusive because of the presence of artifacts caused by metal hardware; the diagnosis of spinal stenosis was then confirmed by lumbar myelo-­ computed tomography. The most common cause of phantom radiculopathy was lumbar disc herniation, occurring in more than 80% of cases (mainly at L4–L5, L5–S1 level, or both). In one patient, S1 radiculopathy was secondary to an incorrectly positioned sacroiliac screw. Radiologists should be attentive to the paradoxical nodular hypertrophy of the sciatic nerve and lumbosacral plexus that has been previously described in young patients following lower limb above-knee amputations. Also, the presence of a terminal neuroma of the residual lower limb is not rare. Furthermore, patients should be assessed with appropriate imaging tools to exclude hip, sacroiliac joint, and knee disorders. Consultations with experts such as neurologists, orthopedists, physical therapists, and rheumatologists can aid in differential diagnoses. To the best of our knowledge, the contribution of electrodiagnostic studies has never been made in patients with phantom sciatica.

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Further Reading

Aydin SM, Zou SP, Varlotta G, Gharibo C.  Successful treatment of phantom radiculopathy with fluoroscopic epidural steroid injections. Pain Med. 2005;6:266–8. https://doi. org/10.1111/j.1526-­4637.2005.05041.x. Bogdasarian RN, Cai SB, Tran BNN, Ignatiuk A, Lee ES. Surgical prevention of terminal neuroma and phantom limb pain: a literature review. Arch Plast Surg. 2021;48:310–22. https://doi.org/10.5999/ aps.2020.02180. Boroumand MR, Schulz D, Uhl E, Krishnan KG.  Tibioperoneal short circuiting for stump neuroma pain in amputees: revival of an old technique. World Neurosurg. 2015;84:681–7. https://doi. org/10.1016/j.wneu.2015.04.038. Brown WA.  Post amputation phantom limb pain. Dis Nerv Syst. 1968;29:301–6. Brown MD, Hornicek FJ, Lebwohl NH, Phantom sciatica. A case report. J Bone Joint Surg Am. 1997;79:252–3. https://doi. org/10.2106/00004623-­199702000-­00014. Chung BM, Lee GY, Kim WT, Kim I, Lee Y, Park SB. MRI features of symptomatic amputation neuromas. Eur Radiol. 2021;31:7684–95. https://doi.org/10.1007/s00330-­021-­07954-­2. Collins KL, Russell HG, Schumacher PJ, Robinson-Freeman KE, O’Conor EC, Gibney KD, et  al. A review of current theories and treatments for phantom limb pain. J Clin Invest. 2018;128:2168–76. https://doi.org/10.1172/JCI94003. Croci D, Fandino J, Marbacher S. Phantom radiculopathy: case report and review of the literature. World Neurosurg. 2016;90:699.e19–23. https://doi.org/10.1016/j.wneu.2016.02.006. Daniilidis K, Stukenborg-Colsman CM, Ettinger M, Windhagen H. Huge sciatic neuroma presented 40 years after traumatic above knee amputation. Technol Health Care. 2013;21:261–4. https://doi. org/10.3233/THC-­130719. DeGregoris G, Diwan S. Phantom radiculitis effectively treated by fluo110.4 Treatment Options and Prognosis roscopically guided transforaminal epidural steroid injections. Pain Physician. 2010;13:505–8. Regarding sciatic pain, first-line treatment consists of con- Ernberg LA, Adler RS, Lane J. Ultrasound in the detection and treatment of a painful stump neuroma. Skelet Radiol. 2003;32:306–9. servative measures, including rest, analgesics, oral anti-­ https://doi.org/10.1007/s00256-­002-­0606-­9. inflammatory agents, neuropathic drugs, muscle relaxants, Fedele L, Bianchi S, Raffaelli R, Zanconato G, Zanette G.  Phantom and physical therapy. endometriosis of the sciatic nerve. Fertil Steril. 1999;72(4):727–9. The first cases published before the 2000s were treated https://doi.org/10.1016/s0015-­0282(99)00305-­2. through surgical decompression resulting in the resolution of Finneson BE, Haft H, Krueger EG.  Phantom limb syndrome associated with herniated nucleus pulposus. J Neurosurg. 1957;14:344–6. phantom radicular pain for more than 1 year. In more recently https://doi.org/10.3171/jns.1957.14.3.0344. reported cases, patients were treated with fluoroscopically Keil G. So-called initial description of phantom pain by Ambroise Paré. guided translaminar or epidural steroid injection alone, with “Chose digne d’admiration et quasi incredible”: the “douleur ès parties mortes et amputées”. Fortschr Med. 1990;108:62–6. long-term pain relief. Kerimoglu U, Canyigit M.  Paradoxic hypertrophy of the sciatic Methods for treating PLP are not well standardized. nerve in adult patients after above-knee amputation. Acta Radiol. Treatments include, but are not limited to, analgesia, mirror 2007;48:1028–31. https://doi.org/10.1080/02841850701545854. therapy, acupuncture, medications (including tricyclic anti- King AB. Phantom sciatica. AMA Arch Neurol Psychiatr. 1956;76:72– 4. https://doi.org/10.1001/archneurpsyc.1956.02330250074010. depressants, selective serotonin reuptake inhibitors, gabaM, Hunter JE, Malata CM.  Sciatic neuroma presenting forty pentinoids, antiseizure medications, sodium channel Kitcat years after above-knee amputation. Open Orthop J. 2009;3:125–7. blockers, ketamine, opioids, and nonsteroidal anti-­ https://doi.org/10.2174/1874325000903010125. inflammatory drugs), surgery (sympathectomy, dorsal-root Klein SM, Eck J, Nielsen K, Steele SM.  Anesthetizing the phantom: peripheral nerve stimulation of a nonexistent entry-zone lesions, cordotomy, and rhizotomy), invasive and extremity. Anesthesiology. 2004;100:736–7. https://doi. noninvasive neuromodulation procedures, neuroma injecorg/10.1097/00000542-­200403000-­00039. tions and cryoablation techniques, as well as traditional or Krajewski R, Krzymiński T. Atypical pain syndrome after amputation cooled radiofrequency ablation. of the lower limb. Neurol Neurochir Pol. 1984;18:83–5.

1026 Lipton DE, Nagendran T. A rare cause of stump pain—herniated lumbar disc. A case report. Ala Med. 1989;58:39–40. Moll K.  Sciatica as the cause of thigh stump pain. Munch Med Wochenschr. 1961;103:567–8. Moll K, Salanky K. Ischias as the cause of pain in amputation stumps. Orv Hetil. 1958;99:294. Pavy TJ, Doyle DL. Prevention of phantom limb pain by infusion of local anaesthetic into the sciatic nerve. Anaesth Intensive Care. 1996;24:599–600. https://doi.org/10.1177/0310057X9602400517. Perazzini F. Ruptured intervertebral disc in leg amputees. Z Orthop Ihre Grenzgeb. 1952;82:110–6.

110  Phantom Sciatic Pain Smuck M, Christensen S, Lee SS, Sagher O. An unusual cause of S1 radicular pain presenting as early phantom pain in a transfemoral amputee: a case report. Arch Phys Med Rehabil. 2008;89:146–9. https://doi.org/10.1016/j.apmr.2007.08.135. Sonmez E, Yilmaz C, Caner H, Altinors N.  Lumbar disc herniation as a rare cause of stump pain. Case report. J Neurosurg Spine. 2008;8:398–9. https://doi.org/10.3171/SPI/2008/8/4/398. Sperry BP, Cheney CW, Conger A, Shipman H, McCormick ZL. Cooled radiofrequency ablation of a large sciatic neuroma at the infrapiriformis foramen for recalcitrant phantom limb pain in a below-knee amputee. Pain Med. 2021;22:223–6. https://doi.org/10.1093/pm/ pnaa154.

Intracranial Funicular Sciatica

111

111.1 Generalities and Relevance Most cases of sciatic radicular pain have a spinal origin. However, sciatica can be the main presenting symptom in some patients with intracranial lesions. For some authors, this pain is a true “sciatica,” while for others it is only referred to pain known as “sciatica-like leg pain.” Whatever the designation, this is a false localizing presentation that may lead to a missed or delayed diagnosis as well as a possible risk of avoidable operation, particularly when: • The pain is the major symptom. • There is no other neurologic symptom (isolated pain). • There is a co-existing lumbosacral degenerative lesion. According to Larner, a “false localizing sign” can be defined as a confusing clinical condition in which the anatomical situation of the lesion causing neurologic symptoms is distant or remote from the anatomical site predicted by neurologic examination. This referred pain is also called tract pain or “Funicular Pain.” The concept of the “False localizing sign” was first proposed by the English neurologist James Stansfield Collier (1870–1935) in 1904. He observed an additional “false localizing sign” in 12.4% of cases (20 from 161) with intracranial tumors studied clinically and pathologically. According to the position of the causative lesion, false localizing signs can be caused by intraspinal (c.f. Chap. 44), intracranial, or other lesions. The exact pathophysiology of funicular pain due to intracranial lesions is poorly understood. Typically, the pain is attributed to two main mechanisms:

Fig. 111.1  Illustration of the cortical sensory homunculus as seen in the coronal section of the brain. The primary sensory cortex is located in the post-central gyrus of the parietal lobe. Note that the area controlling the lower limb is located medially to the interhemispheric region in the paracentral lobule (stars)

(b) Interruption of the pathways of pain modulation.

In addition, concomitant lower limb motor weakness may be caused by irritation of the descending lateral corticospinal tract (e.g., at the dorsal part of the posterior limb of the inter (a) Irritation of the ascending spinothalamic tract (e.g., at nal capsule) and/or the somatomotor cortex (pre-central the posterior portion of the putamen and the dorsal part gyrus in the posterior frontal lobe) (Figs. 111.2 and 111.3). of the posterior limb of the internal capsule just adjacent The parasagittal area (paracentral lobule) is located at the to the thalamus) and/or the somatosensory cortex (post-­ lower limb of the homunculus. central gyrus in the anterior parietal lobe) (Fig. 111.1).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0_111

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111  Intracranial Funicular Sciatica

Besides the mechanical injury mentioned above, chemical inflammatory factors have been involved. The neurologic lesions can be secondary to: • • • •

Direct neurologic tract compression or displacement. Tract invasion and/or destruction (inflammation, edema). Brain parenchyma, hypoxia, or ischemia. A combination of these three mechanisms.

Only a few cases of sciatica as a false localizing sign were reported in the literature, mainly in patients with contralateral parasagittal or interhemispheric tumors, demyelinating diseases, or neurovascular lesions (e.g., hemorrhage or ischemia).

Fig. 111.2  Illustration of the cortical motor homunculus as seen in the coronal section of the brain. The primary motor cortex is located in the pre-central gyrus of the frontal lobe. Note that the area controlling the lower limb is located medially to the interhemispheric region in the paracentral lobule (stars)

Fig. 111.3  Illustration of the left brain cortical anatomy with the location of the pre-central and post-central gyri. Note the Arabic transcription of the word “Allah” meaning God in Islam (in green color) which makes it possible to remember and find the following important structures: supramarginal gyrus, post-central gyrus, pre-central gyrus, and Broca’s area

Pre-central gyrus

Rolandic fissure (central sulcus) Broca’s area

Post-central gyrus Supramarginal gyrus

Sylvian fissure (Lateral sulcus)

111.3  Imaging Features

1029

111.2 Clinical Presentations

111.3 Imaging Features

Unlike radicular pain, “funicular pain” is continuous, not exacerbated by root stretching (straight leg raising test), diffuse/vague and poorly localized, non-dermatomal distribution, deep, contralateral to intracranial compression, and does not correlate with physical findings. Sciatic pain is frequently not an isolated finding but part of a more extensive neurological syndrome. Some accompanying signs and symptoms may have an important diagnostic value for differentiation between the intracranial lesion and lumbosacral radiculopathy such as:

Cases with no traditional lumbosacral radicular pattern should always be alert to a possible cause of a central nervous system lesion at a higher level even intracranially. Magnetic resonance imaging is now the primary imaging modality of choice that may indicate the exact intracranial topography of the lesions, their exact margins, and inner structures, as well as their relationships with adjacent structures. Electromyography may be performed in the evaluation of a concomitant denervated muscle. The majority of patients with sciatica as a false localizing sign of a contralateral lesion may be associated with one of the following diseases:

• Sensory deficit over the ipsilateral L5 and S1 dermatomes. • Focal motor or sensory seizures beginning in the foot. • Urinary or fecal incontinence. • Headache. • Mental changes as a part of the frontal lobe syndrome. • Presence of upper motor neuron findings such as positive Babinski’s sign, increased deep tendon reflexes, or ankle clonus. Fig. 111.4 Parasagittal extra-axial meningioma (dotted circle) with mass effect on the paracentral lobule as seen on axial CT scan (a), axial (b), and sagittal (c) post-gadolinium T1-weighted MRI as well as on coronal (d) T2-weighted MRI

• Parasagittal or interhemispheric meningioma (extra-axial) (Figs. 111.4 and 111.5) • Metastasis (intra-axial) (Fig. 111.6) • Glioma (intra-axial) (Figs. 111.7, 111.8, and 111.9) • Ischemic stroke (especially anterior cerebral artery territory)

a

b

c

d

1030 Fig. 111.5 Falx interhemispheric (extra-axial) meningioma (stars) manifesting as isolated unilateral sciatic pain. Axial CT scan (a), axial (b), and coronal (c) post-gadolinium T1-weighted MRI as well as sagittal (d) T2-weighted MRI

Fig. 111.6 Parasagittal intra-axial metastasis (arrows) on the right (paracentral lobule) in a patient who presented with contralateral leg pain only. Axial brain CT scan before (a) and after (b) contrast administration

111  Intracranial Funicular Sciatica

a

b

c

d

a

b

111.3  Imaging Features Fig. 111.7  Case 1. Parasagittal brain glioma (dotted circles) of the pre-cental gyrus as seen on axial CT scan before (a) and following (b) contrast injection. Note the position of the central sulcus (Rolandic fissure) (arrows)

1031

a

b

a

c

b

d

e

Fig. 111.8  Case 1. Glioma of the left paracentral lobule as shown on sagittal (a), coronal (b), axial (c, d) post-gadolinium T1-weighted MRI, and axial FLAIR sequences (e). Note the location of the central sulcus (arrows)

1032 Fig. 111.9  Case 1. Stereotactic biopsy of the brain lesion using the Leksell stereotactic frame (a). Biopsy samples (b)

Fig. 111.10 Parasagittal post-central brain vasculitis (arrows) in a young patient who presented with lower limb pain and paresthesia without motor weakness. Axial FLAIR (a, b), sagittal T1- (c), and coronal (d) T2-weighted MRI. (Courtesy of Pr. Oussama Cherkaoui Rhazouani)

111  Intracranial Funicular Sciatica

a

b

a

b

c

d

• Demyelinating plaque • Vasculitis (Fig. 111.10) • Lenticulo-capsular hematoma

111.4 Treatment Options and Prognosis Subsequent management is pathology-dependent.

There was an improvement in the sciatic pain in the patients who had undergone surgical removal of the causative parasagittal lesion (especially tumors). Outcomes and prognosis are related to the causative lesions, co-existing symptoms, and potential underlying diseases.

Further Reading

Further Reading Akhaddar A, Akhaddar H.  A new learning approach for identifying cortical brain areas around the central sulcus using the name of Allah. Surg Neurol Int. 2019;10:244. https://doi.org/10.25259/ SNI_554_2019. Atac K, Ulas UH, Erdogant E, Gokcil Z. Foot drop due to cranial gunshot wound. Mil Med. 2004;169:568–9. https://doi.org/10.7205/ milmed.169.7.568. Baysefer A, Erdoğan E, Sali A, Sirin S, Seber N. Foot drop following brain tumors: case reports. Minim Invasive Neurosurg. 1998;41:97– 8. https://doi.org/10.1055/s-­2008-­1052025. Bielsa C, André M, Schmidt J, Georget AM, Chazal J, Dordain G, Aumaître O. Paralyzing sciatica of central origin. Rev Med Interne. 1997;18:730–1. https://doi.org/10.1016/s0248-­8663(97)83755-­1. Bilić H, Hančević M, Sitaš B, Bilić E. A rare case of parasagittal meningioma causing isolated foot drop: case report and review of the literature. Acta Neurol Belg. 2021;121:555–9. https://doi.org/10.1007/ s13760-­019-­01255-­8. Carolus AE, Becker M, Cuny J, Smektala R, Schmieder K, Brenke C.  The interdisciplinary management of foot drop. Dtsch Arztebl Int. 2019;116:347–54. https://doi.org/10.3238/arztebl.2019.0347. Collier J.  The false localizing signs of intracranial tumor. Brain. 1904;27:490–508. https://doi.org/10.1093/brain/27.4.490. Davis M, Lucatorto M.  The false localizing signs of increased intracranial pressure. J Neurosci Nurs. 1992;24:245–50. https://doi. org/10.1097/01376517-­199210000-­00003. Djekidel M, Harb W. A case of foot drop as an expression of brain metastases? Neurologist. 2006;12:274–5. https://doi.org/10.1097/01. nrl.0000231731.90889.27. Dolev A, Robinson D, Yassin M. A central nervous system tumor mimicking a lumbar spine pathology causing acute foot drop: a case report. J Orthop Case Rep. 2018;8:78–81. https://doi.org/10.13107/ jocr.2250-­0685.1222. Goia E, Hamilton L, Chan J, Wei XC, Mah JK, Rho JM. Unilateral foot drop as an initial presentation of a brain tumor in a child. J Child Neurol. 2014;29:955–8. https://doi.org/10.1177/0883073813479172. Gómez Rodríguez N, Formigo Rodríguez E, Ferreiro Seoane JL, Durán Muñoz O. Chronic pain simulating lumbago/sciatica as the initial manifestation of multiple sclerosis. An Med Interna. 1996;13:353–4.

1033 Kim JS.  Central post-stroke pain or paresthesia in lenticulocapsular hemorrhages. Neurology. 2003;61:679–82. https://doi.org/10.1212/ wnl.61.5.679. Kim KW, Park JS, Koh EJ, Lee JM. Cerebral infarction presenting with unilateral isolated foot drop. J Korean Neurosurg Soc. 2014;56:254– 6. https://doi.org/10.3340/jkns.2014.56.3.254. Larner AJ.  False localising signs. J Neurol Neurosurg Psychiatry. 2003;74:415–8. https://doi.org/10.1136/jnnp.74.4.415. Lee YS, Wang PY. Foot drop caused by a brain tumor: a case report. Acta Neurol Taiwanica. 2009;18:130–1. Louw JA.  The differential diagnosis of neurogenic and referred leg pain. SA Orthop J. 2014;13:52–6. Oktem NB, Tari R, Kotil K, Bilge T. Cerebral contusion as a rare cause of foot drop: case report. Turk Neurosurg. 2012;22:99–101. https:// doi.org/10.5137/1019-­5149.JTN.2962-­10.1. Ricarte IF, Figueiredo MM, Fukuda TG, Pedroso JL, Silva GS. Acute foot drop syndrome mimicking peroneal nerve injury: an atypical presentation of ischemic stroke. J Stroke Cerebrovasc Dis. 2014;23:1229– 31. https://doi.org/10.1016/j.jstrokecerebrovasdis.2013.07.009. Santiago-Palma J, Jimenez J, Barna S, Messina K.  Radicular pain in a patient with aqueductal cerebral stenosis. PM R. 2009;1:884–6. https://doi.org/10.1016/j.pmrj.2009.07.004. Tsang BK, Macdonell R. Multiple sclerosis—diagnosis, management and prognosis. Aust Fam Physician. 2011;40:948–55. Tucker AM, Niu T, Nagasawa DT, Everson R, Sedighim S, Buitrago Blanco MM. CT-negative, MRI GRE-positive primary motor cortex contusion causing isolated foot drop. Surg Neurol Int. 2016;7:S756– 8. https://doi.org/10.4103/2152-­7806.193727. Tural S, Konya D, Sun IH, Gercek A, Ozgen S, Pamir NM. Foot drop: the first sign of an intracranial tumor? J Clin Neurosci. 2007;14:490– 2. https://doi.org/10.1016/j.jocn.2006.01.028. Westhout FD, Paré LS, Linskey ME. Central causes of foot drop: rare and underappreciated differential diagnoses. J Spinal Cord Med. 2007;30:62–6. https://doi.org/10.1080/10790268.2007.11753915. Young WF, Weaver M, Mishra B.  Surgical outcome in patients with coexisting multiple sclerosis and spondylosis. Acta Neurol Scand. 1999;100:84–7. https://doi.org/10.1111/j.1600-­0404.1999. tb01042.x.

Index

A Abdominopelvic/retroperitoneal tumors anatomic structures, 893 clinical presentations, 898–899 mechanisms, 893 origin, 893 paraclinic features, 899–900 primary/secondary sources, 893 prognosis, 900 treatment, 900 Acetabular labrum, 993 Active denervation changes, 961 Acute gluteal/thigh compartment syndrome, 961 Airway, breathing, and circulation (ABCs), 768 Aneurysm, 903–905 Ankylosing spondylitis (AKSP) clinical presentations, 619, 620 definition, 619 extraskeletal structures, 619 history, 619 HLA-B27, 619 incidence, 619 inflammatory process, 619 mechanisms, 619 paraclinic features, 620–625 sacroiliac joints, 619 treatment options and prognosis, 625, 626 Anterior retroperitoneal LDH (ARLDH), 345 anterior zone, 345 axial views, 345 clinical presentations, 346 concomitant spinal stenosis, 347 imaging features, 346–349 neurological presentations, 345 traditional midline approach, 349 treatment, 349 Antiviral drugs, 1013 Arachnoid cysts classification, 729 clinical presentations, 729, 730 definition, 729 history, 729 imaging features, 730, 731 primary spinal forms, 729 secondary spinal forms, 729 treatment options and prognosis, 731 Arachnoiditis ossificans, 679, 681 clinical presentations, 685 definition, 685 factors, 685 history, 685 imaging features, 686, 687

pathogenesis, 685 treatment options and prognosis, 687 types, 685 Arachnoid layer, 685 Articular theory, 993 Avicenna, 15 Axial spondyloarthritis, see Ankylosing spondylitis Axonal and myelin degeneration, 967 Axonotmesis, 967, 970 B Baastrup disease clinical presentation, 870 degenerative modifications, 869, 870 etiology, 869, 870 imaging features computed tomography (CT) scan, 870, 871 fluorodeoxyglucose-positron emission tomography (FDG-­ PET), 870 magnetic resonance imaging (MRI), 870–873 plain radiographs, 870 posterior lumbosacral lesions, 870 short tau inversion recovery (STIR) sequences, 870 incidence, 870 pseudarthrosis, 869 treatment, 873 Back-pocket sciatica, 949 Beatty test, 951 Benign neurogenic tumors, 900, 987 Benign schwannoma, 900 Bertolotti’s syndrome, 98, 531 Castellvi classification, 689, 690 clinical presentations, 690 definition, 689 incidence, 689 LSTV, 689 mobility, 689 paraclinic features, 690–695 treatment options and prognosis, 695, 696 Bilateral acetabular protrusion, 105 Bilateral posterior heel spurs, 113 Bilobed paraspinal granuloma, 212 Bitten apple appearance, 375 Bowstring disease, 60 Bragard’s sign/test, 86 C Calcified synovial cyst, 149 Calcium pyrophosphate dihydrate crystal deposition disease (CPPD), 645

© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. Akhaddar, Atlas of Sciatica, https://doi.org/10.1007/978-3-031-44984-0

1035

1036 Candle wax dripping, 642 Castellvi classification, 689, 690 Cauda equina cavernomas, 795 Cauda equina lesions, 604, 605 Cauda equina syndrome (CES), 64, 70, 179, 365, 534, 538, 559, 571, 577, 620, 654, 779, 783, 788, 870 Cavernous epidural angioma, 166 Cerebrospinal fluid (CSF), 783 Chalk stick/carrot stick fractures, 620 Chemical inflammatory factors, 1028 Chicken pox, 1011 Chondrocalcinosis, 645 Chronic exertional compartment syndrome, 963, 964 Chronic painful lymphedema, 111 Clasp-knife deformity, 697 Coagulopathy, 781 Common peroneal nerve entrapment (CPNE) clinical presentation, 1006, 1007 deep branch, 1005 etiologies, 1005, 1006 paraclinic features, 1007, 1008 prognosis, 1008 superficial branch, 1005 treatment, 1008 Common peroneal neuropathy, 1005 Comorbid spine disorders, 64 Compartment syndrome, 963 Comprehensive pathophysiologic processes, 1019 Compression test, 930 Compression theory, 346 Compressive mononeuropathy, 1005 Conjoined nerve root (CNR), 156 anatomy, 701 clinical presentations, 702 developmental/embryological anomaly, 701 diagnostic confusion, 702 imaging features, 702–706 incidence, 701 spontaneous radicular pain, 702 treatment options and prognosis, 706, 707 Contralateral lumbar disc herniation clinical presentations, 436 false localizing sign, 435 myelo-radiculography, 435 paraclinic features, 436–437 pathophysiological mechanisms, 436 surgical management, 437 treatment, 437 Contralateral lumbosacral radicular symptom, 437 Conus medullaris, 70, 577, 578, 598, 721–723 Conus medullary lesions (CML) back pain, 597 clinical presentations, 604, 605 etiologies, 599–604 imaging features, 605, 606 incidence, 597 lumbosacral radicular symptoms, 597 lumbosacral spine, 597, 599 pathophysiology, 597 treatment options and prognosis, 606 Conus medullary syndrome, 577 Cordonal sciatica, 609 Cram test, 85 Credit-carditis, 949, 959, 960

Index Credit-card-wallet sciatica, 949 Cupping technic (Hijama), 176 Cyclic/catamenial sciatica, 919 Cyclic sciatic pain, 919 D De Anquin’s disease (DAS) characterization, 697 clinical presentations, 698 history, 697, 698 imaging features, 698, 699 incidence, 697 treatment options and prognosis, 699, 700 Decompression sickness (DS), 1015–1017 Deep gluteal space, 947, 949 Deep gluteal syndrome (DGS) anatomic structures, 947–949 associated symptoms, 950 clinical evaluation, 950, 951 deep gluteal space, 947, 949 greater sciatic foramen, 947, 948 internal iliac vessels with sciatic nerve, 948 paraclinic features, 951 piriformis muscle, 947, 948 prognosis, 953 sciatic nerve, 947 subtypes, 949 treatment, 952, 953 Deep infiltrating intrapelvic endometriosis, 921 Deep infiltrative endometriosis, 921 Deep vein thrombosis, 108 Degenerative scoliosis clinical presentations, 521–522 conservative treatment, 528 coronal deviation, 522, 524 imaging features, 522–528 lumbosacral spine, 521 sagittal T2-weighted MRI, 527 sciatica, 521 surgical treatment, 528 Degenerative spine diseases, 1023 Demyelinating plaque, 1032 Diffuse idiopathic skeletal hyperostosis (DISH) clinical presentations, 641, 642 definition, 641 history, 641 lumbar spine, 641 paraclinic features, 642, 643 risk factors, 641 thoracic spine, 641 treatment options and prognosis, 643, 644 Direct intrafascicular injection, 955 Direct nerve compression, 960 Discal cysts, 150 clinical presentations, 417 conservative treatment, 418 degenerative spinal joint disease, 417 etiology, 417 histopathology study, 417 imaging features, 418 nerve decompression, 418 neurologic deficits, 418 overview, 417 postoperative complications, 418, 419

Index Discogenic sciatica, 173 activity modifications, 174 axial lumbosacral CT scan, 175, 176 complementary and alternative therapies, 176 conservative medical management, 173 endoscopic techniques, 190, 191 good/excellent and poor prognoses, 217 intradural LDH, 421 lumbar canal stenosis, 221 medications, 173 patient education, 177 physical therapy programs, 174 post-operative management, 217–222 preoperative sagittal MRI, 219 sacral hiatus epidural infiltration, 176 sciatic scoliotic list, 224 sequels, 222 surgical complications arachnoiditis, 204 deep subcutaneous abscess, 199 definition, 193 dural tear, 194 epidural/extradural fibrosis, 203 epidural hematomas, 208 errors, 210–214 failed back surgery syndrome, 205 FBSS, 205 infections, 198 kneeling operative positioning, 207 lumbar pedicle instrumentation, 208 mortality, 214 neurological complications, 202 nonsurgical (medical) complications, 214 postoperative arachnoiditis, 204 postoperative facial swelling, 207 postoperative pseudomeningocele, 196 postoperative wound problems, 208 pseudoarthrosis, 209 radicular injury, 202 recurrence of LDH, 203 reoperation, 208 retroperitoneal blood vessel injuries, 209 spinal lumbar instability, 208 thromboembolic complications, 208 wrong disc level exploration, 205 surgical outcomes, 217 surgical treatment, 179 automated percutaneous discectomy, 189 bilateral laminectomy, 179 chemonucleolysis, 189 IDET, 190 intradiscal surgical techniques (ISTs), 189 lumbar disc herniation (LDH), 179 open discectomy, 179 percutaneous lumbar nucleoplasty (PLN), 190 posterolateral approach, 190 therapeutic injections, 174 three-dimensional CT scan, 175 Distraction test, 930, 931 Diving decompression, 1015 Double crush syndrome (DCS), 432, 941 bimodal decompression, 1021 clinical presentations, 431, 1020 common proximal and distal sites, 1020 comprehensive pathophysiologic processes, 1019

1037 conservative treatment, 433 definition, 431, 1019 distal lesion, 431, 1019 etiologies, 1020 mechanisms, 1019 outcomes, 1021 overview, 431 paraclinic features, 432–433, 1020, 1021 plausible mechanisms, 431 proximal lesion, 431, 1019 surgical treatment, 433 traditional nerve involvement, 431 treatment, 1021 types, 1019 Dural ectasia clinical presentations, 726 grading system, 725 imaging features, 726 lumbosacral area, 725, 726 pathogenesis, 725 symptoms, 725 treatment options and prognosis, 727 Dysesthesias, 535 E Electrophysiologic evaluation, sciatic hernia, 937 Empty thecal sac sign, 681 Empyema, 669, 675 Endometriosis clinical manifestation, 919 clinical presentations, 920 cyclic/catamenial sciatica, 919 definition, 919 genetic and environmental factors, 919 incidence, 919 paraclinic features, 920 prognosis, 922 size, 919 treatment options, 921–922 Enlarged dural sac, see Dural ectasia Enthesopathy, 641 Eosinophilic granuloma (EOG), see Langerhans cell histiocytosis Epidural abscesses clinical presentations, 670 development, 669 empyema, 669 imaging features, 670–672 intraspinal infections, 669 laboratory findings, 672 predisposing factors, 669 spinal epidural space, 669 treatment options and prognosis, 672, 673 Epidural gas pseudocyst clinical presentation, 875 imaging features, 875–878 incidence, 875 overview, 875 treatment, 879 Epidural lipomatosis clinical presentations, 571 etiology, 571 magnetic resonance imaging, 571–575 obesity, 571 treatment options and prognosis, 575

1038 Epidural non-vertebral tumors (ENVT) clinical presentations, 568 epidural metastasis, 560 MALT lymphoma, 565 non-vertebral tumors, 559 operative view, 568 overview, 559 paraclinic features, 568 spinal imaging, 569 treatments, 569 Epidural schwannomas, 569 Exostosis, 978, 983 Extradural fibrous entrapment, 161 Extrafascicular injection, 955 Extraneural hematoma, 1001 Extrapelvic extrinsic sciatic neuropathy, 978 Extrapelvic hematomas causes-related sciatica, 1001 clinical presentations, 1001, 1002 outcomes, 1003 paraclinic features, 1002 prognosis, 1003 treatment, 1002, 1003 types, 1001 Extrapelvic musculoskeletal and soft tissues tumors anatomic structures, 977 clinical evaluation, 978 paraclinic features, 978–980, 982, 983 prognosis, 984 sources, 977 treatment, 984 types, 977 Extrapelvic vascular lesions clinical presentation, 998 etiologies-related sciatica, 997 gluteal artery aneurysm, 998 gluteal venous varicosities, 998 mechanism of, 997 outcomes, 1000 paraclinic features, 998–999 pathologic, structural, and hemodynamic changes, 997 persistent sciatic artery aneurysm, 997 prognosis, 1000 pseudoaneurysms, 998 treatment, 999 F FABER test, 85, 930, 931 Facet joint, 49, 627, 629 FADER test, 85 Failed Back Surgery Syndrome (FBSS), 205 FAIR test, 950 False localizing sign, 609, 1027–1029 Far-out syndrome, 531 Fasciitis ossificans, 973 Fasciotomy, 962, 964, 965 Fat-wallet syndrome, 949, 959, 960 Femoral condylar osteomyelitis, 107 Femoral neck fracture, 105 Femoral neuralgia, 4 Femoral stretch test, 85 Fibrodysplasia ossificans progressiva, 973 Fibular tunnel, 1005 Filum terminale syndrome, 709 First-line therapy, 900 Flaval cysts, see Ligamentum flavum

Index Flowing candle wax, 642 Foot drop, 1005, 1006 Foraminal and extraforaminal lumbar disc herniations (FELDH), 262 imaging features, 263 lateral/foraminal sequestrated disc fragment, 267 Sagittal T2-weighted MRI, 265 overview, 261 surgical strategy, 269 treatment options, 269 Forestier’s disease, see Diffuse idiopathic skeletal hyperostosis Freiberg test, 950 Funicular pain, 1027, 1029 Furcal nerve, 335 G Gaenslen’s test/maneuver, 930, 931 Ganglion cyst, 993 See also Posterior longitudinal ligament (PLL) cyst Ganglioneuroma, 587, 588 Ganglionic cysts, 993, 994 Gas embolism, 1015 Gastrointestinal/genitourinary tract infections, 907 Glioma, 1029, 1031 Gluteal artery (GArt) aneurysm, 998, 999 Gluteal hernia, see Sciatic hernia Gluteal/high intracompartmental pressure, 964 Gluteal intramuscular injection (GIMIJ) clinical presentation, 955 complication, 955 diagnosis, 955 paraclinical features, 956 prevention, 956 shut up and butt out, 956 treatment options and prognosis, 956 Gluteal/thigh compartment syndromes, 959, 961, 964 Gluteal/thigh fasciotomy, 965 Gluteal venous varicosities, 998 Gout clinical presentations, 645 crystal deposition disease, 645 definition, 645 facet joints, 645 paraclinic features, 646, 647 treatment options and prognosis, 647 Gouty arthritis, 645 Granulomatous inflammatory reaction, 213 Gunshot wounds (GSWs), 767 H Hamstring syndrome, 947, 950–952 Hand-Schüller-Christian disease, 649 Hernia incisurae ischiadicae, see Sciatic hernia Herpes simplex virus (HSV), 1011, 1013 Herpes zoster virus (shingles) infection causes, 1011 clinical presentations, 1011–1013 paraclinic features, 1013 prognosis, 1013–1014 treatment, 1013 Heterotopic bone formation, 973 Heterotopic ossification (HOS) acquired causes, 973 Brooker classification, 973 clinical presentation, 974

Index Della Valle classification, 973 genetic, 973 nongenetic, 973 normal compact and cancellous bones, 974 paraclinic features, 974, 975 pathophysiology, 974 prognosis, 976 treatment, 975 HLA-B27, 619 Hoffmann-Tinel-sign, 920 Human immunodeficiency virus (HIV), 907 Hyperbaric oxygen therapy, 962, 965, 1016 Hypertrichosis, 715 I Iatrogenic incidental durotomy, 429 Incorrect positioning, 959–961 Induction theory, 919 Inflammatory disorders, 94 Intracompartmental pressures, 964 Intracranial funicular Sciatica, 1027–1030, 1032 Intracranial hypotension, 800 Intradiscal electrothermal annuloplasty (IDEA), 190 Intradural lumbar disk herniation (LDH), 421 anatomical localization, 421 annulus fibrosus, 421 clinical presentations, 422 discogenic sciatica, 421 fibrin glue reinforcement, 426 iatrogenic incidental durotomy, 425 imaging features, 422–424 mechanism of, 422 MRI features, 425 sagittal T2-weighted MRI, 424 schematic representation, 421 treatment, 425 Intradural lumbosacral tumors (IDLSTum) causes, 577, 578 CES and conus medullaris syndrome, 577, 578 clinical presentations, 578–585, 587–590, 592–594 filum terminale, 577 imaging features, 579, 580 nerve sheath tumors, 577 pathophysiology, 577 Intradural schwannoma, 169 Intraneural ganglionic cyst (INGC), 993, 994 Intraneural hematoma, 1001 Intraneural perineurioma, 987 Intraneural/perineural neurotoxic substances, 955 Intrapelvic and retroperitoneal vascular lesions basic mechanism, 903 clinical presentations, 904 congenital, acquired, or idiopathic causes, 903 delayed diagnosis, 905 etiological factors, 903 imaging tools, 904, 905 paraclinic features, 904–905 pathologic, structural, and hemodynamic changes, 903 prognosis, 905 treatment, 905 Intrapelvic lymphoma, 899 Intraradicular disc herniation clinical presentation, 427, 428 exact localization, 427 exact mechanism, 428

1039 imaging features, 428–429 intraoperative views, 430 overview, 427 schematic representation, 427 treatment, 429 Intraspinal funicular sciatica clinical presentations, 609, 610 definition, 609 false localizing sign, 609 imaging features, 610, 612, 613, 615–617 neurologic lesions, 609 pathophysiology, 609 risk, 609 treatment options and prognosis, 617 Intrinsic sciatic nerve tumors benign neurogenic tumors, 987 clinical presentation, 988 downstream/upstream, 987 histological diagnosis, 987 paraclinic features, 988–990 prognosis, 990 treatment, 990 Inverted Mercedes Benz sign, 780, 784 Ischemic stroke, 1029 Ischemic theory, 346 Ischialgia, 3 Ischiatic hernia, see Sciatic hernia Ischiocele, see Sciatic hernia Ischiofemoral impingement test, 951 Isolated L5/S1 radiculopathy, 907 Ivory vertebra, 632 K Kernohan notch-like phenomenon, 435 Kissing spines syndrome, see Baastrup disease L Langerhans cell histiocytosis (LCH) clinical presentations, 649, 650 history, 649 paraclinic features, 650 reticulo-endothelial system, 649 skeletal system, 649 treatment options and prognosis, 651 Lasègue test, 951, 1013 Lenticulo-capsular hematoma, 1032 Leptomeningeal cysts, see Leptomeningeal cysts Letterer-Siwe disease, 649 Ligamentum flavum clinical presentation, 845 histopathology study, 845 imaging features, 845–848 neurological disturbance, 845 pathogenesis, 845 recurrence, 849 synovial/ganglion cysts, 845 treatment, 848, 849 Ligamentum flavum hematoma clinical presentation, 791 histopathology, 791 imaging features, 791, 792 overview, 791 pathogenesis and etiology, 791 treatment, 792, 793

1040 Ligamentum flavum ossification (LFO) causes, 851 clinical presentation, 851 definition, 851 histopathology study, 851 imaging features, 852–854 prevalence, 851 prognosis, 854 treatment, 854 Lindner’s sign, 86 Localized hypertrophic neuropathy, see Intraneural perineurioma Lotus neuropathy, 959 “Lotus position” in yoga, 960 Lower limb, 968 Lower limb compartment syndrome, 961 causes, 963 clinical presentations, 964 with contiguous necrotizing fasciitis, 963 with debridement and skin grafting, 963 etiologies, 963, 964 missed/late diagnosis, 965 morbidity and mortality rate, 965 outcome, 965 paraclinical features, 964 prognostic factor, 965 treatment options, 964, 965 Lower limb pain, 1024 Lumbar adhesive arachnoiditis arachnoiditis ossificans, 679 cause, 679 clinical presentations, 680 definition, 679 factors, 679 histopathology, 679 imaging features, 681, 682 treatment options and prognosis, 683 Lumbar disc herniation (LDH), 21, 48, 58, 120, 121, 147, 179 anterior retroperitoneal zone, 240 antero-posterior plain film, 247 apophyseal ring fracture, 159 axial lumbosacral CT scan, 256 bilateral approach, 185 cavernous hemangioma, 168 central zone, 239 classification, 239 clinical presentations, 243–245 conjoined nerve root (CNR), 156 differential diagnosis, 147 discal cyst, 149 disc extrusion, 239 discitis, 153 enlarged nerve root, 157 epidural abscess, 155 epidural gas, 150 epidural hematoma, 167 extradural non-vertebral tumors, 164 extraforaminal zone, 240 extrusion, 239 foraminal and extraforaminal, 182, 240 imaging features, 246–255 intraoperative fluoroscopy, 179 intraoperative views, 257 invasive microdiscectomy approach, 184 knee-chest position, 180 ligamentum flavum, 182 lumbar epidural varices (LEV), 168

Index MaXcess* tubular retractor system, 188 METRx* tubular retractor system, 189 nerve root tumors, 165 neuroimaging, 250–251 operative view, 184 osteophytes, 151 outcome and prognosis, 258 palpation and identification, 181 paramedian disc herniation, 252 posterior longitudinal ligament (OPLL), 152 postoperative disorders, 160–164 protrusion, 239 sciatic scoliosis, 245 spinal hematomas, 167 spontaneous regression C5–C6 disk herniation, 366 clinical presentations, 367–368 clinical symptoms, 370, 371 definition of, 365 extruded and migrated L4–L5 disk herniation, 368 lumbar axial CT scan, 370 mechanism, 365 overview, 365 paraclinical features, 368–369 treatment, 370 subarticular zone, 239 surgical muscular retractor, 182 synovial cysts, 148 treatment options, 255–256 tumors, 164 unilateral approach, 180 unilateral posterolateral (extracanal) approach, 183 Lumbar epidural varices (LEVs) clinical manifestations, 788 clinical presentation, 788 epidural venous system, 787 extensive varices, 788 imaging features, 788, 789 local varices, 788 pathogenesis, 787, 788 segmentary varices, 788 symptomatic LEV, 787, 788 treatment, 789 Lumbar intervertebral disc calcification, 378 Lumbar microdiscectomy, 185 Lumbar spinal stenosis (LSS), 441 central and lateral recess stenosis, 442 clinical presentations, 461 degenerative canal stenosis, 459 degenerative spinal stenosis, 470 endoscopic technics, 466 etiologies, 442 grading system, 441 intraoperative view, 471 isthmic spondylolisthesis, 451 laminectomy via posterior bilateral approach, 465 management, 464 neurogenic claudication, 474 neurologic symptoms, 441 nonoperative treatment, 468 paraclinic features, 462–463 posterior longitudinal ligament, 452 Schizas grading system, 442 sciatic pain recurrence, 473 treatment, 464 trefoil appearance, 446

Index zygapophyseal facet joint hypertrophy, 441 Lumbar spondylolysis, 477 clinical presentations, 478 congenital defects, 477 continuous double-hump sign, 485 endoscopic technics, 488 failed back surgery syndrome, 477 intervertebral foramina., 477 intraoperative views, 489 isthmic stress fracture, 482 paraclinic features, 478 prevalence of, 478 surgical intervention, 488 treatment, 488 Lumboradicular pain, 619 Lumbosacral extraforaminal stenosis (LSES) causes of, 531 clinical presentations, 534 dysesthesias, 535 overview, 531 paraclinic features, 534–535 pseudoarticulation, 533 treatment, 535 unilateral posterolateral (extracanal) approach, 535 Lumbosacral herpes zoster, 1011 Lumbosacral nerve roots, see Nerve roots extradural fibrous entrapment Lumbosacral plexopathy, 893, 895, 898–900 Lumbosacral plexus, 930, 1025 Lumbosacral radicular pain, 4, 1024 Lumbosacral radiculopathy, 103 Lumbosacral spinal tumors (LSTum), 537 benign and malignant spinal tumors, 537 biologic findings, 540 clinical presentations, 538 diagnosis of, 539 etiological treatment, 556 microscopic image, 542 osteoblastoma, 552 papillary thyroid carcinoma, 538 paraclinic features, 538–540 percutaneous transpedicular approach, 556 solitary plasmacytoma, 549 spinal imaging, 540 treatment, 556 tumors, 537 vertebroepidural aggressive hemangioma, 555 Lumbosacral spine, 627 Lumbosacral spine fractures and dislocations (LSFD) anatomy and biomechanical characteristics, 743 classification, 743, 744 clinical presentation, 744 by falls, 743 by motor vehicle accidents, 743 outcome and prognosis, 752 paraclinic features computed tomography (CT) scan, 745–751 electromyography (EMG), 747 magnetic resonance imaging (MRI), 747, 749 plain radiographies, 746 pathologic fractures, 743 sciatica, 743, 744 sporting accidents, 743 treatment, 751, 752 Lumbosacral transitional vertebra (LSTV), 689, 690 Lumbosacral vertebra, 25 Lymphoma, 977, 980

1041 M Malignant peripheral nerve sheath tumors (MPNSTs), 893, 898–900, 987, 988 Marfan syndrome, 725 Massive lumbar disc herniation (MALDH) axial view, 313 clinical presentations, 314 imaging features, 314–315 overview, 313 plain film radiography, 319 prognosis, 324–325 sequestrated disc fragment, 322 treatment options, 324 undiagnosed giant, 316 Matrix metalloproteinase (MMP), 365 Mechanical injury, 1028 Mechanosensitivity, 58 Meningeal cysts, 733 Meningoradiculitis, 1013 Metaplastic theory, 919 Metastasis, 1029 Meyerding’s radiographic classification, 510 Migrated lumbar disc herniation (MigLDH), 279 clinical presentations, 280 conservative management, 293 coronal views, 279 differential diagnosis, 280 dural weakness, 293 etiopathogenic mechanism, 280 operative view, 290 paraclinic features, 280–281 percutaneous endoscopic lumbar discectomy, 293 Missile injuries, 767 MR myelography (MRM), 132 MR neurography (MRN), 132, 978 Multifocal neuropathy, 941, 1019 Multiplanar reconstructions (MPR), 686 Muscle denervation and atrophy, 994 Muscle membrane instability, 961 Mycobacterium tuberculosis, 666 Myelography, 134, 679 Myositis ossificans, 973 N Naffziger sign/test, 86 Neidre and MacNab’s classification, 41 Nerve action potential (NAP), 956 Nerve conduction studies, 961 Nerve injection injury (NII), 956 Nerve injury, 955 Nerve root fibers, 734 Nerve roots extradural fibrous entrapment clinical presentation, 825 etiologies, 825 fibrous adhesive entrapment, 825 imaging features, 825 pathogenesis, 825 treatment, 825 Nerve roots herniation and entrapment clinical symptoms, 831 dural tear, 827, 829, 830 factors, 827, 831 imaging features, 831 mechanisms, 827 structures, 827, 828 thecal sac, 827, 830 treatment, 831, 832

1042 Neurilemmoma, see Schwannoma Neurinoma, see Schwannoma Neurofibromas, 893, 899, 900, 987, 988, 990 Neurofibromatosis type 1 (NF-1), 898, 899, 987, 988 Neurologic decompression sickness, 1015 Neurologic lesions, 1028 Neurologic pain, 990 Neurolymphomatous tumors, 989 Neuropathic residual pain, 994 Neurotmesis, 967, 970 Nitrogen, 1015 Non-discogenic sciatica causes, 915 clinical presentations, 916 during pregnancy, 915 fetal position, 915, 916 imaging features, 916 mechanism of injury, 915 treatment, 916 Non-missile injuries, 767 Nonsteroidal anti-inflammatory drugs (NSAIDs), 625 O Ossification of the posterior longitudinal ligament (OPLL) clinical presentation, 861 etiology, 861 frequency, 861 histopathology, 861 imaging features, 861–866 outcome, 866 overview, 861 prevalence, 861 treatment, 866 Osteitis deformans, 631 Osteochondroma, 978, 983 Osteoporosis, 755 P Pace sign, 950, 951 Pagetic vertebral ankylosis, 632 Paget’s disease clinical presentations, 631, 632 history, 631 incidence, 631 mechanisms, 631 paraclinic features, 632, 633 treatment options and prognosis, 634 Painful metatarsophalangeal arthritis, 113 Painful sciatic lumbosacral plexus endometriosis, 900 Painful sciatic nerve endometriosis, 921 Pain-relieving drugs, 625 Paracentral lobule, 1027–1031 Paraganglioma, 589, 590 Paralabral cysts, 993 Paralysis, types, 955 Paralytic foot drop, 956 Paramedian muscle splitting technique, 272 Para-osteoarthropathy, see Heterotopic ossification Parasagittal/interhemispheric meningioma, 1029 Paraspinal muscle appearance, 142 Paresthesia, 3 Patellofemoral osteoarthritis, 108 Pathophysiologic mechanisms bowstring disease, 60

Index compression mechanisms, 58 immunological mechanisms, 59 inflammatory mechanisms, 59 lumbosacral discogenic radicular pain, 57 neuropathy, 57 neurophysiologic effects, 59 plexopathy, 57 psychological disorders, 59–60 radiculopathy, 57 vascular mechanisms, 59 Pediatric lumbar disk herniations (LDHs), 351 clinical presentation, 356 clinical presentations, 355 imaging features, 357 operative view, 354 outcomes, 359 overview, 351 sagittal reconstructions, 357 treatment, 358 Pelvic and intrapelvic infections anatomic structures, 907 clinical presentations, 908 contamination, 907 imaging features, 908–912 isolated L5/S1 radiculopathy/pure sciatic peripheral mononeuropathy, 907 laboratory findings, 912 outcome, 913 pathogens, 907 treatment, 912 Penetrating spine injuries clinical presentation, 768 imaging assessment, 768–771 missile injuries, 767 neurological symptoms and deficits, 767 non-missile injuries, 767 outcomes and prognosis, 772 timing of onset and progression, 767 treatment, 771, 772 Percutaneous aspiration of the cyst, 994 Percutaneous laser disc decompression (PLDD), 190 Perineural cyst, see Tarlov cysts Peripheral mononeuropathies, 1015 Peripheral nerve injury, 967 Peritoneal diverticulum, 919 Peroneal nerve neuropathy, 959 Persistent sciatic artery (PSA) aneurysms, 997–999 Phantom leg pain (PLP), 1024 Phantom limb pain (PLP), 1023–1025 Phantom limb sensation, 1023 Phantom lumbosacral radiculopathy, 1023 Phantom radicular pain, 1025 Phantom radiculopathy, 1025 Phantom sciatica, 1024, 1025 Pigmented villonodular synovitis (PVNS) clinical presentations, 627 etiology, 627 history, 627 incidence, 627 paraclinic features, 627–629 treatment options and prognosis, 629 Piriformis syndrome, 947, 949–951, 953 Plexiform neurofibroma, 987 Polymicrobial infections, 666 Posterior epidural migration of lumbar intervertebral disk fragments (PEMLIFs), 327 axial view, 327

Index clinical presentations, 328 development of, 327 differential diagnoses, 333 imaging features, 328 intraoperative view, 331, 333 microsurgical technics, 334 treatment, 333 Posterior longitudinal ligament (PLL) cyst anterolateral spinal epidural space, 857 clinical presentation, 857, 858 etiology, 857 histopathology, 857 imaging features, 858 treatment, 859 Posterior ring apophysis separation (PRAS), 861 calcified herniated disc, 373 clinical presentations, 375 conservative management, 391 diagnostic features, 375 etiologies of, 391 histopathologic appearance, 375 intraoperative and postoperative complications, 393 intraoperative view, 395 limbus vertebral fracture, 373 lumbar axial CT scan, 381 nonoperative treatment, 391 overview, 373 pathogenesis of, 374 Personal classification, 374 sagittal section, 373 sagittal T2-weighted MRI, 386 spinal imaging, 378 spontaneous regression, 392 Takata classification, 374 unilateral approach, 393 Postherpetic neuralgia, 1014 Postoperative sciatica clinical presentation, 821, 822 computed tomography (CT) scan, 816, 818–822 etiology, 801 magnetic resonance imaging (MRI), 802–814, 822 outcome and prognosis, 823 plain radiography, 822 predictive factors, 801–802 treatment, 822, 823 Pott’s disease, 658, 659 Pregnancy, LDH, 361 clinical presentations, 362 imaging features, 362 outcomes, 363 pathophysiologic mechanisms, 361 scannopelvimetry, 362 surgical complications, 363 treatment, 362 Progressive osseous heteroplasia, 973 Prolonged immobilization, 959–961 Pseudoaneurysm, 904, 905, 998 Pseudoarticulation, 696 Pseudogout clinical presentations, 645 crystal deposition disease, 645 definition, 645 facet joints, 645 paraclinic features, 646, 647 treatment options and prognosis, 647 Pseudomeningoceles, 827

1043 Pseudo-sciatica, 924 Psoriasis, 619, 620 Pure lumbosacral neuropathy, 1001 Pure sciatic peripheral mononeuropathy, 907 Pyramidal muscle, 947–953 R Rbdominopelvic/retroperitoneal tumors, 893 Recurrent lumbar disc herniation (R-LDH) axial lumbar, 402 clinical presentations, 401 complications, 414 definition, 401 discogenic sciatica, 410 imaging features, 402 polypoid mass hypointense, 402 postoperative risks, 401 sciatic pain recurrence, 407 surgical options, 414 surgical technique, 413 treatment, 413 Relaxin, 915 Retrograde menstruation, 919 Rhabdomyolysis, 961–965 Rheumatoid arthritis (RA) clinical presentations, 637, 638 erosive features, 637 facet joints and vertebral endplates, 637 history, 637 lumbar spine lesions, 637 paraclinic features, 638 peripheral joints, 637 prevalence, 637 sciatica, 637 treatment options and prognosis, 638, 639 S Sacral plexus, 25 Sacral stress fractures (SSF) classification, 763, 764 clinical presentation, 764 fatigue fractures, 763 imaging and biological studies, 764, 765 insufficiency fractures, 763 pathologic fractures, 763 prognosis, 765 treatment, 765 Sacral thrust test, 930 Sacroiliac joint disorders clinical presentations, 929–932 etiology, 929 paraclinic features, 932 pathologies and injuries, 925 prognosis, 932 pseudo-sciatica and true sciatic pain, 924 treatment, 932 Sacroiliitis, 923, 925, 930, 932 Sacrosciatic hernia, see Sciatic hernia Sacrum, 733 Sarcoma, 893, 895, 899, 977, 979, 980 Scannopelvimetry, 362 Scelalgia, 3 Schober test, 89 Schwannoma, 895, 898, 900, 987, 988

1044 Sciatica, 3, 645 Arabic and Persian civilization, 13–17 biblical period, 8–10 cautery scars, 230 chondrocytes proliferation, 54 clinical examination, 69 discogenic sciatica, 69 hip abduction, 81 hip adduction, 81 lumbosacral plexopathy, 70 lumbosacral spine, 72 patient history, 69–71 peripheral neuropathies, 71 postural deformities, 73 psychological factors, 90 psychosocial factors, 90 psychotic disorders, 90 trunk lateral flexion, 73 clinical presentations, 631, 632 definitions, 3 development of, 48 DISH, 641 eighteenth century, 17–18 epidemiology, 48, 66 epidural and selective nerve root blocks, 145 etiological classifications, 49–51 Greco-Roman period, 10–13 history, 7, 631 imaging evaluations, 118 imaging examinations, 133 imaging modalities coronal lumbosacral spinal, 143 CT scan, 128 discography, 127 magnetic resonance imaging, 128–133 myelography, 125 plain radiography, 125 strengths and weaknesses, 117 incidence, 631 ironing, 229 laboratory investigations, 145 laboratory tests, 145 LSFD, 744 lumbar disc herniation (LDH), 48, 63, 66 lumbosacral spine, 131 antero-posterior plain film, 131 plain film radiographs, 132 plain radiographs, 129 mechanisms, 631 muscle strength grading, 80 natural history, 63 neurophysiological studies, 124–125 nineteenth century, 18–19 nonmedical literature, 232 overview, 47 paraclinic features, 632, 633 paraclinical evaluations, 117 paravertebral muscle atrophy, 49 physical examination, 71 Bragard’s sign/test, 75 Cram test, 72 crossed straight leg raising test, 72 FABER test, 72 FADER test, 75 femoral stretch test, 72

Index heel walking test, 76 Lindner’s sign, 75 Naffziger sign/test, 75 sitting knee extension test, 75 straight leg raising (SLR) test, 72 tiptoe walking test, 75 rectal and genital examination, 71 representation of, 53 resorption/regression, 65 risk factors, 48 scarification scars, 231 spinal etiologies, 118 spontaneous regression, 65 traditional therapeutic practices, 227–231 treatment options and prognosis, 634 twentieth century, 19–21 word cloud, 4 Sciatic hernia anatomic defect, 935 clinical diagnosis, 936 clinical presentation, 936 definition, 935 neurovascular structures, 935, 936 paraclinic features, 936, 937 pelvic anatomy, 935 prognosis, 937 treatment, 937 Sciatic lumbosacral plexopathy clinical presentation, 889 definition, 883, 884 etiologies, 884–889 imaging studies, 889, 890 pain, weakness, and sensory loss, 884 pathological involvement, 884 pathophysiology, 884 prevalence, 884 prognosis, 890 treatment, 890 Sciatic nerve, 1024, 1025 anatomical variations, 43 compression, 998 damage, 960, 1015 decompression, 952 endometriosis, 919, 921 entrapment, 949 histological architecture, 26 histological structures, 29 intervertebral disc, 29, 38 intervertebral foraminal area, 41–42 lumbar nerve roots, 40 lumbar spine, 29 lumbosacral spine, 26, 29 anterior view, 30 lateral view, 32 posterior view, 31 motor and sensory supply, 42 motor distribution, 43 origin and course, 25 overview, 25 peripheral nerve of the lower limb, 968 peroneal division, 26 peroneal nerve, 42 piriformis muscle, 28, 44 posterior lumbar musculature, 39 posterior view, 44

Index reinforcement, 965 sensory supply, 43 tibial nerve, 42 Sciatic neuritis, 955 Sciatic neuropathy, 1015 due to external nerve pressure, 959 incidence, 960, 968 predisposing factors, 960 See also Sciatic peripheral neuropathy Sciatic notch, 935 Sciatic pain, 629, 1023, 1025 Sciatic pain in name only (SPINO), 93 ankle pain, 103 buttock pain, 103 cardiorespiratory diseases, 101 complex regional pain syndrome, 105 fibromyalgia syndrome, 105 foot pain, 103 gastrointestinal diseases, 101 genitourinary diseases, 101 hip pain, 101 inappropriate (nonorganic) symptoms, 114 intracranial diseases, 113 knee pain, 103 leg pain, 103 magnetic resonance imaging (MRI), 93 muscular tenderness, 103 myelopathies, 96–97 peripheral nerves, 105 physical examination, 114 plexopathies, 101 proctological diseases, 101 psoas iliac bursitis, 101 psychological and psychiatric disorders, 113–114 psychosocial factors, 113 radiculopathies, 97–101 referred pain, 93 spinal lesions, 94–96 stump pain, 105 tendino-bursitis, 101 Sciatic peripheral neuropathy causes, 941 clinical presentations, 944 etiology, 941–944 paraclinic features, 944, 945 vs. peripheral nervous system, 941 prognosis, 945 surgical indications, 945 treatment, 945 Sciatic-related intrapelvic infections, 908 Scoliosis, 534 Scottie Dog Model, 479, 511 Seated piriformis stretch test, 951 Sequestrated lumbar disc herniation (SeqLDH), 297 clinical presentations, 298 differential diagnosis, 310 endoscopic interlaminar approach, 311 foraminal sequestrated disc fragment, 308 free fragment sizes, 297 gadolinium injection, 304 operative view, 301 paraclinic features, 298–300 peripheral ring enhancement, 306 spontaneous regression, 310 treatment, 310

1045 Short tau inversion recovery sequence (STIR), 620 Sitting knee extension test, 86 Soft tissue lipoma, 978 Soft tissue metastasis, 899, 980 Spina bifida, 697, 698, 700 Spina bifida occulta, 37 Spinal canal stenosis, 620 Spinal cavernous angiomas (SpCA) causes, 795 clinical presentation, 795, 796 etiologies, 795 imaging, 796, 797 pathogenesis, 795 pathologic, structural, and hemodynamic changes, 795 treatment, 798 Spinal epidural angiolipoma, 569 Spinal epidural hematoma clinical presentation, 776 definition, 775 factors, 775 imaging features, 776, 777 intraspinal hematomas, 776 pathophysiology, 775 treatment, 777 Spinal epidural meningiomas, 569 Spinal hygromas clinical symptoms, 799 imaging features, 799 pathologies, 799 treatment, 799, 800 Spinal instability, 634, 649, 746 Spinal non-discogenic etiology, 49 Spinal pathologic fractures (SPF) causes, 755 clinical presentation, 756 etiologies, 755 incidence and prevalence, 755, 756 lifetime risk, 755 mechanisms, 755 osteoporosis, 755 paraclinic features computed tomography (CT) scan, 756–760 fluorodeoxyglucose positron emission tomography (FDG-PET) scan, 758 magnetic resonance imaging (MRI), 757 percutaneous vertebral biopsy, 758, 761 prognosis, 761 progressive collapse, 755 treatment, 761 Spinal sciatica, 335 bilateral sciatic pain, 339 clinical presentations, 336 concomitant herniated disc, 342 conservative management, 342 false localizing sign, 335 normal anatomical distribution, 336 paraclinic features, 336 pathophysiology, 335 surgical decompression, 342 surgical management, 342 Spinal subarachnoid hematoma clinical signs and symptoms, 783 definition, 783 etiological factors, 783 imaging features, 784 literature review, 783 treatment, 784

1046 Spinal subdural hematoma clinical presentation, 779 definition, 779 factors/etiologies, 779 imaging features, 779–781 treatment, 781 Spinous engagement syndrome, see De Anquin’s disease Spondylarthropathies, 929 Spondylodiscitis clinical presentations, 654 development, 653 imaging features, 655–661, 663–666 isolated discitis, 653 laboratory findings, 666 modes of distribution, 654 sciatica, 653 treatment options and prognosis, 666, 667 types, 653 Spondylolisthesis bilateral facet joint, 498 clinical presentations, 509–510 degree of slippage, 495 endoscopic technics, 514 etiologies, 497 interarticularis defect, 503 intraoperative view, 514, 518 neurologic deficits, 509 nocturnal pain, 509 operative view, 519 outcomes, 514 overview, 495 paraclinic features, 510–514 pseudo-lumbar disc herniation, 502 risk factors, 497 sciatic pain, 497 spino-pelvic sagittal alignment, 514 treatment, 514 unusual and fracture forms, 497 Staghorn renal stone, 103 Stenosis, 641, 644 Straight leg raising (SLR) test, 85, 510 Stretch injury, 960 Stump pain, 1023 Subdural abscesses clinical presentations, 675, 676 development, 675 imaging features, 676 intraspinal canal infections, 675 lumbar, 675 predisposing factors, 675 suppurative material, 675 Suppuration, 670, 676 Syndesmophyte, 620 Synovial cysts, 993 clinical presentation, 836 cuboid/pseudostratified membrane, 835 etiology, 835 imaging features computed tomography (CT) scan, 836, 837 magnetic resonance imaging (MRI), 836, 838–841 treatment, 842 unilateral/bilateral, 836 Syringomyelia, 721

Index T Tarlov cysts asymptomatic cases, 734 classification, 733–736 clinical presentation, 735 imaging features, 735–740 prognosis, 741 symptomatic cases, 734 theories, 734 treatment, 741 Terminal ventricle, 721 Tethered spinal cord syndrome (TSCS) clinical presentations, 714, 715 diagnose, 709 etiologies, 709 imaging features, 715–717 neurological manifestations, 709–714 signs and progressive symptoms, 712 spinal cord tethering, 709 treatment options and prognosis, 717, 718 Thigh thrust test, 930 Tiptoe walking test, 87 Toilet bowl neuropathy, 959 Tophaceous gout, 645 Traumatic sciatic nerve lesions clinical presentation, 968–970 etiologies, 967 histological structures, 968 outcomes, 970 paraclinic features, 970 preventive measures, 971 prognosis, 971 treatment options, 970 True sciatic pain, 924 Truncal sciatica, 920 Trunk extension ability test, 74 Tuberculous spondylodiscitis, 154 Typical peripheral nerve, 968 U Unilateral peripheral mononeuropathy, 987 Ureteric sciatic hernias, 936 V Valleix phenomenon, 944 Varicella-zoster virus (VZV), 1011, 1013 Varicosis, 787 Varix, 789 Vascular lesions-related sciatica, 903 Vascular malformation, 779, 780, 784 Vasculitis, 1032 Ventriculus terminalis (VTER) cerebrospinal fluid, 721 clinical presentation, 721 clinical symptoms, 721 definition, 721 history, 721 imaging features, 722 residual ependymal cyst, 721 treatment options and prognosis, 723

Index Vertebra plana, 650 Vertebral osteomyelitis clinical presentations, 654 imaging features, 655–661, 663–666 isolated discitis, 653 laboratory findings, 666 modes of distribution, 654 sciatica, 653 treatment options and prognosis, 666, 667 types, 653 Viral reactivation, 1011, 1013

1047 W Wallet neuritis, 949, 959–961 Walletosis, 959, 960 Wiltse posterolateral paraspinal approach, 187 Y Yeoman’s test, 930 Z Zooster-induced sciatica, 1013