Spinal Neurosurgery [1 ed.] 2018029143, 9780190887773

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Spinal Neurosurgery

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NEUROSURGERY BY EXAMPLE Key Cases and Fundamental Principles Series edited by: Nathan R. Selden, MD, PhD, FACS, FAAP Volume 1: Peripheral Nerve Surgery, Wilson and Yang Volume 2: Surgical Neuro-​Oncology, Lonser and Elder Volume 3: Spinal Neurosurgery, Harrop and Maulucci

 

Spinal Neurosurgery Edited by

James S. Harrop, MD, FACS Professor, Departments of Neurological and Orthopedic Surgery Director, Division of Spine and Peripheral Nerve Surgery Neurosurgery Director of Delaware Valley SCI Center Thomas Jefferson University Philadelphia, Pennsylvania and

Christopher M. Maulucci, MD, FACS Associate Professor of Neurological Surgery Director of Spine Surgery Tulane University New Orleans, Louisiana

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1 Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship, and education by publishing worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and certain other countries. Published in the United States of America by Oxford University Press 198 Madison Avenue, New York, NY 10016, United States of America. © Oxford University Press 2019 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by license, or under terms agreed with the appropriate reproduction rights organization. Inquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above. You must not circulate this work in any other form and you must impose this same condition on any acquirer. Library of Congress Cataloging-​in-​Publication Data Names: Harrop, James S., editor. | Maulucci, Christopher M., editor. Title: Spinal neurosurgery /​edited by James S. Harrop, Christopher M. Maulucci. Description: New York, NY : Oxford Unversity Press, [2019] | Includes bibliographical references. Identifiers: LCCN 2018029143 | ISBN 9780190887773 (pbk.) Subjects: | MESH: Spine—​surgery | Spinal Diseases—​surgery | Spinal Injuries—​surgery | Neurosurgical Procedures—​methods Classification: LCC RD533 | NLM WE 727 | DDC 617.4/​71059—​dc23 LC record available at https://​lccn.loc.gov/​2018029143 This material is not intended to be, and should not be considered, a substitute for medical or other professional advice. Treatment for the conditions described in this material is highly dependent on the individual circumstances. And, while this material is designed to offer accurate information with respect to the subject matter covered and to be current as of the time it was written, research and knowledge about medical and health issues is constantly evolving and dose schedules for medications are being revised continually, with new side effects recognized and accounted for regularly. Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulation. The publisher and the authors make no representations or warranties to readers, express or implied, as to the accuracy or completeness of this material. Without limiting the foregoing, the publisher and the authors make no representations or warranties as to the accuracy or efficacy of the drug dosages mentioned in the material. The authors and the publisher do not accept, and expressly disclaim, any responsibility for any liability, loss or risk that may be claimed or incurred as a consequence of the use and/or application of any of the contents of this material. 9 8 7 6 5 4 3 2 1 Printed by WebCom, Inc., Canada

 

Contents

Series Editor’s Preface  vii Contributors  ix 1. Odontoid Fracture Type II  1 Daniel Tarazona and Alexander R.Vaccaro 2. Cervical Fracture Dislocation  11 Jason Liounakos, G. Damian Brusko, and Michael Y. Wang 3. Occipitocervical Dislocation  21 Alexander B. Dru and Daniel J. Hoh 4. Central Cord Injury  31 Bizhan Aarabi, Charles A. Sansur, David M. Ibrahimi, Mathew Kole, and Harry Mushlin 5. Atlantoaxial Instability  41 Jonathan M. Parish and Domagoj Coric 6. Basilar Invagination and Cranial Settling  49 Benjamin D. Elder and Jean-​Paul Wolinsky 7. Cervical Myelopathy: Lordosis  63 Randall J. Hlubek and Nicholas Theodore 8. Cervical Myelopathy: Kyphosis  71 Mario Ganau, So Kato, and Michael G. Fehlings 9. Ossification of the Posterior Longitudinal Ligament: Cervical  81 Todd D.Vogel, Hansen Deng, and Praveen V. Mummaneni 10. Cervical Radiculopathy Due to Central Disc: ACDF/​Arthroplasty  93 Mazda K.Turel and Vincent C.Traynelis 11. Cervical Radiculopathy: Lateral Disc Foramintomy  101 Michael Karsy, Ilyas Eli, and Andrew Dailey 12. Thoracic Disc Herniation  109 Derrick Umansky and James Kalyvas 13. Thoracolumbar Burst Fractures  123 Omaditya Khanna, Geoffrey P. Stricsek, and James S. Harrop 14. Thoracic Cord Compression: Extradural Tumor  133 Tej D. Azad, Anand Veeravagu, John K. Ratliff, and Atman Desai

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Contents

15. Spinal Cord Tumor: Intramedullary  141 Rajiv R. Iyer and George I. Jallo 16. Spinal Cord Tumor: Intradural Extramedullary  149 Michael A. Galgano, Jared Fridley, and Ziya Gokaslan 17. Radiation-​Sensitive Spine Tumor  159 Adam M. Robin and Ilya Laufer 18. Cauda Equina Syndrome  175 Emily P. Sieg, Justin R. Davanzo, and John P. Kelleher 19. Lumbar Stenosis  183 Miner N. Ross and Khoi D. Than 20. L4–​L5 Degenerative Spondylolisthesis  191 Rani Nasser, Scott Zuckerberg, and Joseph Cheng 21. Isthmic Spondylolisthesis  199 Evan Lewis and Charles A. Sansur 22. Lumbar Degenerative Scoliosis  207 Michael LaBagnara, Durga R. Sure, Christopher I. Shaffrey, and Justin S. Smith 23. Flat Back Deformity  215 Yusef I. Mosley and James S. Harrop 24. Diskitis  225 Jacob R. Joseph, Brandon W. Smith, and Mark E. Oppenlander 25. Epidural Abscess  235 Hector G. Mejia Morales and Manish K. Singh 26. Nonsurgical Spinal Diseases  243 Lahiru Ranasinghe and Aimee M. Aysenne Index  253

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Series Editor’s Preface

I am delighted to introduce this volume of Neurosurgery by Example:  Key Cases and Fundamental Principles. Neurosurgical training and practice are based on managing a wide range of complex clinical cases with expert knowledge, sound judgment, and skilled technical execution. Our goal in this series is to present exemplary cases in the manner they are actually encountered in the neurosurgical clinic, hospital emergency department, and operating room. In this volume, Dr. Jim Harrop, Dr. Christopher Maulucci, and their contributors share their extensive wisdom and experience with all major areas of spinal neurosurgery. Each chapter contains a classic presentation of an important clinical entity, guiding readers through assessment and planning, decision-​making, surgical procedure, after care, and complication management. “Pivot points” illuminate the changes required to manage patients in alternate or atypical situations. Each chapter also presents lists of pearls for the accurate diagnosis, successful treatment, and effective complication management of each clinical problem. These three focus areas will be especially helpful to neurosurgeons preparing to sit for the American Board of Neurological Surgery oral examination, which bases scoring on these three topics. Finally, each chapter contains focused reviews of medical evidence and expected outcomes, helpful for counseling patients and setting accurate expectations. Rather than exhaustive reference lists, the authors provide lists of high-​priority additional reading recommended to deepen understanding. The resulting volume should provide you with a dynamic tour through the practice of spinal neurosurgery, guided by some of the leading experts in North America. Additional volumes cover each subspecialty area of neurosurgery using the same case-​ based approach and board review features. Nathan R. Selden, MD, PhD Campagna Professor and Chair Department of Neurological Surgery Oregon Health and Science University Portland, Oregon

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Contributors

Bizhan Aarabi, MD, FRCSC, FACS Professor, Neurosurgery Director of Neurotrauma, R. Adams Cowley Shock Trauma Center Department of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland Aimee M. Aysenne, MD, MPH Director of Neurocritical Care Department of Clinical Neurosciences Tulane University, School of Medicine New Orleans, Louisiana Tej D. Azad, BA Medical Student Department of Neurosurgery Stanford University School of Medicine Stanford, California G. Damian Brusko, BS Department of Neurological Surgery The Miami Project to Cure Paralysis University of Miami Miller School of Medicine Miami, Florida Joseph Cheng, MD, MS Professor of Neurosurgery Frank H. Mayfield Chair Department of Neurological Surgery University of Cincinnati Health Cincinnati, Ohio

Domagoj Coric, MD Chief, Department of Neurosurgery Carolinas Medical Center Carolina Neurosurgery and Spine Associates Charlotte, North Carolina Andrew Dailey, MD Professor Department of Neurosurgery University of Utah Salt Lake City, Utah Justin R. Davanzo, MD Department of Neurological Surgery Penn State Health Milton S. Hershey Medical Center Pennsylvania, Pennsylvania Hansen Deng, BS Medical Student Department of Neurological Surgery University of California, San Francisco San Francisco, California Atman Desai, MD Assistant Professor Department of Neurosurgery Stanford University School of Medicine Stanford, California Alexander B. Dru, MD University of Florida Department of Neurosurgery Gainesville, Florida

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Contributors

Benjamin D. Elder, MD, PhD Assistant Professor of Neurosurgery, Orthopedic Surgery, and Biomedical Engineering Mayo Clinic School of Medicine Rochester, Minnesota Ilyas Eli, MD Resident Department of Neurosurgery University of Utah Salt Lake City, Utah Michael G. Fehlings, MD, PhD, FRCSC, FACS Vice Chair Research Professor of Neurosurgery McLaughlin Scholar in Molecular Medicine Co-​Chair Spinal Program University of Toronto Gerry and Tootsie Halbert Chair in Neural Repair and Regeneration Head, Spinal Program Toronto Western Hospital Toronto, Ontario, Canada Jared Fridley, MD Assistant Professor of Neurosurgery Brown University Department of Neurosurgery Providence, Rhode Island Michael A. Galgano, MD Clinical Instructor of Neurosurgery Brown University Department of Neurosurgery Providence, Rhode Island Mario Ganau, MD, PhD, FACS Spine Fellow Toronto Western Hospital Toronto, Ontario, Canada Ziya Gokaslan, MD Professor and Chair Brown University Department of Neurosurgery Providence, Rhode Island x

James S. Harrop, MD, FACS Professor, Departments of Neurological and Orthopedic Surgery Director, Division of Spine and Peripheral Nerve Surgery Neurosurgery Director of Delaware Valley SCI Center Thomas Jefferson University Philadelphia, Pennsylvania Randall J. Hlubek, MD Department of Neurosurgery Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona Daniel J. Hoh, MD Associate Professor Dunspaugh-​Dalton Endowed Professorship Department of Neurological Surgery University of Florida Gainesville, Florida David M. Ibrahimi, MD Assistant Professor Department of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland Rajiv R. Iyer, MD Department of Neurosurgery The Johns Hopkins University School of Medicine Baltimore, Maryland George I. Jallo, MD Professor of Neurosurgery, Pediatrics and Oncology Director, Institute for Brain Protection Sciences Johns Hopkins All Children’s Hospital St. Petersburg, Florida Jacob R. Joseph, MD Department of Neurosurgery University of Michigan Ann Arbor, Michigan

 

Contributors

James Kalyvas, MD Neurosurgeon Ochsner Clinic Foundation New Orleans, Louisiana

Evan Lewis, MD Neurosurgeon Baptist Medical Group–​Neurosurgery Pensacola, Florida

Michael Karsy, MD, PhD Resident Department of Neurosurgery University of Utah Salt Lake City, Utah

Jason Liounakos, MD Resident Department of Neurological Surgery Univeristy of Miami Miller School of Medicine Miami, Florida

So Kato, MD Spine Fellow Toronto Western Hospital Toronto, Ontario, Canada John P. Kelleher, MD Department of Neurological Surgery Penn State Health Milton S. Hershey Medical Center Pennsylvania, Pennsylvania Omaditya Khanna, MD Resident Thomas Jefferson University Hospital Philadelphia, Pennsylvania Mathew Kole, MD Resident in Training Department of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland Michael LaBagnara, MD Assistant Professor of Neurological Surgery University of Tennessee Semmes-​Murphey  Clinic Memphis, Tennessee Ilya Laufer, MD Department of Neurosurgery Memorial Sloan Kettering Cancer Center New York, New York

Christopher M. Maulucci, MD, FACS Associate Professor of Neurological Surgery Assistant Residency Program Director School of Medicine Tulane University New Orleans, Louisiana Hector G. Mejia Morales Medical student Tulane University School of Medicine New Orleans, Louisiana Yusef I. Mosley, MD Department of Neurosurgery Thomas Jefferson University Philadelphia, Pennsylvania Praveen V. Mummaneni, MD Joan O’Reilly Endowed Professor Vice Chairman University of California, San Francisco Neurosurgery San Francisco, California Harry Mushlin, MD Resident in Training Department of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland

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Contributors

Rani Nasser, MD Clinical Instructor of Neurosurgery University of Cincinnati Health Cincinnati, Ohio Mark E. Oppenlander, MD Assistant Professor Department of Neurosurgery University of Michigan Ann Arbor, Michigan Jonathan M. Parish, MD Resident Physician Carolinas Medical Center Charlotte, North Carolina Lahiru Ranasinghe, BS Medical Student Department of Clinical Neuroscience Tulane University School of Medicine New Orleans, Louisiana John K. Ratliff, MD Professor Department of Neurosurgery Stanford University School of Medicine Stanford, California Adam M. Robin, MD Department of Neurosurgery Memorial Sloan Kettering Cancer Center New York, New York Miner N. Ross, MD, MPH Resident Physician Department of Neurological Surgery Oregon Health and Science University Portland, Oregon Charles A. Sansur, MD Associate Professor Department of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland

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Christopher I. Shaffrey, MD John A. Jane Professor of Neurological Surgery Division Head Spinal Surgery Professor of Orthopaedic Surgery University of Virginia Medical Center Charlottesville, Virginia Emily P. Sieg, MD Department of Neurological Surgery Penn State Health Milton S. Hershey Medical Center Pennsylvania, Pennsylvania Manish K. Singh, MD Assistant Professor of Neurological Surgery Director of Spine Surgery Program Tulane University School of Medicine New Orleans, Louisiana Brandon W. Smith, MD, MS Department of Neurosurgery University of Michigan Ann Arbor, Michigan Justin S. Smith, MD, PhD Harrison Distinguished Professor Neurological Surgery University of V   irginia Medical Center Charlottesville,Virginia Geoffrey P. Stricsek, MD Resident Thomas Jefferson University Philadelphia, Pennsylvania Durga R. Sure, MD Department of Neurosurgery University of Virginia Charlottesville, Virginia Daniel Tarazona,  MD Department of Orthopedics Rothman Institute Philadelphia, Pennsylvania

 

Contributors

Khoi D. Than, MD Assistant Professor Neurological Surgery Oregon Health and Science University Portland, Oregon

Anand Veeravagu,  MD Assistant Professor Department of Neurosurgery Stanford University School of Medicine Stanford, California

Nicholas Theodore,  MD Department of Neurosurgery Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona

Todd D. Vogel, MD Minimally Invasive and Complex Spine Fellow Department of Neurological Surgery University of California, San Francisco San Francisco, California

Vincent C. Traynelis, MD Professor Department of Neurosurgery Rush University Medical Centre Chicago, Illinois Mazda K. Turel, MBBS Clinical Fellow in Cerebrovascular and Bypass Surgery Department of Neurosurgery Rush University Medical Centre Chicago, Illinois Derrick Umansky, MD Resident Department of Neurosurgery Tulane University School of Medicine New Orleans, Louisiana Alexander R. Vaccaro, MD, PhD, MBA Department of Orthopedic Surgery Rothman Institute (President) Philadelphia, Pennsylvania

Michael Y. Wang,  MD Chief of Neurosurgery University of Miami Hospital Professor Departments of Neurological Surgery and Rehabilitation Medicine University of Miami School of Medicine Miami, Florida Jean-​Paul Wolinsky,  MD Department of Neurosurgery and Oncology Clinical Director of the Johns Hopkins Spine Program Johns Hopkins University Baltimore, Maryland Scott Zuckerberg, MD, MPH Co-Director Research of the Vanderbilt Sports Concussion Center Research Group Department of Neurological Surgery Vanderbilt University Medical Center Nashville, Tennessee

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Odontoid Fracture Type II Daniel Tarazona and Alexander R. Vaccaro

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Case Presentation

A 79-​year-​old woman presents to the emergency department after falling at a nursing home. She denies loss of consciousness. She arrived in a cervical collar placed prior to transfer with a chief complaint of neck pain. She denies any paresthesias or weakness. She is hemodynamically stable and is awake, alert, and oriented. Upon physical examination there is midline cervical spine tenderness without step-​offs or deformities. A neurological exam revealed 5/​5 motor strength throughout, no sensory deficits, 1+ DTR throughout, and a normal rectal examination.

Questions

1. What is the likely diagnosis? 2. What is the most appropriate imaging modality? 3. How are odontoid fractures classified?

Assessment and Planning

Based on the history and physical exam, the surgeon suspects a cervical spine fracture. The differential diagnosis includes injuries to the upper cervical, subaxial cervical, and upper thoracic spine. Due to the initial concern for a cervical spine injury, spine precautions are maintained and a dedicated computed tomographic (CT) scan of the cervical, thoracic, and lumbar spine is obtained revealing a type II odontoid fracture.

Oral Boards Review: Diagnostic Pearls

1. The Anderson and D’Alonzo classification for odontoid fractures lends prognostic information for risk of nonunion and assists with treatment planning. 2. CT scan is the preferred imaging modality with high inter-​and intrarater agreement. It also assists with diagnosis of concomitant spinal injuries.20 3. CT or magnetic resonate (MR) angiography should be considered if vertebral artery injury is clinically suspected. Initial radiographic evaluation of the cervical spine includes anteroposterior (AP), lateral, and open-​mouth odontoid views and CT of the cervical spine. Magnetic

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Anderson and D’Alonzo

Type I

Type II

Type III

Figure 1.1  Anderson and D’Alonzo. resonance imaging (MRI) is warranted with neurologic injury or concern for concomitant ligamentous injury. If posterior instrumentation is anticipated, then a CT angiogram may be obtained to evaluate for potential vascular anomalies that would preclude safe C2 pars, C2 pedicle, C1–​C2 transarticular, or C1 lateral mass screw placement. Odontoid fractures can be classified into three types as described by Anderson and D’Alonzo (Figure 1.1).3 Type I odontoid fractures represent an avulsion fracture of the tip of the odontoid through the alar ligament. Type II is the most common C2 fracture pattern and is defined by a fracture line at the base of the odontoid. Type II fractures have the greatest risk of nonunion due to the disruption of the tenuous blood supply.Type III fractures occur through the vertebral body and extend into the superior articular facets. Greater vascularity in the C2 body results in a low nonunion rate with cervical orthosis for this fracture type. Grauer and colleagues proposed subclassifying type II fractures to guide treatment decisions (Figure 1.2).Type IIA are transverse fractures, type IIB are angled anterosuperior to posteroinferior, and type IIC are either angled from anteroinferior to posterosuperior or are comminuted fractures.23 This fracture classification is useful when considering an odontoid screw as patients with a IIC are not appropriate for odontoid screw fixation. In the present case, CT of the spine demonstrates a displaced type II odontoid fracture with type IIC obliquity (Image 1)  and a C3 right transverse process fracture. There is no apparent cord compression. A CT angiogram does not reveal any vascular insult or anomalies (Figure 1.3).

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Grauer

Type II Subclass A (Nondisplaced)

Type II Subclass B (Displaced transverse or ant superior to post inferior)

Type II Subclass C (Comminuted or ant inferior to post superior)

Figure 1.2  Grauer classification.

Figure 1.3  Sagittal view of cervical spine showing type IIC odontoid fracture.

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Questions

1. What are risk factors for nonunion? 2. How should management be approached in a patient of advanced age? 3. How do these clinical and radiological findings influence surgical planning?

Decision-​Making

No uniform treatment algorithm has been established for odontoid fractures. Instead, each case should be tailored with special considerations for comorbidities, concomitant injuries, prior functional status, neurological status, and fracture morphology. Treatment options are also based on the risk of nonunion, favoring surgical intervention for patients with a higher risk of nonunion. Known risk factors for nonunion include age 50 years or greater, comminution, greater than 5 mm of posterior displacement, fracture gap of more than 1 mm, more than 4 days between injury and treatment, and greater than 10 degrees of angulation. Furthermore, there is extensive literature demonstrating a decrease in mortality with operative fixation and an improvement in health-​related quality of life outcomes in type II fractures in the geriatric population.18,19,24 Adults with a type II fracture without nonunion risk factors can be managed in a hard collar or a halo vest to prevent subsequent displacement. Most commonly, adults with risk factors for nonunion or geriatric patients who may safely undergo anesthesia are treated with a posterior C1–​C2 fusion. In the properly selected patient, an odontoid screw may be beneficial, but this has been demonstrated to lead to a high risk of dysphagia in the elderly as well as screw pull-​out in the setting of osteopenia/​osteoporosis.16,26 The management of type II odontoid fractures in the elderly has changed in the past decade. Historically, acceptable outcomes with asymptomatic stable fibrous nonunions in the elderly have been reported.4 More recent literature supports operative management for patients 65 years or older, reporting improved functional outcomes and union rates, no difference in complications, and a trend toward improved mortality.19 However, an increased risk of complications can be seen in surgically treated patients 80 years or older.24 Rigid external immobilization (halo vest) is contraindicated in the elderly due to high morbidity and mortality rates.5 They generally have lower overall functional reserve and decreased pulmonary function, so prolonged immobilization could have morbid implications. Consequently, more surgeons are advocates for early surgical intervention, and there is a growing body of evidence to support this as well.18–​20,22,24 There are multiple surgical treatments for odontoid fractures with the most commonly used being segmental fixation consisting of C1 lateral mass with either C2 pedicle or pars screws. Other options included an anterior odontoid osteosynthesis and C1–​C2 transarticular screw fixation. While posterior instrumentation demonstrated greater rates of osseous union, anterior odontoid osteosynthesis avoids fusion of the C1–​C2 articulation, which is responsible for 50% of cervical rotation. Each option has unique advantages and disadvantages which should be balanced with the fracture pattern, body habitus, and patient expectations. In this case, due to the displacement and instability of the odontoid fracture, as well as the potential serious complications of immobilization, the surgeon opted

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Odontoid Fracture Type II

for surgical fixation. The surgeon elected for C1–​C2 posterior instrumented fusion. Anterior screw osteosynthesis is often not indicated because of the patient’s age and potential for fixation failure due to poor screw purchase with osteoporosis, as well as the fact that lag screw fixation would result in translation and displacement with a type IIC fracture. Body habitus is also an important consideration as this patient’s obesity makes anterior odontoid osteosynthesis technically challenging to place a screw due to the trajectory. Surgical Procedure

As previously mentioned, there are multiple surgical options for type II odontoid fracture but here the focus will be on segmental C1–​C2 instrumentation and fusion (C1 lateral mass technique, Figure 1.4). Positioning and Preparation

The patient should undergo intubation with in-​line cervical immobilization to prevent excessive neck hyperextension. This may be done with a GlideScope or as a fiber-​optic intubation.The Mayfield clamp is applied after intubation. Neuromonitoring is routinely utilized, and preintubation and prepositioning somatosensory and transcranial motor evoked potentials (SSEPs and tcMEPs) are recorded. The patient is then positioned prone with the neck in a slightly flexed position followed by repeat SSEPs and tcMEPs. The cervical spine is prepped and draped in sterile fashion. If iliac crest bone graft harvesting is required, then the posterior iliac crest should also be prepped and draped. Approach

A midline longitudinal incision is utilized. Intraoperative radiographs should be taken to confirm spinal levels. Particular care should be taken to stay in the midline and follow the midline raphe for an avascular approach. Subperiosteal dissection of the posterior elements of C2 and inferior arch of C1 is performed. Avoid sharp dissection lateral to the C1 lateral masses and cephalad to the C1 ring to reduce risk of injuring the vertebral artery. As dissection extends from the base of the C1 arch to the C1 lateral masses, significant bleeding from the venous plexus in this region may be encountered.

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Figure 1.4  (A) C1 lateral mass technique. (B) Retraction of C2 nerve root and exposure of lateral mass.

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Procedure

Fluoroscopy is initially used to confirm adequate position of C1 relative to C2. Next, the starting point of the C2 pars screw is determined. A pilot hole is made approximately 2–​3 mm proximal to the C2–​C3 facet joint and slightly laterally (2–​3 mm) to the palpated medial border of the C2 isthmus. The drill is angled cephalad and slightly medial along the path of the C2 isthmus and advanced to the predetermined unicortical depth. Next, a probe is used to confirm the absence of bony breach, the tract is tapped, and the screw is placed. Following placement of C2 pars screw, fluoroscopy is then used to help identify the starting point and trajectory of the C1 lateral mass screw. Prior to screw placement, the C2 nerve root must be gently retracted inferiorly, exposing the bony anatomy (Figure 1.5). The entry point is identified 5 mm lateral to the medial aspect of the lateral mass and just caudal to the C1 posterior arch. A drill can be used to cannulate the lateral mass, aimed approximately 10 degrees medial with fluoroscopy guiding a cephalad parallel trajectory to the midpoint of the C1 anterior arch. Depth gauge measurements can then confirm the screw length and size prior to its insertion into the lateral mass. This is repeated for the contralateral C1 lateral mass. Screw positions are checked under lateral fluoroscopy and rods are placed. The C2 lateral masses and inferior arch of C1 is decorticated and a structural graft is placed in the C1–​C2 interspace. Final x-​rays are then taken to confirm hardware positioning.

Oral Boards: Management Pearls

1. Evaluation of vertebral artery anatomy with preoperative imaging, minimizing sharp dissection around the cephalad edge of the atlas, and using a superomedial trajectory of C1 lateral mass screw trajectory will reduce the risk of injury to the vertebral artery. 2. Suboptimal lateral fluoroscopic imaging for C1–​C2 instrumentation can result in improper screw placement and neurologic or vascular injury. 3. C1–​C2 polyaxial screw and rod fixation does not require direct odontoid anatomic reduction, and intraoperative reduction by manipulation can be achieved using direct manipulation of the C1 posterior arch.

Pivot Points

1. If an aberrant vertebral artery is present, then an alternative operative technique, such as a C2 laminar screw, should be considered. C1–​C2 transarticular screw and C2 pedicle screw placement should be avoided with aberrant anatomy. 2. Although the lateral mass screw placement may initially appear to be without complication, if the screw tip is in close proximity to the vertebral artery, normal pulsatile flow may result in delayed damage to the vessel. Any concern for excessive screw length should prompt screw removal, with a shorter screw subsequently inserted.

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Odontoid Fracture Type II

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B

Figure 1.5  (A,B) Anteroposterior and lateral view of cervical spine with posterior C1–​C2 fusion. Aftercare

It is recommended that patients undergoing fixation of type II odontoid type fractures be placed in a cervical orthosis and admitted for close monitoring of potential postoperative complications. In geriatric patients, a soft collar is used, but in high-​energy injuries a hard collar is used. The patient can be mobilized immediately after surgery. Follow-​up imaging should be obtained at 2 weeks and 6–​8 weeks to ensure there is no early hardware failure (Figure 1.5). Also, functional radiographs in flexion and extension can be obtained to evaluate stability 3–​6 months after surgery. Once initial healing and maintenance of stability is established, the patient may be weaned from the cervical orthosis. Complications and Management

The different complications of surgery are largely dependent on the approach and technique used.These complications can be further categorized into intraoperative and postoperative complications. Intraoperative Complications

Neurovascular injuries are the most concerning intraoperative complications. With a posterior approach, one of the feared complications is injury to the vertebral artery with screw malposition. An anomalous vertebral artery further increases the risk of injury, especially with C1–​C2 transarticular or C2 pedicle screw placement. Preoperative imaging should be closely evaluated for aberrant vessels. Careful intraoperative technique, avoiding C2 pedicle screws with aberrant vertebral artery anatomy, and directing the C1 lateral mass screw superomedially is essential to avoid vertebral artery damage.13 Damage to a single vertebral artery may be asymptomatic with intact contralateral supply, but bilateral injury can be catastrophic. With an anterior approach, careful retraction and dissection should be used to avoid injury to the internal carotid and esophagus. Other potential rare complications 7

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include neurologic injury from past-​point drilling or excessive depth of the anterior odontoid screw. Postoperative Complications

Following a posterior cervical approach, occipital neuralgia is a common complaint. To minimize the risk, the C2 nerve root should be gently retracted downward and protected with a Penfield dissector during lateral mass screw placement. Additionally, partially threaded screws are used at C1. Wound complications are also more common with a posterior approach.17 Sterile technique, antibiotics, and proper wound irrigation help reduce the risk of infection. Surgical site infections with any concern for deep extension should be addressed with surgical debridement. Following an anterior approach, dysphagia can be common and may necessitate the use of a feeding tube.27 This approach can be further complicated by aspiration pneumonia, which should be promptly treated with antibiotics.11,27 Hoarseness or vocal cord paralysis may ensue from neurapraxia or ischemic injury to the superior laryngeal and recurrent laryngeal nerves, respectively. Patients should also be closely monitored for signs of respiratory distress as this may be a sign of a retropharyngeal hematoma, which should be emergently surgically evacuated. Failure of instrumentation and pseudarthrosis can complicate the postoperative recovery. Routine follow-​up radiographs are scrutinized for evidence of union. CT scans can be utilized if the surgeon is concerned for nonunion.

Oral Boards Review: Complications Pearls

1. If there is an inadvertent injury to the vertebral artery, bleeding should be immediately controlled with primary vascular repair, temporary insertion of screw into the drilled hole, or by occlusion with a hemostatic agent or bone wax. If hemorrhage control is not possible and ligation is planned, intraoperative angiography should be performed.28 Contralateral screw placement should not be attempted to avoid bilateral injury. 2. C2 neuralgia can be a result of C1 lateral mass screw placement or excessive traction during exposure of lateral mass. 3. Bicortical fixation of lateral mass screw could place the internal carotid artery at risk for injury.10 4. The congenital arcuate foramen can be confused with the C1 lamina and must be identified to avoid vertebral artery injury

Evidence and Outcomes

The optimal surgical technique for type II odontoid fractures remains a matter of debate, with both anterior odontoid screw fixation and posterior cervical atlantoaxial fusion being acceptable choices.16,24 However, a posterior approach is especially indicated in geriatric patients and when anterior approaches are contraindicated in cases such as type IIC odontoid fracture, associated C1–​C2 injury, nonreducible fractures, nonunion, large body habitus with a barrel chest, severe kyphosis, and severe osteoporosis.16 Posterior

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Odontoid Fracture Type II

C1–​C2 fusions may also be used for salvage of an anterior fixation failure. Overall, posterior atlantoaxial fixation has been associated with a high rate of fusion, approaching 100%, with a low complication rate thus making it a very effective treatment option for type II odontoid fractures.12 When appropriately indicated, anterior screw fixation can provide similar clinical results.24 Another previous area of uncertainty was the optimal management of elderly patients; however, there has been a significant amount of research in the past decade demonstrating the superiority of surgery. Vaccaro et al. conducted a multicenter, prospective cohort study comparing operative and nonoperative treatments for patients 65 years of age or older. The study revealed better outcomes, lower nonunion rates, no difference in complication rates, and a nonsignificant trend toward lower mortality.19 Schroeder et al. performed a systematic review that found a decrease in both short-​and long-​term mortality in patients treated surgically. However, there is likely an upper age to surgery.24 Schoenfeld et al. conducted a retrospective study, and, although patients between 65 and 74 years old who underwent surgery had lower mortality rates, there was no difference when patients approached 85 years of age.22 References and Further Readings

1. Boos N, Aebi M, eds. Spinal Disorders:  Fundamentals of Diagnosis and Treatment. Berlin: Springer-​Verlag;  2008. 2. Keller S, Bieck K, Karul M, et  al. Lateralized odontoid in plain film radiography:  Sign of fractures?—​A comparison study with MDCT. RöFo—​Fortschritte Auf Dem Geb Röntgenstrahlen Bildgeb Verfahr. 2015;187(09):801–​807. doi:10.1055/​s-​0035-​1553237. 3. Anderson LD, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg Am. 1974;56(8):1663–​1674. 4. Pal D, Sell P, Grevitt M.Type II odontoid fractures in the elderly: An evidence-​based narrative review of management. Eur Spine J. 2011;20(2):195–​204. doi:10.1007/​s00586-​010-​1507-​6. 5. Majercik S, Tashjian RZ, Biffl WL, Harrington DT, Cioffi WG. Halo vest immobilization in the elderly: A death sentence? J Trauma. 2005;59(2), 350–​358. 6. Goel A. Treatment of odontoid fractures. Neurol India. 2015;63(1):7. doi:10.4103/​ 0028-​3886.152657. 7. Robinson Y, Robinson A-​L, Olerud C. Systematic review on surgical and nonsurgical treatment of type II odontoid fractures in the elderly. BioMed Res Int. 2014;2014. doi:10.1155/​ 2014/​231948. 8. Posterior C1–​ C2 Fusion, ClinicalKey. https://​www-​clinicalkey-​com.ezproxy.rowan.edu/​ #!/​content/​book/​3-​s2.0-​B9781437715200000279. Accessed May 1, 2016. 9. Bodon G, Patonay L, Baksa G, Olerud C. Applied anatomy of a minimally invasive muscle-​ splitting approach to posterior C1–​C2 fusion:  An anatomical feasibility study. Surg Radiol Anat SRA. 2014;36(10):1063–​1069. doi:10.1007/​s00276-​014-​1274-​x. 10. Seal C, Zarro C, Gelb D, Ludwig S. C1 lateral mass anatomy: Proper placement of lateral mass screws. J Spinal Disord Tech. 2009;22(7):516–​523. doi:10.1097/​BSD.0b013e31818aa719. 11. Dailey AT, Hart D, Finn MA, Schmidt MH, Apfelbaum RI. Anterior fixation of odontoid fractures in an elderly population: Clinical article. J Neurosurg. 2010;12(1):1–​8. 12. Harms J, Melcher RP. Posterior C1–​C2 fusion with polyaxial screw and rod fixation. Spine. 2001;26(22):2467–​2471.

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13. Gautschi OP, Payer M, Corniola MV, Smoll NR, Schaller K, Tessitore E. Clinically relevant complications related to posterior atlanto-​axial fixation in atlanto-​axial instability and their management. Clin Neurol Neurosurg. 2014;123:131–​135. doi:10.1016/​j.clineuro.2014.05.020. 14. Spine Surgery Basics, Springer. http://​link.springer.com.ezproxy.rowan.edu/​book/​ 10.1007%2F978-​3-​642-​34126-​7. Accessed May 1, 2016. 15. Wang L, Liu C, Zhao Q-​H, Tian J-​W. Outcomes of surgery for unstable odontoid fractures combined with instability of adjacent segments. J Orthop Surg. 2014;9:64. doi:10.1186/​ s13018-​014-​0064-​9. 16. Joaquim A, Patel A. Surgical treatment of type II odontoid fractures: Anterior odontoid screw fixation or posterior cervical instrumentation fusion. Am Assoc Neurosurg. 2015:38(4):E11. 17. Harel R, Stylianou P, Knoller N. Cervical spine surgery:  Approach-​related complications. World Neurosurg. 2016;94:1–​5. 18. Chapman J, Smith JS, Kopjar B, et  al. The AOSpine North America Geriatric Odontoid Fracture Mortality Study:  A retrospective review of mortality outcomes for operative versus nonoperative treatment of 322 patients with long-​ term follow-​ up. Spine. 2013;38(13):1098–​1104. 19. Vaccaro AR, Kepler CK, Kopjar B, et al. Functional and quality-​of-​life outcomes in geriatric patients with type-​II dens fracture. J Bone Joint Surg. 2013;95(8):729–​735. 20. Barker L, Anderson J, Chesnut R, Nesbit G, Tjauw T, Hart R. Reliability and reproducibility of dens fracture classification with use of plain radiography and reformatted computer-​aided tomography. J Bone Joint Surg (Am). 2006;88(1):106–​112. 21. Koivikko MP, Kiuru MJ, Koskinen SK, Myllynen P, Santavarita S, Kivisaari L. Factors associated with non-​union in conservatively treated type II fractures of the odontoid process. J Bone Joint Surg (Br). 2004;86-​B:1146–​1151. 22. Schoenfeld AJ, Bono CM, Reichmann WM, et al. Type II odontoid fractures of the cervical spine:  Do treatment type and medical comorbidities affect mortality in elderly patients? Spine. 2011;36(11):879–​885. 23. Grauer JN, Shafi B, Hilibrand AS, et al. Proposal of a modified, treatment-​oriented classification of odontoid fractures. Spine J. 2005;5(2):123–​129. 24. Schroeder GD, Kepler CK, Kurd M, et al. A systematic review of the treatment of geriatric type II odontoid fractures. Neurosurgery 2015;77:S6–​S14. 25. Smith HE, Kerr SM, Maltenfort M, et al. Early complications of surgical versus conservative treatment of isolated type II odontoid fractures in octogenarians: A retrospective cohort study. J Spinal Disord Tech. 2008;21(8):535–​539. 26. Andersson S, Rodrigues M, Olerud C. Odontoid fractures: High complication rate associated with anterior screw fixation in the elderly. Eur Spine J. 2000;9(1):56–​59. 27. Vasudevan K, Grossberg JA, Spader HS, Torabi R, Oyelese AA. Age increases the risk of immediate postoperative dysphagia and pneumonia after odontoid screw fixation. Clin Neurol Neurosurg. 2014;126:185–​189. 28. Peng CW, Chou BT, Bendo JA, Spivak JM. Vertebral artery injury in cervical spine surgery:  Anatomical considerations, management, and preventive measures. Spine J. 2009;9(1):70–​76.

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Cervical Fracture Dislocation Jason Liounakos, G. Damian Brusko, and Michael Y. Wang

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Case Presentation

A 30-​year-​old man was transferred to a local level 1 trauma center by emergency medical services (EMS) 3 hours after diving into a shallow pond head first. He presents with a Glasgow Coma Scale (GCS) score of 15, without loss of consciousness, and states that immediately after the dive he was unable to move his arms or legs. He also complains of an intermittent burning sensation in his arms and neck pain. He is rigidly immobilized on a backboard with strict spine precautions. His blood pressure is 90/​60 mm Hg with a heart rate of 55 bpm. Detailed physical examination is significant for 5/​5 strength in deltoids, 4+/​5 in biceps, and 0/​5 distally. He has absent rectal tone. Biceps reflexes are 2+ bilaterally. Brachioradialis, triceps, patellar, and achilles reflexes are absent bilaterally. Hoffman sign is negative, and no clonus or plantar response is equivocal. Sensation to pin prick and light touch is preserved throughout, including the perianal region.

Questions

1. What is the most likely diagnosis? 2. At what level is the suspected injury? 3. What is the international standardized classification system used for spinal cord injury? 4. What imaging examinations are most appropriate to accurately diagnosis the injury? 5. Describe common fracture patterns associated with cervical facet dislocations.

Assessment and Planning

Given the acute onset of symptoms in an otherwise healthy patient sustained after an obvious traumatic injury, the on-​call neurosurgeon suspects a traumatic spinal cord injury. Spinal cord injuries in the cervical spine are frequently associated with cervical fracture dislocation. An initial complete trauma evaluation is necessary to rule out other injuries, particularly in the setting of neurogenic shock where hypotension may be related to hemorrhagic shock rather than to a loss of sympathetic tone secondary to the spinal cord injury. Until the injury has been identified and stabilized, strict spine precautions are necessary, particularly in the setting of an incomplete spinal cord injury (as in this case). Instability due to a fracture predisposes the patient to further injury

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and risks worsening neurological status so the utmost care must be taken in patient positioning and transfers. Assuming a spinal cord injury is present, a complete neurological exam will often accurately reveal the level of injury. In this patient with grossly intact deltoid and biceps strength and nothing below, the level of injury is likely C5. Given the presence of intact sensation, this injury is classified as incomplete American Spinal Injury Association (ASIA) B. The complete guide to the ASIA neurologic exam and ASIA Impairment Scale is provided in the References and Further Reading section. The neurologic level is defined as the most caudal level with normal function. Importantly, to accurately diagnose a complete (ASIA A) injury, the function of the most caudal spinal segments (S4–​S5) must be evaluated and found to be absent. Per the 2013 update to the Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injury provided by the Congress of Neurological Surgeons (CNS), computed axial tomography (CT) is the recommended initial imaging study for symptomatic trauma patients. CT will quickly and accurately uncover the level of bony injury, if present, and guide further workup and treatment. Magnetic resonance imaging (MRI) is extremely useful after the patient has been initially stabilized to assist in determining the extent of neurologic injury, the presence of active compression of the spinal cord, and, perhaps somewhat more controversially, the safety of closed reduction in the presence of facet dislocation. Disrupted or herniated discs occur in one-​third to one-​half of patients with cervical facet dislocations. It has been argued that prereduction MRI is important to identify a traumatic disc herniation that has the potential to exacerbate spinal cord compression if closed reduction is performed. In the worst-​case scenario, this could potentially lead to an incomplete injury becoming complete. It is further argued that, in the presence of such a disc herniation, treatment should proceed with anterior cervical discectomy, followed by open reduction and internal fixation. Interestingly, however, only a few reports of such complications exist, and numerous studies have failed to demonstrate an association between a traumatic herniated disc and postreduction neurologic deterioration in the awake patient. Even so, the practice at many institutions, including our own, typically involves urgent MRI in the awake patient with an incomplete spinal cord injury and cervical fracture dislocation. In our case, CT demonstrated a grade 2 anterolisthesis of C5 on C6 (Figure 2.1A) with complete dislocation (“jumped” or “locked” facet) of the right facet joint (Figure 2.1B) and subluxation (“perched” facet) of the left facet joint (Figure 2.1C), associated with a flexion teardrop-​type fracture of C6. An MRI was subsequently obtained (Figure 2.2) that did not demonstrate an obvious disc herniation. Clearly evident injury to the spinal cord and posterior ligamentous complex was indicated by the presence of high T2 signal in both. Cervical facet dislocations are caused by hyperflexion and posterior distraction with or without a rotational component. Rotational injury is often a major component of unilateral facet dislocations. They are commonly seen after high-​energy trauma such as motor vehicle and diving accidents. When the inferior articulating process of the rostral vertebra dislocates anteriorly to the superior articulating process of the caudal vertebra, the condition is commonly referred to as “jumped” or “locked” facets. When the inferior articulating process sits superior to the superior articulating process, the facets are

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Figure 2.1  Computed tomography (CT) scan demonstrating cervical fracture dislocation at the C5–​C6 level. A grade 2 anterolisthesis of C5 on C6 exists (A). The right facet is fully dislocated (jumped) with the inferior articulating process of the C5 vertebra dislocated anteriorly to the superior articulating process of C6 (B). By comparison, the left facet is perched (C).

referred to as being “perched.” Unilateral facet dislocation often results in a grade 1 anterolisthesis. Isolated unilateral facet dislocation may present with monoradiculopathy secondary to nerve root compression at the level of the neural foramen. Bilateral facet dislocations often result in a more significant degree of anterolisthesis (often greater than 50%) with a high incidence associated spinal cord injury. In addition to facet dislocation, hyperflexion, distraction, rotational, and axial loading forces may result in fractures that include simple compression fractures, fractures of the facet joint including the superior or inferior articulating processes and the pars interarticularis, and flexion teardrop fractures. In this case, a nonclassical but teardrop-​ type fracture of C6 is present. Flexion tear drop fractures are highly unstable as they involve both the anterior and posterior columns, demonstrating severe ligamentous disruption of the facet joint, ligamentum flavum, and posterior longitudinal ligament.They often result in damage to the anterior spinal cord, as in this patient presenting with motor, but not sensory, deficits. Fractures of the anteroinferior corner of the affected vertebral body are classically seen, and retrolisthesis of the rostral vertebral body over the

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Figure 2.2 T2-​weighted magnetic resonance image (MRI) depicting significant spinal canal comprise as a result of the cervical fracture dislocation at C5–​C6 with increased T2 signal present in the spinal cord but without evidence of a grossly herniated disc at that level.

caudal one may be present. These fractures require surgical fixation as the primary form of treatment as they are highly unstable.

Oral Boards Review: Diagnostic Pearls

1. The physical examination is the most important component in the initial evaluation of cervical spine trauma. a. A complete neurologic evaluation and ASIA grade is important in determining prognosis. b. A palpable step-​off may be felt, likely indicating a severe dislocation injury. 2. Depending on the mechanism of injury, there may be other bodily injuries associated with cervical spine trauma, and a full trauma evaluation is indicated. Even in the setting of spinal cord injury, hemodynamic instability should raise concern for other sites of hemorrhage, rather than simply being attributed to neurogenic shock. 3. The 2013 update to the Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injury recommend CT scan as the best first imaging study to be performed in the setting of cervical spine trauma. If not available, plain radiographs are recommended. 4. Cervical dislocations occur as a result of flexion and rotational (in the case of unilateral facet dislocation) forces. Fractures with the same mechanism may be associated, and these include simple compression fractures, fractures of the facet complex, and flexion teardrop fractures.

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5. Much controversy surrounds whether prereduction MRI should be performed in a patient with a cervical fracture dislocation injury. According to the most recent guidelines, MRI should be performed prior to closed reduction in a patient who cannot reliably be examined during the procedure, or, if the procedure fails, prior to anterior or posterior open surgical reduction and fixation. It has been reported that disc herniation may be found on MRI anywhere between one-​third to one-​half of the time; however, their clinical significance remains largely uncertain.

Questions

1. After a diagnosis is made, what is the next best step in management, and when should this be performed? 2. What different techniques may be used to reduce facet dislocations? 3. How does a patient’s mental status influence the decision to proceed with closed reduction?

Decision-​Making

Cervical facet dislocations are unstable injuries, and their initial management should focus on reduction followed by internal fixation or external immobilization. Reduction should be performed expeditiously, particularly in the setting of ongoing spinal cord compression and/​or incomplete spinal cord injury as reduction potentially may lead to improvement in neurologic status and ongoing compression may lead to worsening neurologic injury. Closed reduction may be performed via craniocervical traction or via cervical manipulation under anesthesia. Alternatively, open surgical reduction may also be performed. Treatment algorithms vary widely between institutions, and no concrete evidence supports one over the other; however, it appears that craniocervical traction in an awake patient is likely more safe than cervical manipulation under anesthesia as a method of closed reduction. Numerous studies have been conducted on the efficacy of closed reduction for unilateral and bilateral facet dislocation injuries, showing an 80–​90% success rate with closed reduction and an approximately 1% risk of permanent neurological complications. Closed reduction via craniocervical traction may be performed with Gardner-​Wells tongs and sequential application of weight while closely monitoring the patient’s neurologic exam and using fluoroscopy to confirm reduction. The CNS’s guidelines for the acute management of cervical spine and spinal cord injuries suggests that closed reduction not be performed in a sedated or obtunded patient as they are unable to be adequately assessed for any neurologic deterioration as a result of the procedure. Rather, an MRI should be performed first to rule out any complicating injuries that could preclude closed reduction. If closed reduction fails, MRI is recommended prior to attempting open surgical reduction and fixation for the purposes of planning the approach and assessing the need for anterior decompression and discectomy prior to reduction and fixation.

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Questions

1. What options are available for internal fixation and external immobilization? 2. How do the results of halo orthosis immobilization compare to surgical fixation? 3. What are the major complications associated with ACDF? 4. How should the occurrence of a new neurologic complaint or deficit encountered during the process of closed cervical reduction be managed?

Surgical Procedure

Cervical fracture dislocation injuries are highly unstable, and internal fixation or external immobilization is necessary to prevent recurrent injury and possible neurologic compromise. After closed reduction, external immobilization via a halo orthosis is an option. Alternatively, open or closed reduction may be followed by internal surgical fixation. Protocols vary from center to center. Halo immobilization is a fairly morbid and quality-​of-​life affecting treatment and, for this reason, has fallen out of favor at our institution. While external immobilization can be used to treat these injuries, it does not seem to be as effective or reliable at producing successful results compared to surgical fixation. A  2002 study directly comparing the halo orthosis and anterior arthrodesis in the treatment of flexion teardrop fractures favored surgery, finding a 20% failure rate in the halo group as well as significantly worsened cervical kyphosis on follow-​up. No significant postoperative complications occurred in the surgical group. Internal fixation may be performed anteriorly, posteriorly, or circumferentially. According to the 2013 CNS guidelines, all such procedures are effective, and the decision on how to proceed must be made on a case-​by-​case basis. Anterior surgery has the benefit of supine surgery, a straightforward dissection, the ability to remove a herniated disc prior to open reduction, and a relatively benign complication profile. A downside is that open reduction may be somewhat more difficult than a posterior approach. The posterior approach allows for easier access to the facet joints to facilitate reduction. This is followed by lateral mass screw and rod placement. Posterior cervical fusion has a somewhat higher morbidity than anterior cervical discectomy and fusion (ACDF), and a theoretical risk neurologic injury exists when turning the patient prone. Circumferential fusion may be necessary for extremely unstable injuries, although surgical morbidity particularly due to position and time of surgery are significantly higher. At our institution, we prefer a management strategy of urgent MRI to evaluate for any compressive anterior pathology, followed by open reduction and ACDF. The patient is placed in a Mayfield head holder, and, after the discectomy is performed, the dislocated facet joints are reduced manually via slight flexion and distraction. If necessary, further distraction may be accomplished by using a Cobb elevator placed in the disc space.

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Oral Boards Review: Management Pearls

1. Cervical fracture dislocation injuries are highly unstable. Even if closed reduction is performed successfully, either internal fixation or external immobilization is necessary as there may be a high rate of recurrence and subsequent neurologic injury. 2. Anterior or posterior approaches to internal fixation are both effective, and the approach should be decided on a case-​by-​case basis, taking into account the need for neurologic decompression.

Pivot Points

1. If, during closed reduction, the patient begins to experience new neurologic symptoms, the last weight placed should be removed and the patient reassessed by physical exam and fluoroscopy. More than likely, the procedure will need to be aborted. At that point, it is recommended to proceed with MRI and open reduction and fixation. 2. Based on the literature, prereduction MRI showing a cervical herniated disc in conjunction with facet dislocation does not necessarily mandate discectomy prior to reduction; however, this is the bias at our institution.

Aftercare

Postoperative care for cervical fusion following traumatic fracture dislocation is fairly straightforward and entails wearing a rigid cervical collar for 8 weeks per our institution’s protocol, followed by plain radiographs versus CT scan (depending on the extent of injury) to assess for bony healing. However, because of the significant morbidity and physiologic derangements associated with spinal cord injury, an intensive care unit (ICU) level of care is necessary. Spinal shock is commonly associated with acute spinal cord injury. Spinal shock is characterized by a temporary loss in motor, sensory, and autonomic function below the neurologic level that gradually returns in four phases. Areflexia in phase 1 lasts about 2 days (as seen in our case). In phase 2, some initial reflexes return during days 2–​4 post-​ injury, with early hyperreflexia appearing during phase 3 and lasting approximately a month. Finally, phase 4 may last up to a year following the injury and is characterized by hyperreflexia and spasticity. Spinal shock should not be confused with neurogenic shock, which involves hypotension and bradycardia resulting from damage to the autonomic fibers within the spinal cord, although these complications may occur together (as in our patient). In the ICU, blood pressure augmentation should be utilized to maintain a mean arterial pressure (MAP) greater than 80 mm Hg for approximately 1 week. This serves to maintain adequate systemic perfusion in the face of neurogenic shock, as well as to provide maximal safe perfusion to the spinal cord in the hopes of facilitating potential neurologic recovery. Anticholinergic medications such as atropine may be used in the

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setting of symptomatic bradycardia. Higher level cervical injuries result in disruption of the phrenic nerve and may lead to inadequate ventilation. These patients may require mechanical ventilation if PaO2 is less than 70 mm Hg or PaCO2 is greater than 45 mm Hg. Foley catheterization will be necessary until the patient is systemically stable, and neurogenic bladder causes a significant problem. Autonomic dysreflexia is another common problem facing spinal cord injury patients. Frequent patient repositioning, range of motion exercises (to combat spasticity), and early management of pressure ulcers is necessary. Finally, kinetic therapy via a rotorest bed may also be beneficial as a cardiovascular and respiratory prophylactic measure. Complications and Management

Complications of rigid external fixation with a halo orthosis commonly include pin loosening, pin site infection, and discomfort. Other rarer complications include skull fracture and injury to the supratrochlear and/​or supraorbital nerves. Because of the fairly high incidence of morbidity associated with the halo vest, our center has largely abandoned its use. ACDF is generally a low-​morbidity procedure; however, significant complications may occur. Postoperative dysphagia is the most common complication. Efforts at minimizing the degree of and time under retraction may reduce its incidence, but the etiology is likely multifactorial. While largely transient, a short course of steroids may be beneficial in severe cases. Recurrent laryngeal nerve palsy and vocal cord paresis may result from division or traction injuries to the nerve during exposure and/​or retraction. Careful dissection, minimizing time under retraction, deflation of the endotracheal tube cuff after the self-​ retaining retractors are placed, and, as argued by some studies, a left-​sided approach may minimize its occurrence. In general, symptomatic injuries are transient, however otolaryngology referral may be indicated. Postoperative wound hematoma is a potentially catastrophic complication of the anterior approach. A large retrospective review by Fountas et al. found a 5.6% chance of this complication with 24 of 57 affected patients requiring emergent surgical evacuation. If respiratory compromise is suspected, emergent evacuation of the hematoma is indicated. Durotomy and cerebrospinal fluid (CSF) leak may occur in a very small percentage of patients, and this should be treated with the prompt placement of a lumbar drain and careful attention to a watertight wound closure. In the majority of cases, several days of CSF diversion and head of bed elevation will resolve the leak. Durotomy is more common in posterior cervical cases where laminectomies are performed, but because of the wider exposure, these tears should be attempted to be closed primarily. Placement of a dural substitute or sealant may also be beneficial. Other rare but catastrophic complications of ACDF include vertebral artery injury and esophageal or pharyngeal perforation. This likely occurs in less than 1% of cases. For esophageal injuries, prompt intraoperative identification and primary repair by a general surgeon is paramount as unidentified injuries may lead to mediastinitis and overwhelming infection. Care should be taken during lateral dissection and when performing foraminotomies to avoid vertebral artery injury. At our center, any vertebral artery injury

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is treated with packing and emergent angiogram to assess the injury and potentially sacrifice the artery. Similarly, the vertebral arteries are at risk when instrumenting the cervical spine posteriorly. The screw should not be removed if an injury is suspected. The wound should be packed and, at our institution, prompt referral to the endovascular suite should be initiated. In regards to the patient with an unstable cervical fracture and spinal cord injury, simple maneuvers such as patient transfers and positioning could have serious consequences. Strict spine precautions are necessary at all times to prevent the production or worsening of a neurologic injury.

Oral Boards Review: Complications Pearls

1. Minimizing time under retraction and deflation of the endotracheal tube once the self-​retaining retractors are placed may minimize the risk of postoperative dysphonia. 2. Postoperative dysphagia is more common in three-​level procedures compared to one-​or two-​level procedures. 3. CSF leak encountered during ACDF should be treated with several days of lumbar drainage and is successful in most cases.

Evidence and Outcomes

Level 1 evidence suggests that both anterior and posterior approach surgeries are effective at treating cervical fracture dislocation injuries. One prospective randomized controlled trial found that, compared to posterior fixation, ACDF was associated with less postoperative pain, higher rate of fusion, better alignment, and fewer postoperative wound infections. Numerous cohort studies have found similar results. Closed reduction of cervical dislocations is associated with high success rates and a low rate of neurologic complications, ranging from 1% to 4%. References and Further Reading

Anissipour AK, Agel J, Baron M, Magnusson E, et  al. Traumatic cervical unilateral and bilateral facet dislocations treated with anterior cervical discectomy and fusion has a low failure rate. Global Spine J. 2017;7(2):110–​115. doi: 10.1177/​2192568217694002. Epub Apr 6, 2017. https://​www.ncbi.nlm.nih.gov/​pubmed/​28507879 Belirgen M, Dlouhy BJ, Grossbach AJ, et al. Surgical options in the treatment of subaxial cervical fractures: A retrospective cohort study. Clin Neurol Neurosurg. 2013;115(8):1420–​1428. doi:  10.1016/​j.clineuro.2013.01.018. Epub Mar 5, 2013. https://​www.ncbi.nlm.nih.gov/​ pubmed/​23481897 Casha S, Christie S. A systematic review of intensive cardiopulmonary management after spinal cord injury. J Neurotrauma. 2011;28(8):1479–​1495. doi: 10.1089/​neu.2009.1156. Epub Apr 8, 2010. https://​www.ncbi.nlm.nih.gov/​pubmed/​20030558 Ditunno JF, Little JW,Tessler A, et al. Spinal shock revisited: A four-​phase model. Spinal Cord. 2004 Jul;42(7):383–​395. https://​www.ncbi.nlm.nih.gov/​pubmed/​15037862

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Fisher CG, Dvorak MF, Leith J, et al. Comparison of outcomes for unstable lower cervical flexion teardrop fractures managed with halo thoracic vest versus anterior corpectomy and plating. Spine (Phila Pa 1976). 2002;27(2):160–​166. https://​www.ncbi.nlm.nih.gov/​pubmed/​ 11805662 Fountas KN, Kapsalaki EZ, Nikolakakos LG, et al. Anterior cervical discectomy and fusion associated complications. Spine (Phila Pa 1976). 2007;32(21):2310–​2317. https://​www.ncbi.nlm. nih.gov/​pubmed/​17906571 Kirshblum SC, Burns SP, Biering-​Sorensen F, et  al. International standards for neurological classification of spinal cord injury (revised 2011). J Spinal Cord Med. 2011;34(6):535–​546. doi:  10.1179/​204577211X13207446293695. https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​ PMC3232636/​ Kwon BK, Fisher CG, Boyd MC, et  al. A prospective randomized controlled trial of anterior compared with posterior stabilization for unilateral facet injuries of the cervical spine. J Neurosurg Spine. 2007;7(1):1–​12. https://​www.ncbi.nlm.nih.gov/​pubmed/​17633481 Lee JY, Nassr A, Eck JC, et al. Controversies in the treatment of cervical spine dislocations. Spine J. 2009 May;9(5):418–​423. doi: 10.1016/​j.spinee.2009.01.005. Epub Feb 23, 2009. https://​ www.ncbi.nlm.nih.gov/​pubmed/​19233734 Song KJ, Lee KB. Anterior versus combined anterior and posterior fixation/​fusion in the treatment of distraction-​flexion injury in the lower cervical spine. J Clin Neurosci. 2008;15(1): 36–​42. https://​www.ncbi.nlm.nih.gov/​pubmed/​18061456 Walters BC, Hadley MN, Hurlbert RJ, et  al. Guidelines for the management of acute cervical spine and spinal cord injuries:  2013 update. Neurosurgery. 2013;60 Suppl 1:82–​91. doi:  10.1227/​01.neu.0000430319.32247.7f. https://​www.ncbi.nlm.nih.gov/​pubmed/​ 23839357

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Occipitocervical Dislocation Alexander B. Dru and Daniel J. Hoh

3

Case Presentation

A 28-​year-​old woman presents to the emergency department after being struck by a car at high speed while changing a tire on the side of a road. The patient arrives intubated for airway protection and with a cervical collar in place. She has multiple deep lacerations to the head and neck, an open left humerus fracture, and a distended abdomen. She has no significant past medical or surgical history. Upon arrival, the patient’s vital signs are blood pressure 130/​71, pulse 79, respiratory rate 14 (mechanically ventilated), and temperature 37.1°C. Neurologic examination (off sedation) is remarkable for a Glasgow Coma Scale (GCS) of 7T (does not open eyes, intubated, localizes right greater than left upper extremity to noxious stimuli). Cranial nerve examination is consistent with pupils of 2 mm, equal and reactive to light, intact corneal reflexes, and present cough and gag reflexes. On motor examination, the patient weakly withdraws all four extremities, right greater than left.

Questions

1. What radiologic studies are indicated as part of the initial neurosurgical evaluation (imaging modality and anatomic area to image)? 2. What is the most appropriate management of the cervical collar? 3. In the setting of a potential spinal cord injury (SCI), what is the importance of cardiopulmonary vital signs?

Assessment and Planning

Given a history of high-​energy mechanism of injury to the head and neck, the initial neurosurgical survey includes evaluation for acute intracranial pathology and spinal column injury resulting in instability and/​or spinal cord or nerve compression. The patient should be assessed for both possibilities with an emergent head computed tomography (CT) and full spine CT. Since the patient has depressed mental status, the patient should be maintained in a cervical collar until cervical spine CT and further clinical assessment is made. If the patient is suspected of having a potential cervical SCI, heart rate and blood pressure should be closely monitored for neurogenic shock. Upper cervical SCI can result in impaired respiratory motor function. A secure airway should be confirmed at time of the initial survey.

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Occipitocervical dislocation (or atlanto-​occipital dislocation, AOD) is a highly unstable injury to the cranio-​cervical junction (Figure 3.1). Historically, AOD was only reported in autopsy findings likely due to a high rate of mortality related to severe cervical spine instability and concomitant upper cervical SCI. Currently, AOD is estimated to cause up to 35% of fatalities in motor vehicle collisions and 10% of fatal cervical spine injuries. Better management by first responders, established advanced trauma life support protocols, and modern imaging modalities have contributed to improved survival rate after traumatic AOD. AOD is typically a result of high-​ energy deceleration forces. Distraction with hyperextension-​flexion, often with a rotational component, are necessary to cause forces significant to disrupt the robust ligamentous attachments at the occipital-​cervical junction. Mortality is likely related to dislocation at the craniocervical junction causing upper cervical spinal cord compression and acute respiratory dysfunction and/​or hemodynamic instability secondary to neurogenic shock. Immediate immobilization in the field (e.g., cervical collar) followed by prompt diagnosis and external stabilization (e.g.,

A

C

B

D

Figure 3.1  Radiograph (A), computed tomography (CT) sagittal (B), coronal (C), and three-​dimensional reconstruction (D) of demonstrating atlanto-​occipital dislocation (AOD).

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Occipitocervical Dislocation

halo vest) may prevent or mitigate neurologic injury, with some patients presenting as neurologically intact or with an incomplete SCI. SCI can be a result of dislocation leading to compression, contusion, laceration, or ischemia of the spinal cord. SCI at the cranio-​cervical junction can present with a variety of complete or incomplete motor and sensory deficits. Bell cruciate paralysis is an incomplete syndrome unique to the cranio-​cervical junction characterized by weakness of the upper extremities with little to no involvement of lower extremity muscle groups. The pattern of injury is secondary to midline damage to the upper pyramidal decussation. The somatotopy of the decussation is such that the injured upper extremity motor fibers cross more superomedially, whereas the spared lower extremity fibers are inferolateral in the medulla. Other associated neural and vascular injuries are often observed in the setting of AOD. Individual cranial nerves are susceptible to injury following AOD, specifically lower cranial nerves IX, X, XI, and XII as they traverse the jugular or hypoglossal foramen. Most commonly, cranial nerves IX, X, and XI are affected due to tethering and traction within the jugular foramen. The hypoglossal nerve (CN XII) may be at high risk if there is a concomitant fracture of the occipital condyle extending into the hypoglossal canal. Carotid and vertebral artery injuries may occur due to stretching or laceration, with either intimal tears, dissection, or thrombosis. Pontomedullary subarachnoid blood may be an indication of AOD with posterior circulation injury.Vertebral artery injury can result in posterior inferior cerebellar artery distribution ischemia with a lateral medullary syndrome characterized by cerebellar dysmetria; ipsilateral cranial nerve V, IX, X, and XI deficits; an ipsilateral Horner syndrome; and contralateral loss of pain and temperature sensation.

Oral Boards Review: Diagnostic Pearls

1. Prompt multiplanar CT imaging is crucial to the timely and accurate diagnosis of AOD. a. Displacement of the occipital condyle from C1 lateral mass by more than 2 mm (adults) or more than 4 mm (children) indicates potential AOD. 2. One should have a high index of suspicion for AOD if: a. High cervical SCI is present without evidence of cervical fracture and/​or dislocation in the subaxial spine. b. Bell cruciate paralysis is present with only upper extremity paralysis. c. Isolated lower cranial nerve dysfunction (e.g., IX, X, XI, XII) is present. d. Subarachnoid blood is present at the pontomedullary junction. e. Significant soft-​tissue swelling (e.g., retropharyngeal) is present at the upper cervical spine.

Questions

1. Describe the utility of x-​ray, CT, and magnetic resonance imaging (MRI) in the diagnosis and management of AOD.

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2. Describe image-​based diagnostic criteria for AOD. 3. What are two classification systems for AOD?

Decision-​Making

The diagnosis of AOD is made based on imaging studies. Historically,AOD was identified using two-​dimensional lateral plain x-​ray characterizing the radiographic relationship between structures of the skull base and upper cervical vertebrae. With the advent of modern CT imaging technology, the current gold standard for diagnosing AOD is with multiplanar thin-​slice CT. A basic knowledge of lateral x-​ray criteria for AOD, however, may be helpful in understanding the pathophysiology of AOD and for supplementary diagnostic evaluation in questionable cases. The Harris method or “rule of twelves” calculates the basion-​axial interval (BAI) and basion-​dental interval (BDI) (Figure 3.2A). BAI is the distance between the vertical extension of the posterior cortex of C2 and the posterior-​most tip of the basion. BDI is the distance from the tip of the dens to the basion. In normal adults, both BAI and BDI should be less than 12 mm. The Powers ratio is the ratio of two distances (Figure 3.2B). The numerator is the distance between the tip of the basion to the ventral midpoint of the posterior arch of C1. The denominator is the distance from the tip of the opisthion to the dorsal midpoint of the anterior arch of C1. A ratio greater than 1 suggests anterior dislocation of the head relative to the spine. Multiplanar CT imaging provides the highest sensitivity and specificity for diagnosing AOD. The condyle-​C1 interval (CCI) is measured by selecting four equidistant points

A

B

C

Figure 3.2  (A) The Harris method. In the radiograph, the basion-​dental interval (BDI; white) and basion-​axial interval (BAI; yellow) are both greater than 12 mm. (B) The Powers ratio. The numerator is the distance between the tip of the basion to the ventral midpoint of the posterior arch of C1. The denominator is the distance from the tip of the opisthion and the dorsal midpoint of the anterior arch of C1. A ratio of greater than 1 suggests atlanto-​occipital dislocation (AOD). (C) The condyle–​C1 interval (CCI). Four equidistant points along the articulating surface of the occiput–​C1 joint on sagittal CT are measured. AOD is suspected if the average of the four measurements is greater than 2 mm in adults or greater than 4 mm in children.

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along the articulating surface of the occiput–​C1 joint on sagittal or coronal CT (Figure 3.2C). AOD is suspected if the average of the four measurements is greater than 2 mm in adults or greater than 4 mm in children. Additional imaging modalities may be useful in further characterizing the extent of injury after AOD. MRI is generally not required for routine diagnosis, but it provides superior visualization of neurologic and soft tissue structures. Particularly in the setting of neurologic deficit, MRI may elucidate the underlying etiology, whether spinal cord compression, contusion, ischemia, or epidural hematoma. MRI may also identify ligamentous disruption at the occipital-​cervical articulation, as well as elsewhere in the cervical spine (e.g., transverse ligament). CT angiography may identify associated vascular injuries with potential risk of thromboembolic stroke. There are two major classification systems for AOD. The Traynelis Classification System characterizes the direction of head dislocation relative to the spine (Figure 3.3). Type 1 is ventral head dislocation, type 2 is vertical displacement, and type 3 is dorsal dislocation relative to the cervical spine.The Bellbarba system is based on imaging findings in neutral position as well as with controlled test traction. It is designed to assess spinal stability and facilitate management decision-​making. Type 1 AOD is considered stable. It is characterized by both BAI and BDI within 2 mm of normal and less than 2 mm displacement with traction. Type 2 AOD is unstable. It is characterized by both BAI and BDI within 2 mm of normal, but significant displacement with test traction. Type 3 AOD is also unstable and demonstrates BAI and BDI values of greater than 2 mm of normal in neutral position.

Questions

1. What is the immediate management of AOD? 2. What is the risk of cervical traction in AOD? 3. What are the goals of surgical treatment? 4. What is potential loss of range of motion after surgical treatment?

Surgical Procedure

AOD is an acute, highly unstable injury with potential risk of permanent upper cervical SCI. Once the diagnosis is made, the patient should be placed in immediate external immobilization with strict cervical spine precautions. Patients presenting with acute trauma are usually already in a cervical collar. Halo vest immobilization generally provides better stabilization of the cranio-​cervical junction than a rigid cervical collar alone, and securing the patient in a halo vest should be considered. Ultimately, AOD is a result of disruption of the ligamentous attachments between the occiput and the upper cervical spine. Therefore, external bracing alone is unlikely to provide long-​term healing and stability. Reduction of AOD and internal fixation and fusion across the occipital-​cervical junction is generally recommended for definitive treatment. In the setting of polytrauma with cardiopulmonary compromise, it is appropriate to maintain the patient in halo external immobilization with strict cervical precautions until the patient is stable enough to be safely taken to the operating room.

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Figure 3.3 The Traynelis classification system. Type 1 (top) is ventral head dislocation. Type 2 (middle) is vertical displacement. Type 3 (bottom) is dorsal dislocation relative to the cervical spine.

The role of closed reduction with traction for AOD is controversial. Due to instability at the occipital-​atlantal articulation with potential for further vertical head displacement and neurovascular injury, one should generally avoid traction. There is a reported 10% risk of neurologic deterioration with the use of traction in the setting of AOD. The goals of surgical treatment are to immediately stabilize the cranio-​cervical junction with internal fixation, decompress the spinal cord by reduction and/​or removal of any compressive lesions, and provide long-​term maintenance of correction with arthrodesis.Various posterior surgical techniques for stabilization have been described with current approaches generally involving screw fixation of the occiput and upper cervical spine connected by occipital plate-​rod constructs (Figure 3.4). Determining how many cervical levels are necessary for fixation depends on individual patient anatomy, bone integrity, and the presence of other concomitant cervical injuries. The cranio-​ cervical junction can be a challenging region in which to achieve successful arthrodesis. Various autologous (e.g., iliac crest, rib harvest), allogeneic, and synthetic graft options supplemented by graft wiring techniques may be used to optimize fusion rate.

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Occipitocervical Dislocation

Figure 3.4  Occipital–​C4 fusion for internal stabilization of atlanto-​occipital dislocation (AOD). Surgical treatment for AOD often involves stabilization across the occiput–​C2, thereby eliminating motion across both the occipital-​atlantal and atlantal-​axial articulations. As a result, patients can expect loss of 50% of head flexion/​extension and 50% of right–​left rotation. Adult patients with subaxial cervical spondylosis and baseline restricted range of motion may experience even greater overall functional impairment. This permanent loss of range of motion should constitute an important part of the preoperative discussion with patients and caregivers to appropriately align expectations after surgery.

Oral Boards Review: Management Pearls

1. AOD is a highly unstable injury and patients should be immediately placed in a rigid external orthosis. A halo vest generally provides better immobilization at the occipital-​cervical junction than a rigid cervical collar. 2. Definitive treatment for AOD generally involves reduction with surgical decompression (if needed) and stabilization across the occipital–​cervical junction. a. Current surgical stabilization techniques include screw fixation of the occiput and the cervical spine with a connecting occipital plate-​rod construct. b. Determining adequate points of fixation in the cervical spine depends on the patient’s individual anatomy and bone integrity.

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3. Perioperative intensive care management may be necessary to treat cardiopulmonary issues related to neurogenic shock and upper cervical SCI leading to diaphragm paralysis. a. Neurogenic shock is best treated with dopamine and phenylephrine. The presence of bradycardia and hypotension that fail to respond to intravenous fluids suggest neurogenic rather than hypovolemic shock.

Aftercare

Early postoperative care after surgical treatment for AOD is generally determined by the extent of neurologic deficits and other associated injuries. Patients with cardiopulmonary compromise from cervical SCI should be managed in an intensive care unit until hemodynamic and respiratory issues are stabilized. Hypotension and bradycardia in the setting of acute cervical SCI should alert for potential neurogenic shock. Management consists of intravenous sympathomimetic agents and fluid resuscitation. Patients with upper cervical SCI with diaphragmatic paralysis and who fail ventilator weaning should be expeditiously transitioned from an endotracheal tube to a tracheostomy. Aggressive pulmonary toilet and respiratory rehabilitation should be implemented to reduce risk of pneumonia. Additional SCI management should be directed toward preventing venous thromboembolic, urinary tract, and pressure ulcer complications. Patients with adequate surgical reduction and internal fixation generally do not require supplementary external bracing. Continued postoperative use of a rigid cervical collar or halo vest may lead to skin breakdown or halo pin site complications and can impede rehabilitation. Patients with poor bone mineral density or with high risk of instrumentation failure, however, may benefit from additional postoperative external orthosis, and may be considered in select individuals. Serial routine follow-​up should be performed at regular intervals up to generally 12 months postoperative to assess for neurologic function and for eventual successful fusion. Maintenance of correction, stable instrumentation, and the presence of bridging bone across the occipital-​cervical junction indicate bony healing. Complications and Management

Surgical complications after occipital-​cervical fusion include those that may be encountered after any posterior spine fusion including surgical site infection, blood loss, cerebrospinal fluid leak, pseudarthrosis, and instrumentation failure. New postoperative neurologic deficits after surgery are uncommon. Given the relatively favorable spinal canal-​to-​spinal cord ratio at the craniocervical junction, direct injury to the spinal cord during surgery is rare. Placing patients prone with AOD, however, can potentially cause new neurologic deficits given the highly unstable injury and risk of further dislocation during positioning. Positioning patients in a halo vest with pre-​and postpositioning electrophysiologic spinal cord monitoring and intraoperative fluoroscopy are measures that may reduce this risk. The course of the vertebral artery as it traverses the cranio-​cervical junction can be variable, and preoperative assessment of its anatomy is recommended prior to screw placement, specifically at C1 and C2. Bilateral vertebral artery injuries are generally fatal,

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and therefore, careful evaluation for any vertebral artery anomalies (e.g., unilateral dominant, torturous) or associated traumatic occlusion (e.g., dissection) should be made. In situations of an incompetent unilateral vertebral artery, careful consideration should be made to avoid screw placement that may put the contralateral artery at risk. The occipital-​cervical junction is a region that can be challenging to achieve successful arthrodesis. Instrumentation failure with screw loosening or rod fracture on routine postoperative x-​ray indicate likely pseudarthrosis. Late postoperative new onset or worsening pain may be an early sign of failed fusion. Further investigation of suspected pseudarthrosis includes fine-​cut CT imaging to assess for the presence or absence of bridging bone across the occipital–​cervical junction. Asymptomatic pseudarthrosis with intact instrumentation may be treated conservatively. Instrumentation failure, progressive deformity, worsening pain, or new neurologic deficits in the setting of failed fusion may be indications for revision surgery.

Oral Boards Review: Complication Pearls

1. AOD is a highly unstable injury and therefore maintaining strict immobilization is critical. a. Neurologic deterioration may occur with any excessive motion, and therefore cervical traction should generally be avoided. b. Special care should be made in positioning patients prone for surgery, with pre-​and postpositioning fluoroscopy and electrophysiologic spinal cord monitoring. 2. The vertebral artery may be at risk during surgical fixation at the occipital-​ cervical junction due to preexisting anatomic anomalies or secondary to traumatic injury. a. Careful preoperative assessment of both vertebral arteries should be made to avoid potential risk of bilateral vertebral artery compromise. 3. The occipital–​cervical junction is susceptible to pseudarthrosis, which may present with late-​onset pain, neurologic worsening, progressive deformity, or instrumentation failure. a. Evaluation includes multiplanar thin-​cut CT imaging to assess for bridging bone. b. Symptomatic pseudarthrosis should be treated with revision fusion.

Evidence and Outcomes

AOD is relatively uncommon compared to other traumatic cervical spine injuries, which may in part be secondary to a high mortality risk immediately at the time of injury. Existing literature, therefore, regarding treatment, prognosis, and outcomes is limited. Modern advances in care by first responders, emergency trauma services, diagnostic imaging, and spine surgery have likely contributed to better survival. Long-​term outcome after AOD is most likely related to neurologic function at time of initial presentation, including both SCI and any potential concomitant traumatic brain injury. Complete upper cervical SCI portends a worse prognosis than incomplete and lower cervical injuries. Recent literature suggests that early decompression 29

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and stabilization of cervical spine injuries may enhance potential for neurologic recovery. Additionally, better medical management with aggressive rehabilitation and chronic preventative care for SCI-​related complications have improved overall life expectancy post-​SCI. References and Further Reading

Fisher CG, Sun JC, Dvorak M. Recognition and management of atlanto-​ occipital dislocation: Improving survival from an often fatal condition. Can J Surg. 2001;44(6):412–​420. Horn EM, Feiz-​erfan I, Lekovic GP, Dickman CA, Sonntag VK, Theodore N. Survivors of occipitoatlantal dislocation injuries:  Imaging and clinical correlates. J Neurosurg Spine. 2007;6(2):113–​120. Kleweno CP, Zampini JM,White AP, Kasper EM, Mcguire KJ. Survival after concurrent traumatic dislocation of the atlanto-​occipital and atlanto-​axial joints: A case report and review of the literature. Spine. 2008;33(18):E659–​E662. Pang D, Nemzek WR, Zovickian J. Atlanto-​occipital dislocation—​part  1:  Normal occipital condyle-​C1 interval in 89 children. Neurosurgery. 2007;61(3):514–​521. Pang D, Nemzek WR, Zovickian J. Atlanto-​occipital dislocation—​part  2:  The clinical use of (occipital) condyle-​C1 interval, comparison with other diagnostic methods, and the manifestation, management, and outcome of atlanto-​occipital dislocation in children. Neurosurgery. 2007;61(5):995–​1015.

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Central Cord Injury Bizhan Aarabi, Charles A. Sansur, David M. Ibrahimi, Mathew Kole, and Harry Mushlin

4

Case Presentation

A 45-​year-​old police officer sustained a cervical spine “whiplash” injury during a high-​ speed car chase and was momentarily unconscious. Immediately following the motor vehicle collision (MVC), he was unable to move any of his extremities and EMTs were there within 30 minutes of the accident. He gradually regained function in his legs, but his arms were burning, tingling, and powerless. His Glasgow Coma Scale score was 14, his pulse rate 55 bpm, and blood pressure 90/​60 mm Hg. He was complaining of neck pain and severe burning and tingling of his hands and forearms. His cervical spine was tender, his chest clear, and abdomen soft. He was given a liter of normal saline and transferred to the trauma center within 56 minutes. Upon presentation, he was conscious and alert; he was complaining of severe hypersensitivity of his hands and weak arms. His respiratory rate was 12, pulse rate 60 bpm, blood pressure 100/​75 mm Hg, and O2 saturation 99% on room air. Primary and secondary surveys did not reveal additional findings. Following resuscitation, neurosurgery was called to evaluate the patient. Neurological examination showed normal speech and cranial nerves. His American Spinal Injury Association (ASIA) motor score (AMS) was 56 and ASIA Impairment Scale (AIS) grade D (see Table 4.1). His hands and forearms were extremely sensitive to sensory examination and touch. Deep tendon reflexes were absent in the upper extremities but slightly hyperactive in the lower extremities. Digital rectal examination indicated good sensation and volition.

Questions

1. What is the likely neurological diagnosis? 2. What imaging modalities best aid in management? 3. What anatomical regions of the vertebral column would you study in imaging studies? 4. What is the most appropriate timing for imaging studies and treatment?

Assessment and Planning

The composite picture described here is a typical presentation of what is called acute traumatic central cord syndrome (ATCCS). ATCCS is the most frequently encountered

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Table 4.1 ASIA motor score of the presented case

Right Left

C5

C6

C7

C8

T1

L2

L3

L4

L5

S1

4 4

2 3

2 3

1 2

1 2

5 5

5 5

5 5

5 5

5 5

clinical picture of a mild to moderate (AIS grade C or D) incomplete blunt traumatic spinal cord injury (SCI). Dr. R. C. Schneider was the first to describe ATCCS: in his 21 patients, upper extremities were much weaker than the lower extremities, there were varying degrees of sensory loss, and the patients had difficulty with sphincter control.1–​3 Close to half of patients with ATCCS have no radiographically obvious fracture dislocations and instead suffer from congenital or degenerative spinal stenosis (Figure 4.1). Ten of 21 patients in Dr. Schneider’s series had radiographically proven fracture dislocations, and 11 had degenerative spinal stenosis. In another clinical series of 42 patients with ATCCS due to congenital stenosis or disc/​osteophyte complex, 33 (~80%) were AIS grade D at admission.4 These elderly patients sustained their cervical spine hyperextension injury mostly following a mechanical fall during which the spinal cord was presumably pinched between an acutely bulged intervertebral disc and the buckled ligamentum flavum. While the most frequent segmental injury was at C3–​C4, the compressive contusive lesion may be in more than two separate skeletal segments. Approximately 35% of patients with degenerative ATCCS exhibit magnetic resonance imaging (MRI) or computed tomography (CT) evidence

Figure 4.1  Admission imaging studies of the case presented above. Plates A and C indicate right and left lateral computed tomography (CT) views of facet joints and plate B the midsagittal view of the vertebral bodies. There is no evidence of fracture dislocation, and morphology is essentially normal. Plates D, E, and F indicate T2-​ weighted sagittal magnetic resonance imaging (MRI) showing prevertebral soft tissue swelling (long arrow), spinal cord compression with signal change at C3-​C4 (short arrow), and spinal stenosis at three skeletal segments (C3–​C6).

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of extension injury (Extension Distraction Stage 1 of Allen et al.)5 to one or more of the intervertebral discs.4 Under such circumstances, there may be an avulsion fracture of the antero-​inferior edge of the rostral vertebral body at the disc level, and T2-​weighted MRI may indicate signal change at the disc level (mostly at the C6–​C7 disc level). Skeletal stenosis may range from 1 to 5 segments; however, T2-​weighted MRI usually indicates signal change at one short segment of spinal cord, mostly at the C3–​C4 level (Figure 4.1). There may be nonspecific signal change in the prevertebral or supraspinal soft tissues (Figure 4.1). The intramedullary lesion signal change typically is short and within one skeletal segment (Plate E). Postmortem studies indicate that translation of kinetic energy into cytoskeletal damage is dispersed within the posterolateral funiculus of the spinal cord, disrupting neural transmission in the lateral corticospinal tract.6 Minor necrosis of the central gray has been reported; however, in a typical ATCCS exhibiting AIS grades C or D functional loss, there is no intraparenchymal bleeding, as originally suggested by Dr. Schneider.1,2,6,7

Oral Board Review: Diagnostic Pearls

1. Almost 50% of ATCCS patients are those with fracture dislocations. 2. In ATCCS due to hyperextension injuries, morphology is almost always well-​ maintained with no evidence of structural instability. 3. ATCCS due to hyperextension injuries is usually a mild to moderate (AIS grades C and D) SCI. 4. Intramedullary hemorrhage in hyperextension ATCCS is almost always absent. 5. ATCCS primarily involves upper extremities with variable degrees of sensory loss and sphincter dysfunction.

Questions

1. How do clinical and radiological findings influence surgical planning? 2. What is the most appropriate timing for intervention in this patient? 3. What is the best surgical technique to fully decompress the spinal cord under compression? The neurosurgeon confronted with an elderly patient with positive past medical history of comorbidities and hyperextension ATCCS due to multisegmental spinal stenosis bases treatment decisions on certain critical considerations:  (1) the cervical spine in this patient is stable, therefore, there is no urgency for speedy cervical spine anatomical realignment, spinal cord decompression, and internal fixation; (2) the SCI in ATCCS is usually mild to moderate and incomplete; (3) regardless of management, surgical or nonsurgical, significant recovery of neurological deficit over time is almost guaranteed; (4) surgical intervention is usually complex, tedious, meticulous, and may take several hours; and (5) although there is low-​level evidence that decompression within 24 hours may help recovery of function, this issue remains controversial and is usually applied only to the most severe SCI.4,8,9

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Decision-​Making Oral Board Review: Decision-​Making Pearls

1. The spinal cord is usually under compression at one or several skeletal segments. 2. The surgeon has to plan a timely and extensive surgery, taking into consideration a meticulous, multisegmental, complex anterior or posterior approach with or without internal fixation. 3. Though the surgery does not have to be urgent or emergent, the literature is quite varied and inconclusive concerning surgical timing.

Surgical Procedure

Before surgery, one needs to review the imaging studies and look for the following: 1 . Is the patient’s cervical spine kyphotic, straight, or lordotic? 2. How many stenotic skeletal segments are to be dealt with? 3. Where is the site of most stenosis on MRI with signal change? 4. Should the surgical technique be anterior, posterior, or circumferential? 5. Is laminectomy needed? 6. What is the relationship of signal change on MRI and the length of the stenotic canal?

Anterior Cervical Discectomy and Fusion

This surgical technique is suitable when the pressure on the spinal cord is primarily anterior. ACDF is especially indicated in patients who need corrective surgery for sagittal imbalance and the probability of worsening kyphotic deformity is high with laminectomy. Figures 4.2 and 4.3, respectively, belong to the case under discussion and a 60-​ year-​old man with ATCCS and an AMS of 94 following an automobile accident. The first patient has well-​maintained sagittal balance, but the second patient suffers an early kyphotic deformity, and the compression on the cord at C4–​C5 and C5–​C6 dictated an anterior approach. In order to reverse early kyphosis, posterior osteophytes needed to be resected generously, followed by insertion of lordotic implants. In both cases, decompression was enough with no need for laminectomy. Laminoplasty

Laminoplasty is appropriate in patients who do not have prominent soft disc herniation and only suffer from hard disc osteophyte complex across several motion segments with preserved cervical lordosis.10 In the presence of multiple-​segment spinal stenosis and kyphotic deformity, anterior approach or posterior laminectomy and posterior spinal fusion may take precedence (Figure 4.4). Laminoplasty is contraindicated in the presence of fracture dislocations.

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Figure 4.2  Management of the case presented. The patient had three-​level anterior cervical discectomy and fusion (ACDF) with resection of osteophytes and satisfactory decompression of the segmental damage to the cord and spinal stenosis. The patient did not need laminectomy and fusion.

Figure 4.3  A 60-​year-​old man with acute traumatic central cord syndrome (ATCCS) following an automobile accident who was managed by two-​level anterior cervical discectomy and fusion (ACDF) to relieve pressure from the spinal cord. ACDF was particularly indicated since the patient had kyphotic deformity and significant pressure ventrally The surgery resulted in relief of spinal cord compression and kyphotic deformity with no need for laminectomy.

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Figure 4.4  A 43-​year-​old man with acute traumatic central cord syndrome (ATCCS) and managed by laminoplasty, which relieved spinal cord compression while maintaining a modest degree of axial spine movements, with maintenance of the patient’s posterior tension band. Laminectomy

Laminectomy with or without posterior spinal fusion should be considered for multisegmental spinal stenosis with well-​maintained sagittal alignment.We prefer trough laminectomy in patients with severe stenosis and rigid spines. In this technique, a high-​ speed drill is used to remove the outer table of each skeletal segment to the inner table; this is followed by a 2  mm Kerrison Punch to remove the inner table and then lift up the lamina following resection of the ligamentum flavum. At times there are adhesion strands between the dura and the inner table that need to be sectioned with microscissors (Figures 4.5 and 4.6).

Oral Board Review: Surgical Technique Pearls

1. For extensive ACDFs, look for the superior laryngeal nerve at C3–​C4 and inferior thyroid artery and recurrent laryngeal nerve at the level of C6–​C7 skeletal segments. 2. It is vital to resect osteophytes at the level of posterior annulus and then proceed with resection of the posterior longitudinal ligament and complete foraminotomy. 3. Your implants need to be lordotic in order to reverse kyphotic deformity. 4. In patients with straight or kyphotic cervical spine, avoid laminectomy without fusion.

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Figure 4.5  A 33-​year-​old man who sustained acute traumatic central cord syndrome (ATCCS) following a motor vehicle accident. His ASIA motor score was 54, and 24 hours following admission he underwent laminectomy for spinal cord decompression.

Aftercare

1. Venous thromboembolism prophylaxis 72 hours after admission is instituted whether management is non-operative or surgical intervention. 2. Develop a rehabilitation plan as soon as possible. 3. Perform tracheostomy for high cervical AIS grade C or worse patients.

Figure 4.6  Schematic view of trough laminectomy. Two troughs are produced on each side of the lamina followed by removal of the inner tables using a Kerrison rongeur. Incision of the ligamentum flavum will release the lamina, which is removed without aggressive surgery using a Leksell rongeur or the thick footplate of a rongeur over a spinal cord parenchyma tightly compressed by spinal stenosis.

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Preoperative

Five years postop

Figure 4.7 Ten years following successful decompression of the spinal cord, the patient was working in a car dealership suffering from lack of dexterity of his hands (50%), burning and numbness of his hands, and urinary frequency. He was on baclofen for severe spasms and gabapentin for numbness and tingling of his hands. 4 . Discuss a long-​term disability financial coverage plan. 5. Administer medications such as gabapentin or pregabalin for dysesthetic hand and forearm pain. 6. Schedule long-​term MRI studies to present evidence for central cord syrinx. These patients may have an AMS of 100, but their lives are miserable owing to lack of dexterity and presence of dysesthetic pain and paresthesia (Figure 4.7).

Pivot Pearls

1. If a patient presents with ATCCS while being on warfarin or antiplatelet agents, it is recommended to wait until the patient has an appropriate coagulation profile and only then proceed with surgical intervention.

Complication Pearls

1. Management of major venous thromboembolism takes precedence over surgical decompression of the spinal cord. 2. Significant swallowing difficulty should be managed by gastrostomy without too much delay in the nutritional requirements of the patient. 3. AIS grade C patients with ATCCS due to high cervical cord SCI may need short-​term tracheostomy in order to prevent complications such as pneumonia or atelectasis.

References and Further Reading

1. Schneider RC. A syndrome in acute cervical spine injuries for which early operation is indicated. J Neurosurg. 1951;8:360–​367.

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2. Schneider RC, Cherry G, Pantek H. The syndrome of acute central cervical spinal cord injury. J Neurosurg. 1954;13:546–​577. 3. Schneider RC, Thompson JC, Bebin J. The syndrome of acute central cervical spinal cord injury. J Neurol, Neurosurg Psychiatry. 1958;21:216–​227. 4. Aarabi B, Alexander M, Mirvis SE, et al. Predictors of outcome in acute traumatic central cord syndrome due to spinal stenosis. J Neurosurgery Spine. 2011;14:122–​130. 5. Allen BL, Jr., Ferguson RL, Lehmann TR, O’Brien RP. A mechanistic classification of closed, indirect fractures and dislocations of the lower cervical spine. Spine. 1982;7:1–​27. 6. Quencer RM, Bunge RP, Egnor M, et  al. Acute traumatic central cord syndrome:  MRI-​ pathological correlations. Neuroradiology. 1992;34:85–​94. 7. Martin D, Schoenen J, Lenelle J, Reznik M, Moonen G. MRI-​pathological correlations in acute traumatic central cord syndrome: Case report. Neuroradiology. 1992;34:262–​266. 8. Lenehan B, Fisher CG,Vaccaro A, Fehlings M, Aarabi B, Dvorak MF. The urgency of surgical decompression in acute central cord injuries with spondylosis and without instability. Spine. 2010;35 (21 Suppl):S180–​S186. 9. Dvorak MF, Fisher CG, Hoekema J, et al. Factors predicting motor recovery and functional outcome after traumatic central cord syndrome:  A long-​term follow-​up. Spine. 2006;30 (20):2303–​2311. 10. Hirabayashi K, Bohlman HH. Multilevel cervical spondylosis. Laminoplasty versus anterior decompression. Spine. Aug 1 1995;20(15):1732–​1734.

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Atlantoaxial Instability Jonathan M. Parish and Domagoj Coric

5

Case Presentation

An 80-​year-​old man presents with a complaint of neck and bilateral shoulder pain as well as bilateral hand pain and numbness. Patient states the pain has been progressive for 2 months and has been unrelieved by antiinflammatory medication, oral steroids, muscle relaxants, and physical therapy. The patient has a history of rheumatoid arthritis and chronic obstructive pulmonary disease (COPD) with chronic steroid use but no other significant past medical history. The patient describes tingling in his hands, right greater than the left, as well as bilateral hand weakness, noting difficulty with opening jars and buttoning his shirt. The patient also complains of tingling and weakness in his legs and has been using a walker to assist with ambulation over the preceding 6 weeks. The patient denies any difficulties with bowel or bladder control. On examination, patient is alert and appropriate. Motor exam shows 4/​5 strength in his left upper extremity and 4/​5 in his right upper extremity. He has proximal right lower extremity strength of 4/​5 and right distal lower extremity strength 4/​5. He has 4/​5 left lower extremity strength. Sensory exam is intact to light touch and pinprick although the patient complains of paresthesias in his hands and feet. The patient has 2+ equal and symmetric biceps, triceps, patellar, and Achilles deep tendon reflexes. The patient has positive Hoffman sign bilaterally but no clonus or Babinski. Gait is stable with a walker.

Questions

1. What is the likely diagnosis? 2. What is the appropriate imaging modality and anatomical areas to image?

Assessment and Planning

Given the history and physical examination, the clinical picture raises the suspicion for the diagnosis of cervical myelopathy. Cervical spine computed tomography (CT) (Figure 5.1) reveals multiple levels of spondylosis with a soft tissue pannus at C1–​C2 causing severe narrowing of the cervical canal. Cervical magnetic resonance imaging (MRI) (Figure 5.2) reveals severe stenosis with compression of the cervical cord at C1 and signal change at C1–​C2 and multilevel spondylosis without significant cord compression at C5–​T1.The patient is diagnosed with C1–​C2 stenosis with spinal cord compression and myelopathy and is consented for C1–​C2 posterior decompression and fusion.

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Figure 5.1  Sagittal computed tomography (CT) scan of the cervical spine with evidence of rheumatoid pannus causing upper cervical stenosis.

Figure 5.2  Sagittal T2-​weighted magnetic resonance imaging (MRI) of the cervical spine with evidence of severe canal stenosis and associated T2 signal abnormality at  C1–​C2.

 

Atlantoaxial Instability

A number of different imaging modalities can be used to confirm atlantoaxial instability. Plain film radiographs of the cervical spine can be used to assess the atlantodental interval (ADI). The ADI is measured from anterior margin of the dens to the nearest point on the arch of C1. An ADI of greater than 5  mm or greater than 8  mm in rheumatoid arthritis suggests instability and need for C1–​C2 fixation. The posterior atlantodental interval (PADI) is measured from the posterior dens to the anterior aspect of the posterior ring of C1 and defines the neural canal width. A PADI of less than 14 mm suggests needs for decompression and stabilization of the C1–​C2 joint. Cervical CT is necessary to assess the atlantoaxial bony anatomy as well as to assess the foramen transversarium at C1 and C2. In particular, CT scan should be used to estimate screw length and medial/​lateral and cranial/​caudal screw trajectory. Preoperative assessment of the vertebral artery anatomy with cervical CT is imperative for safe C1–​ C2 screw placement. When there is concern for atlantoaxial instability but no clear evidence of pathology on CT or plain films, it is necessary to assess the integrity of the transverse atlantal ligament (TAL). Most commonly, cervical MRI is used to evaluate for any incompetence of the TAL. MRI can also evaluate the extent of cervical cord compression or cord injury that has occurred due to atlantoaxial instability. Flexion-​extension cervical x-​rays can also be used to evaluate for subluxation and TAL injury. Instability of C1–​C2 typically requires surgical intervention for stabilization.

Oral Boards Review: Diagnostic Pearls

1. History and physical exam must evaluate for radicular and myelopathic signs/​ symptoms. 2. Imaging required: a. CT scan with coronal and sagittal reconstruction. b. CT angiography (CTA) may be obtained to assess for vertebral artery anomalies. c. Flexion/​extension x-​rays or MRI to assess TAL integrity. 3. Radiographic measurements. 4. ADI greater than 5 mm or greater than 8 mm in rheumatoid arthritis suggests instability.

Questions

1. What radiological findings influence surgical planning? 2. What is the most appropriate timing for intervention in this patient?

Decision-​Making

When atlantoaxial instability is identified, surgery should be considered, especially if the patient is symptomatic. Signs of atlantoaxial instability are extremely variable, ranging from neck pain to nerve root injury to cervical myelopathy. Trauma and infections are

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indications for acute intervention, whereas congenital or chronic instability may be followed with serial imaging and examinations until the patient becomes symptomatic or stenosis becomes critical. Surgical techniques are numerous, but the overall goal is to decompress neural structures, restore normal or close to normal alignment, and stabilize the atlantoaxial joint.

Questions

1. What are the possible complications from screw placement? 2. If there is concern for intraoperative vertebral injury, how should the procedure be altered?

Surgical Procedure

Surgical fixation options for C1–​C2 stabilization include anterior and multiple posterior techniques. Anterior approach is rarely used but is preferred in cases where patients cannot tolerate prone positioning due to cardiac or pulmonary issues or the posterior bony elements are unsuitable for adequate screw placement. Regardless of surgical approach, care must be taken by the anesthesiologist with cervical precautions during intubation, which is often accomplished by nasal fiber-​optic intubation. Traction may be used to achieve reduction prior to fixation. Anterior approaches include transoral, retropharyngeal, or lateral. It is not uncommon for anterior compressive pathology to necessitate anterior decompression, but anterior C1–​C2 screw/​plate fixation remains rare due to infection and soft tissue healing concerns. For posterior approaches, the patient is positioned prone in military position with the chin tucked and the head in a Mayfield skull clamp. C1–​C2 transarticular screw fixation (Magerl’s technique) has a high rate of fusion, ranging from 90% to 99%.Vertebral artery injury is a major risk with transarticular screws. K-​wires are placed under fluoroscopic guidance starting 1–​2 mm cephalad to the midpoint of the C2–​C3 facet joint and proceeding down the C2 pars interarticularis, across the C1–​C2 joint space and into the lateral mass of C1. This procedure may be accomplished via a standard open technique exposing C1 to C6–​C7 or a less invasive technique utilizing an open exposure of C1–​C2 with bilateral paracentral percutaneous stab incisions at the C6–​C7 level. C1 lateral mass and C2 pars screw/​rod fixation, originally described by Goel and Laheri and modified by Harms and Melcher, provides a safer alternative to transarticular screw fixation by avoiding the vertebral artery anatomy. With exposure of the C1 lateral mass, care should be taken to control bleeding from the C1–​C2 venous plexus during lateral dissection. The vertebral artery in the sulcus arteriosus on top of C1 does not need to be completely exposed for placement of the C1 lateral mass screw. The C2 nerve root should be mobilized inferiorly or can be sacrificed if necessary. There are multiple options for C2 screw placement including pars, pedicle, and translaminar screws. For the C2 pars screws, care should be made to measure the distance to the foramen transversarium on preoperative CT. It is important to verify a sufficient width for C2 pars screw placement so as to not breach medial into the neural canal or lateral into

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the foramen transversarium. The C2 pars screw is angled at a steep trajectory mirroring the C2 pars, generally 20–​30 degrees superior as well as 5–​10 degrees medially. For a C2 pedicle screw placement, the entry point is slightly superior and medial to the pars screw and medially angled approximately 15–​30 degrees. The C2 superior trajectory is less steep than for the pars screw, typically 5–​10 degrees. C2 translaminar screws can be used as a salvage technique for failed C2 pars screws. Screws are placed at the junction of the lamina and spinous process with a trajectory matching the slope of the lamina. Care should be taken to place the screws at appropriate craniocaudal locations so as to not have the translaminar screws intersect. Laminar wiring techniques were initially described as a primary treatment for C1–​ C2 fixation but contemporarily are utilized as an adjunct to screw fixation. Posterior cervical wiring of C1 and C2 was first described by Gallie in 1939. The Gallie technique consists of a graft placed over the C2 spinous process and the posterior arch of C1, which is held in place with steel wire placed under the C1 lamina and looped around the C2 spinous process. Later, Brooks and Jenkins described bilateral graft placement between the C1–​C2 lamina, secured in place by bilateral C1 and C2 sublaminar wires. In the early 1990s, Sonntag modified the Gallie technique with a single sublaminar wire at the C1 and C2 spinous process, wiring to secure a strut-​graft wedged between the posterior arches of C1 and C2. In the presented case, a hybrid technique was utilized with a right C1–​C2 transarticular screw placement and C1 lateral mass and C2 pars screw/​rod construct on the left. A stab incision was made at approximately the C7 level on the right and a K–​wire was placed under fluoroscopic guidance followed by drilling, tapping, and placement of a C1–​C2 transarticular screw under lateral fluoroscopic guidance. Care is taken to maintain control of the K-​wire during all portions of the procedure. The C1 posterior ring and the superior portion of the C2 lamina were then resected to complete the spinal cord decompression. Following decompression, a C1 lateral mass and C2 pars screw was placed on the right (Figure 5.3). Rods were secured from C1 to C2, and local autograft mixed with morselized allograft was placed posterior and posterolaterally over the decorticated posterior elements of C1–​C2 (Figure 5.4).

Figure 5.3  Intraoperative lateral and anteroposterior (AP) cervical x-​rays after right C1–​C2 transarticular and left C1 lateral mass–​C2 pars screw-​rod placement.

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Figure 5.4  Postoperative lateral and anteroposterior (AP) cervical x-​rays.

Oral Boards Review: Management Pearls

1. Appropriate alignment with initial patient positioning is key for transarticular screw placement and appropriate reduction if necessary. 2. Preoperative CT should be reviewed carefully for a high-​r iding vertebral artery or other anomalous vertebral artery pathway prior to deciding type of C2 screw placement.

Pivot Points

1. If patient has subaxial stenosis in addition to C1–​C2 instability, the C1–​C2 construct, regardless of type of posterior technique, can be extended with lateral mass screws and posterior decompression to involve subaxial stenotic levels. 2. Transarticular screw placement requires reduction of C1–​C2 prior to screw placement. If reduction cannot be achieved, lateral mass and C2 pars/​pedicle screw fixation should be used. 3. Translaminar screws may be used as salvage technique if C2 pars/​pedicle screws are unable to be placed. 4. If occipito-​cervical instability is noted intraoperatively, the stabilization/​fusion can be extended up to the occiput.

Aftercare

Postoperative x-​rays may be obtained to confirm screw placement. Patient should be evaluated postoperatively for signs of radicular pain related to screw placement. If the C2 nerve root is sacrificed, patients should be informed of expected occipital numbness or paresthesias. A postoperative CTA should be obtained if there is any concern

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for vertebral injury. Depending on surgeon preference, a cervical collar may be used postoperatively. Patient can be mobilized as early as the night of surgery. A Foley catheter should be removed by postoperative day 1 unless there are underlying bladder concerns. Postoperative cervical x-​rays should be obtained at follow-​up appointments over the next year to confirm bony fusion. Complications and Management

If there is a likely vertebral artery injury noted after drilling/​ tapping the initial transarticular screw, that screw can still be placed to tamponade the bleeding or redirected to a more optimal trajectory. But no attempt should be made to place the contralateral screw due to concerns of potentially catastrophic bilateral vertebral artery injury leading to brainstem stroke. Mean arterial pressure should be elevated to maintain posterior circulation and prevent possible neurological insult. A  postoperative CTA should be obtained to evaluate for thrombosis or dissection or even arteriovenous fistula.

Oral Boards Review: Complications Pearls

1. If there is concern for vertebral artery injury, the contralateral transarticular screw should not be placed, and a lateral mass or pars/​pedicle screw should be placed instead. A postoperative CTA should be obtained to evaluate for thrombosis or dissection. 2. The surgeon should be aware of the C1–​C2 venous plexus and be prepared with cautery/​hemostatic agents to decrease bleeding in this area.

Evidence and Outcomes

Numerous posterior fixation techniques have evolved to address C1–​C2 instability. The Gallie fusion provides good initial fixation in flexion and extension but poor stabilization with rotation and a relatively high nonunion rate approaching 25%. Similarly, the Brooks/​Jenkins fusion provides reasonable biomechanical stability in flexion and extension and has been reported to achieve fusion in the 90% range with the addition of halo immobilization. Of course, halo fixation can be a source of significant morbidity itself. Sonntag and colleagues reported a 97% fusion rate in 36 patients treated with their modification of the Gallie interspinous process technique. The advent of screw fixation techniques brought more rigid biomechanical stability and concomitantly higher fusion rates. Magerl’s C1–​C2 transarticular technique provided increased rotational stability with fusion rates approaching 100%. Stillerman and Wilson reported on 22 patients utilizing a modification of this transarticular technique without additional bone-​wire fusion and reported a 95% fusion rate. Similar clinical results were also achieved by C1 lateral mass fixation and C2 pars fixation, as described by Goel and Laheri, as well as by Harms and Melcher. This technique provides superior biomechanical stability in rotation as well as flexion and extension but with significantly decreased risk of vertebral artery injury. This C1 lateral mass and C2 pars screw/​rod technique has enjoyed widespread adoption.

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References and Further Reading

Brooks AL, Jenkins EB. Atlantoaxial arthrodesis by the wedge compression method. J Bone Joint Surg Am. 1978;60A:279–​284. http://​www.ncbi.nlm.nih.gov.ahecproxy.ncahec.net/​pubmed/​ 348703 Coric D, Branch CL, Wilson JA, Robinson J. Arteriovenous fistula as a complication of C1–​ C2 transarticular screw fixation:  Case report and a review of the literature. J Neurosurg. 1996;85:340–​343. http://​www.ncbi.nlm.nih.gov/​pubmed/​8755766 Coyne TJ, Fehlings MG, Wallace MC, Bernstein M, Tutor CH. C1-​C2 posterior cervical fusion:  Long term evaluation of results and efficacy. Neurosurgery. 1995;37:688–​693. http://​ www.ncbi.nlm.nih.gov/​pubmed/​8559297 Dickman CA, Sonntag VK, Papadopoulos SM, Hadley MN. The inter-​spinous method of posterior atlantoaxial arthrodesis. J Neurosurg. 1991 Feb;74:190–​198. http://​www.ncbi.nlm.nih. gov.ahecproxy.ncahec.net/​pubmed/​1988587 Gallie WE. Fractures and dislocations of cervical spine. Am Surg. 1939;46:495–​499. Goel A, Desai K, Mazumdar D. Atlantoaxial fixation using plate and screw method:  A report of 160 treated patients. Neurosurgery. 2002;51:1351–​1356. http://​www.ncbi.nlm.nih.gov/​ pubmed/​12445339 Goel A, Laheri V. Plate and screw fixation for atlanto-​axial subluxation. Acta Neurochir (Wien). 1994;129(1–​2):47–​53. http://​www.ncbi.nlm.nih.gov.ahecproxy.ncahec.net/​pubmed/​7998495 Harms J, Melcher RP. Posterior C1-​C2 fusion with polyaxial screw and rod fixation. Spine. 2001;26(22):2467–​2471. http://​www.ncbi.nlm.nih.gov.ahecproxy.ncahec.net/​pubmed/​ 11707712 Magerl F, Seemann PS. Stable posterior fusion of the atlas and axis by transarticular screw fixation. In Kehr P, Weidner A (eds.), Cervical Spine (vol. 1). New York: Springer;1987:322–​327. Rahimi SY, Stevens EA,Yeh DJ, Flannery AM, Choudhri HF, Lee MR. Treatment of atlantoaxial instability in pediatric patients. Neurosurg Focus. 2003 Dec 15;15(6):ECP1. http://​www.ncbi. nlm.nih.gov/​pubmed/​15305843 Stillerman CB, Wilson JA. Atlanto-​axial stabilization with posterior transarticular screw fixation: Technical description and report of 22 cases. J Neurosurg. 1993 Jun;32:948–​954. http://​ www.ncbi.nlm.nih.gov/​pubmed/​8327097

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Basilar Invagination and Cranial Settling Benjamin D. Elder and Jean-​Paul Wolinsky

6

Case Presentation

A 65-​year-​old woman with a history of rheumatoid arthritis presented with neck pain, frequent falls, and difficulty with fine motor movements of the hands. On neurological exam, she had full strength but had 3+ reflexes in the upper and lower extremities and positive Babinski and Hoffman signs. A magnetic resonance image (MRI) of the cervical spine demonstrated a pannus formation at C1–​C2 with mild ventral cord compression and T2 signal change. Additionally, lateral flexion-​extension radiographs demonstrated 8 mm of translation of C1 with respect to C2. She was recommended to undergo a C1–​C2 decompression and C1–​C2 arthrodesis, but declined the operation. She neglected to follow-​up but presented 2 years later with increased weakness, particularly in her upper extremities. Additionally, she had been treated for multiple episodes of aspiration pneumonia. On neurological exam, she had 3/​5 strength in her bilateral upper extremities, and 4–/​5 strength in the bilateral lower extremities. She had 3+ reflexes in the bilateral upper extremities, and 4+ reflexes with clonus in the Achilles reflex bilaterally. A computed tomography (CT) image demonstrated new upward translation of the odontoid with extension of the tip of the odontoid 14 mm above the McGregor line (Figure 6.1).

Questions

1. What is the likely diagnosis? 2. How are basilar impression, basilar invagination, cranial settling, and platybasia defined and distinguished? 3. What imaging modalities should be utilized to assess these patients? 4. The presence of what other occipitocervical (OC) pathologies should be assessed? 5. What other disorders are frequently associated with OC pathologies?

Assessment and Planning

The neurosurgeon suspects a diagnosis of basilar impression with cranial settling due to progression of the patient’s C1–​C2 instability from rheumatoid arthritis. Basilar impression, basilar invagination, cranial settling, and platybasia are often used synonymously, but they represent discreet terminology.1 Basilar impression represents

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Figure 6.1  (A) Sagittal computed tomography (CT), (B) axial CT of the posterior fossa, and (C) axial CT at the level of the foramen magnum demonstrating basilar invagination with significant upward translation of the odontoid into the posterior fossa. (Adapted with permission from Wolinsky et al., Endoscopic image-​guided odontoidectomy for decompression of basilar invagination via a standard anterior cervical approach, J Neurosurg Spine 2007;6:184–​191.)

the broader category of OC junction pathologies. Basilar invagination results from migration of the entire spine into the skull base as the skull base remodels or invaginates (Figure 6.2), usually from congenital hypoplasia or dysplasia of various osseous structures at the OC junction or achondroplasia. Common pathologies leading to basilar invagination include osteogenesis imperfecta (most commonly type III), disorders of bone metabolism such as Paget disease, rickets, and hyperparathyroidism. In osteogenesis imperfecta, the load-​bearing capacity of the skull base is exceeded with microfractures in the region of the foramen magnum, leading to gradual deformity and softening of the skull base. OC junction tumors, trauma, and infection can lead to basilar invagination, but usually result in cranial settling. Cranial settling is a form of basilar impression due to C1–​C2 instability (commonly in the setting of rheumatoid arthritis), defined as upward migration (or rotation) of the C2 complex into the cranial vault. Atlanto-​occipital assimilation can develop into cranial settling, with ligamentous laxity at the C1–​C2 level that develops over time. This laxity may result from stress on the C1–​C2 complex from assimilation of the condyles and C1. The lack of flexion-​extension at the craniocervical junction leads to stress at C1–​C2 that ultimately results in the cranial settling. Platybasia is simply deformation and flattening of the skull base that can be found alone or in combination with other OC pathology. Patients with basilar invagination frequently have concurrent Chiari type I malformations, with rates of 54% reported in a series of 190 patients.2 In this series,

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Basilar Invagination and Cranial Settling

Figure 6.2  Sagittal computed tomography (CT) scan of a patient with osteogenesis imperfecta demonstrating basilar invagination with upward migration of the C1–​C2 complex into the cranial vault. (Reproduced with permission from Johns Hopkins University, 2016. All rights reserved. Benjamin Elder and Jean-​Paul Wolinsky.)

most patients presented between the second and fourth decades of life, with earlier and more acute presentation in patients without a concurrent Chiari type I malformation. Many patients reported neck pain, and common physical exam findings in both groups included myelopathy with weakness and paresthesias, gait abnormalities, bowel and/​ or bladder dysfunction, short necks, webbed necks, and lower hairlines. Additionally, patients may present with lower cranial nerve dysfunction depending on the extent of brainstem compression. Basilar invagination was historically identified on open-​mouth anteroposterior (AP) plain film radiographs in which the C1–​C2 facet complex was incompletely visualized. More detailed assessment can be made by determining the relationship of the odontoid tip with the Chamberlain line and McGregor line. Basilar invagination is typically diagnosed with extension of the tip of the odontoid at least 5  mm above the Chamberlain line or more than 7  mm above the McGregor line. Cranial settling is identified with protrusion of the tip of the odontoid more than 4.5  mm above the McGregor line in the setting of rheumatoid arthritis. Currently, CT images with sagittal, coronal, and three-​dimensional reconstructions are ideal for characterizing and defining OC junction abnormalities, particularly as these patients often have complex osseous anatomy with potentially Klippel-​Feil and/​ or cranial assimilation of C1. Additionally, MRI is critical for assessment of neurologic structures and spinal cord and/​or brainstem compression, as well as soft tissue and ligamentous structures. Flexion-​extension radiographs can be used to assess for instability, though caution should be exercised in the setting of often severe spinal cord and brainstem compression. Finally, vascular imaging such as CT angiography or even four-​vessel cerebral angiography is useful to define the vertebral artery anatomy, which may have an aberrant course in the setting of craniocervical pathology.

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Oral Boards Review: Diagnostic Pearls

1. Radiographic imaging with CT scans or lateral radiographs is used to differentiate basilar invagination and cranial settling. a. Basilar invagination: Upward migration of the entire spine into the skull base as the skull base remodels or invaginates. b. Cranial settling: Upward migration (or rotation) of the C2 complex into the cranial vault in the setting of C1–​C2 instability. 2. Each patient should undergo a detailed history and physical exam. Important historical information includes the length of the symptoms, progression of symptoms, and acuity of any changes change in neurological status, as well as presence of any medical comorbidities that may be associated. Important physical exam assessments include visual inspection, assessment of cervical range of motion, and performance of a detailed neurological exam including cranial nerve assessment. 3. Performance of CT imaging of the craniocervical junction is imperative for adequately assessing the potentially complex osseous anatomy. 4. Performance of MRI of the craniocervical junction is required to adequately determine the extent of compression of neurological structures, as well as assess the soft tissue and ligamentous structures. 5. Vascular imaging, typically with CT angiography, is important to adequately identify the vertebral artery anatomy, which may often have an aberrant course in these patients.

Questions

1. What is the most appropriate timing for operative intervention? 2. How do the clinical and radiographic findings influence surgical options? 3. How should cervical traction be used to determine the optimal surgical strategy? 4. What is the importance of oral hygiene prior to surgical intervention? 5. What is the significance of preoperative nutritional status and pulmonary function?

Decision-​Making

If untreated, basilar invagination and cranial settling may lead to significant neurological deterioration and even death. Although no specific criteria for surgical intervention exist, most patients present with some degree of neurological compromise and will require surgical intervention with decompression and stabilization in order to prevent further neurological decline. However, a small subset of patients who present without neurological deficits and with minimal extension of the odontoid into the foramen magnum and no spinal cord or brainstem compression could be followed closely clinically.

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Before surgical intervention, many patients with basilar impression undergo a trial of cervical traction to determine the amount of reduction of the odontoid that may be achieved. However, significant caution should be exercised in patients with significant compression to prevent further neurological injury. In general, low weights (5–​10 pounds) should be used with close neurological monitoring and the angulation of the traction modified to reduce neurological compression, often with the head elevated approximate 15 degrees above the horizontal plane. If the odontoid is completely reducible, the patient may be a candidate for posterior decompression and fusion alone.3 However, if the odontoid cannot be reduced, the patient often requires anterior decompression in conjunction with posterior stabilization (and often posterior decompression as well). There is a spectrum of severity of patients with cranial settling. Initially, there is C1–​C2 instability, followed by C1–​C2 instability with pannus formation. If left untreated, C2 starts to migrate upward and pseudostabilization occurs, with regression of the pannus. This is followed by complete cranial settling. All of these patients require posterior stabilization, but the degree of stabilization is determined by where the patient lies in the spectrum of severity. For C1–​C2 instability with or without a pannus, the patient can be treated with only C1–​C2 instrumented fusion. For early migration of C2 with pseudostabilization, the patient can be treated with reduction and C1–​C2 fusion, or OC fusion if the C1 lateral masses are destroyed. Finally, full cranial settling, if irreducible, requires ventral decompression and OC fusion. As anterior surgical approaches often involve a transoral approach, preoperative assessment of dental hygiene is critical to minimize bacterial contamination of the surgical field. Dental caries and gingivitis require treatment prior to surgery as these may result in hematogenous spread or surgical site infection with a risk of meningitis if a durotomy is encountered. Furthermore, loose dentition should be guarded or prophylactically extracted preoperatively. Also, patients often have lower cranial nerve dysfunction, particularly of the glossopharyngeal, vagus, and hypoglossal nerves. If there is significant dysfunction of these cranial nerves, preoperative tracheostomy placement should be considered. Additionally, patients may have concurrent swallowing dysfunction with resultant poor nutritional status. In these patients, preoperative placement of a percutaneous gastrostomy should be considered to optimize nutritional status preoperatively for improved wound healing. Finally, some patients, both children and adults, may have inadequate mouth opening to establish a sufficient surgical corridor, necessitating use of alternative approaches.

Questions

1. What regions of the craniocervical junction can be approached with the different ventral approaches? 2. What is the significance of the presence of a pannus in terms of the surgical procedure?

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Surgical Procedure Transoral-​Transpharyngeal Approach

Posterior decompression alone is generally inadequate to treat patients in the absence of a reducible basilar invagination and may actually lead to rapid neurological deterioration without concomitant anterior decompression.4,5 The classical surgical approach for treatment of pathology at the ventral craniocervical junction is the transoral-​transpharyngeal approach. This approach provides access to the anterior foramen magnum and from the lower clivus down to possibly as low as the C3 vertebral body, with lateral exposure approximately 14–​20  mm bilaterally off the midline. Injury to the Eustachian tube, hypoglossal nerve, vidian nerve, carotid arteries, and/​or vertebral artery are likely if additional lateral exposure is attempted. The carotid arteries are at higher risk than the vertebral arteries as they usually run approximately 1 cm off midline at C1 and can be right at midline in some patients. While awake, the patient is positioned supine with the head in extension on a horseshoe or, alternatively, in a halo crown attached to the Mayfield brace. Intraoperative neurological monitoring is performed with motor evoked potentials and somatosensory evoked potentials, as well as free running electromyography for lower cranial nerve monitoring. Intubation is performed with a prophylactic tracheostomy or with awake fiber-​optic endotracheal intubation, with the endotracheal tube retracted outside of the surgical field as much as possible. Packing is placed in the throat to prevent flow of blood into the stomach. Oral chlorhexidine gluconate solution is used to prepare the oral cavity, and preoperative intravenous antibiotics are administered.The patient is draped in the usual sterile fashion, with the oral and nasal cavities exposed.The tongue is retracted

Figure 6.3  Intraoperative photograph demonstrating the transoral approach to the craniocervical junction. Self-​retaining retractors keep the mouth open and retract the tongue away from the operative field. Note the red rubber catheter used to retract the soft palate. The initial pharyngeal incision has been made in preparation for exposure of the C1 ring. (Reproduced with permission from Hsu et al., Transoral approaches to the cervical spine, Neurosurgery, 2010;66:A119–​A125.) 54

 

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with a self-​retaining retractor (Figure 6.3), which should be released every 30 minutes to prevent lingual venous congestion. Following injection of 1% lidocaine with 1/​100,000 epinephrine in the posterior pharyngeal mucosa, the mucosa is incised in the midline, from the lower clivus to the superior aspect of the C3 vertebral body, with fluoroscopy or stereotactic navigational guidance. A  myomucosal flap containing the pharyngeal mucosa, constrictor muscles, longus colli, and longus capitis muscles is then elevated off the anterior longitudinal ligament (ALL) and retracted with self-​retaining retractors, and the ventral osseous structures are then exposed with insulated electrocautery.The osseous structures causing ventral compression can then be decompressed in piecemeal fashion using a diamond burr (Figure 6.4). The two layers (pharyngeal muscles and pharyngeal mucosa) should be closed separately in a watertight fashion to minimize the risk of wound dehiscence. When a soft tissue pannus is present around the odontoid, care should be taken during the decompression as the posterior longitudinal ligament and tectorial membrane may be thinned and potentially adherent or even fused to the ventral dura, with a greater potential for intraoperative durotomy. Since the pannus may resolve following posterior stabilization, aggressive ventral decompression may not always be required. Although some surgeons may delay posterior stabilization procedures in order to allow for recovery from the anterior decompression, the craniocervical junction is highly unstable following ventral decompression, even in a halo vest. Therefore, we advocate that the patient be immediately stabilized posteriorly following the ventral decompression. If it is not possible to complete the two-​staged operation in a single day, the patient can be secured in a halo vest and maintained intubated and sedated on flat bedrest until posterior stabilization the following day. If there is a concomitant Chiari type I malformation, or posterior spinal cord and/​ or brainstem compression remains following ventral decompression, posterior decompression is performed as well. The classical approach to posterior stabilization involved a construct with structural rib or iliac crest autograft wired from the occiput to the cervical spine. However, this approach required prolonged immobilization in a halo vest to provide stabilization at the OC junction. Currently, posterior OC rod-​screw constructs are most often used, which provide rigid fixation at the craniocervical junction. Depending on the extent of ventral resection and instability, constructs typically span from the occiput to C2 or C3, but may be extended to C6 or even across the cervicothoracic junction if necessary. An occipital plate is placed, with pedicle, pars, or translaminar screws at C2, and lateral mass screws in the subaxial spine if necessary. C1 screws are rarely placed as it is difficult to bend a rod to fit a plate as well as the C1 lateral mass screws. Extended Transoral Approaches

The detailed surgical techniques for the extended transoral approaches have been described in detail previously.6 If the surgical corridor is inadequate, additional superior and lateral exposure of the lower clivus can be obtained by dividing the soft palate in the midline and deviating the uvula. The soft palate is incised in the midline at the junction with the hard palate and extended down and extended off midline around the uvula. If the soft palate is divided for additional exposure, it should be closed in three layers (nasal mucosa, muscularis, oral mucosa) in a watertight fashion. A maxillary ostomy can 55

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Figure 6.4  Intraoperative photographs showing exposure of the C1 ring (A) and subsequent resection using a diamond burr (B). (C) Intraoperative photograph showing resection of the anterior C1 ring and odontoid, revealing the transverse ligaments. (Reproduced with permission from Hsu et al., Transoral approaches to the cervical spine, Neurosurgery, 2010;66:A119–​A125.)

be added to the transoral-​transpharyngeal approach to provide further exposure of the midline cranial base and middle clivus. A transmandibular circumglossal or transglossal approach can be used to provide exposure from the level of the sella all the way down the cervical spine. Endoscopic Approaches

With additional advances in endoscopic surgery, endonasal or sublabial endoscopic approaches can be used for access to the clivus and even a complete odontoidectomy.7 Also, a transcervical endoscopic approach for odontoidectomy has recently been described.8 This approach uses the standard Smith-​Robinson anterior cervical approach with a transodontoid screw trajectory (Figure 6.5). This allows for exposure from the inferior clivus down to C7 and may allow for ventral decompression in cases which 56

 

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Figure 6.5  Artist’s rendition showing the tubular retractor placed against the anterior cervical spine acting as a working channel for instruments and endoscope. The inset shows the orientation of the patient in the operating room. a = artery. (Adapted with permission from Wolinsky et al., Endoscopic image-​guided odontoidectomy for decompression of basilar invagination via a standard anterior cervical approach, J Neurosurg Spine, 2007; 6:184–​191.)

would otherwise require a maxillary osteotomy (Figure 6.6). Figure 6.7 demonstrates the surgical corridors from these alternative approaches.

Oral Boards Review: Management Pearls

1. Patients with a completely reducible basilar invagination may be treated with posterior decompression and stabilization alone. 2. However, posterior decompression alone is generally inadequate to treat patients without a completely reducible basilar invagination and may actually lead to rapid neurological deterioration. 3. The transoral-​transpharyngeal is the classical gold standard approach for ventral decompression of the craniocervical junction. It provides access from the lower clivus down to as low as the C3 vertebral body, with lateral exposure approximately 14–​20 mm bilaterally off the midline. 4. Posterior stabilization is typically performed with OC screw-​rod constructs, generally with an occipital plate and construct spanning from the occiput down to C2 or C3, but potentially down to C6 or across the cervicothoracic junction if necessary.

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Figure 6.6  (A) Sagittal computed tomography (CT), (B) axial CT of the posterior fossa, and (C) axial CT at the level of the foramen magnum following transcervical endoscopic decompression demonstrating adequate ventral decompression in conjunction with posterior decompression and stabilization. (Adapted with permission from Wolinsky et al., Endoscopic image-​guided odontoidectomy for decompression of basilar invagination via a standard anterior cervical approach, J Neurosurg Spine, 2007;6:184–​191.)

Pivot Points

1. If the basilar invagination is completely reducible with axial cervical traction, a posterior-​only approach (with decompression and stabilization) may be utilized. 2. If the basilar invagination is not completely reducible with cervical traction, then ventral decompression is required with posterior stabilization performed immediately afterward. 3. Additional posterior decompression may be required following ventral decompression if spinal cord and/​or brainstem compression remains, as in the presence of a concomitant Chiari type I malformation.

Aftercare

If a tracheostomy was not performed preoperatively, the patient should remain intubated for 48–​96 hours or until airway and oral edema are adequately reduced. In the absence of a percutaneous gastrostomy, typically placed in patients with poor preoperative nutritional status, a nasogastric tube is placed to allow for adequate enteral nutrition postoperatively. Finally, an external orthosis such as a halo vest or Minerva brace is often

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Figure 6.7  Illustration demonstrating the relevant normal anatomy and operative angles for the (A) sublabial, (B) transoral, and (C) transcervical approaches to the skull base. (Reproduced with permission from Johns Hopkins University, 2009. All rights reserved, Ian Suk. Previously published in Bettegowda et al., Sublabial approach for the treatment of symptomatic basilar impression in a patient with Klippel-​Feil syndrome, Neurosurgery, 2011;69(Suppl 1):77–​82.)

placed for 4–​6 months to provide increased stabilization of the OC junction while fusion is occurring. Complications and Management

Durotomy with cerebrospinal fluid (CSF) leak can be a devastating complication with increased risk of meningitis and wound dehiscence with potential fistula formation. If a CSF leak occurs, primary closure should be attempted, with additional placement of fibrin glue and fascial graft or dural substitute. Additionally, a lumbar subarachnoid drain

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should be placed with drainage of 5–​10 cc/​hr of CSF for 3–​5 days to minimize the risk of continued CSF leakage. The vertebral artery can be injured during lateral exposure beyond 15–​20  mm from the midline or in the presence of aberrant vertebral artery anatomy. The carotid arteries are at higher risk than the vertebral arteries as they usually run approximately 1  cm off midline at C1 and can be right at midline in some patients. Therefore, it is critical that preoperative vascular imaging is reviewed to better understand the vascular anatomy. If there is a vertebral artery injury, direct repair is typically impossible, whereas repair of a carotid artery injury may be attempted. The main goal is to use hemostatic agents to control bleeding, and a formal catheter angiogram should be performed as soon as possible to assess for vessel injury and perform potential endovascular vessel sacrifice. If the soft palate is divided for additional exposure, velopalatine incompetence may occur due to fibrosis of the soft palate or pharynx, with dysphagia, nasal speech, and liquid regurgitation. Pharyngeal retraining and use of a dental obturator can be considered for symptomatic improvement. Additional complications include both superficial and deep surgical site infections, which may require debridement of the wound. Deep infections are typically treated with prolonged courses of intravenous antibiotics, although the surgical hardware can often be left in place. Finally, as with any spinal fusion procedure, there is a risk of pseudarthrosis, which may require surgical revision and a more extensive posterior construct.

Oral Boards Review: Complications Pearls

1. An intraoperative CSF leak can be a devastating complication that should be managed aggressively, with ideally primary closure, placement of fibrin glue and a dural graft, and strong consideration for several days of CSF diversion with a lumbar subarachnoid drain. 2. Vertebral artery injury may occur with excessive lateral exposure or with aberrant vertebral artery anatomy. The carotid arteries are at higher risk than the vertebral arteries as they usually run approximately 1 cm off midline at C1 and can be right at midline in some patients. Preoperative vascular imaging should also be reviewed before surgery. An attempt at hemostasis should be made and catheter angiogram with potential vessel embolization performed as soon as clinically feasible.

Evidence and Outcomes

Randomized controlled trials to determine the optimal treatment approaches for these patients are lacking due to the relative rarity of this constellation of pathologies and the variation in diseases that may result in basilar invagination or cranial settling. However, several large retrospective cohort studies are available. These studies have generally demonstrated that ventral decompression with posterior stabilization and sometimes additional posterior decompression is the optimal treatment approach, but the

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posterior-​only approaches can be considered in patients with completely reducible basilar invagination. As the majority of patients present with neurological deficits including myelopathy and often lower cranial nerve deficits, the treatment goal is to prevent further neurological deterioration and stabilize the craniocervical junction. References and Further Reading

1. Smith JS, Shaffrey CI, Abel MF, Menezes AH. Basilar invagination. Neurosurgery. 66:39–​47,  2010. 2. Goel A, Bhatjiwale M, Desai K. Basilar invagination: a study based on 190 surgically treated patients. J Neurosurg. 88:962–​968, 1998. 3. Hsu W, Zaidi HA, Suk I, Gokaslan ZL, Wolinsky JP. A new technique for intraoperative reduction of occipitocervical instability. Neurosurgery. 66:319–​323; discussion 323–​314, 2010. 4. Menezes AH. Surgical approaches:  Postoperative care and complications “transoral-​ transpalatopharyngeal approach to the craniocervical junction.” Childs Nerv Syst. 24:1187–​1193,  2008. 5. Menezes AH,VanGilder JC.Transoral-​transpharyngeal approach to the anterior craniocervical junction. Ten-​year experience with 72 patients. J Neurosurg. 69:895–​903, 1988. 6. Hsu W, Wolinsky JP, Gokaslan ZL, Sciubba DM. Transoral approaches to the cervical spine. Neurosurgery. 66:119–​125, 2010. 7. Kassam AB, Snyderman C, Gardner P, Carrau R, Spiro R.The expanded endonasal approach: A fully endoscopic transnasal approach and resection of the odontoid process: Technical case report. Neurosurgery. 57:E213; discussion E213, 2005. 8. Wolinsky JP, Sciubba DM, Suk I, Gokaslan ZL. Endoscopic image-​guided odontoidectomy for decompression of basilar invagination via a standard anterior cervical approach. Technical note. J Neurosurg Spine. 6:184–​191, 2007.

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Cervical Myelopathy Lordosis Randall J. Hlubek and Nicholas Theodore

7 Case Presentation

A 65-​year-​old man presents with a chief complaint of numbness in his hands that has been present for more than a year. He reports that he is unable to open jars or lift heavy objects as he used to. He enjoys working with his hands, but he finds it more difficult to complete tasks because of his lack of dexterity. His wife is concerned about his balance and states that he has been falling more frequently. On further questioning, he denies any neck pain or radiating arm pain but does note some neck stiffness. A detailed neurological examination reveals bilateral grip weakness, diffuse hyperreflexia, bilateral Hoffman sign, bilateral positive Babinski reflex, positive Romberg sign, and negative Tinel sign. Motor strength assessment is 4+/​5 bilateral deltoids, 4+/​5 bilateral biceps, 4/​ 5 bilateral triceps, 4−/​5 bilateral grips, and 5/​5 strength in all lower extremity muscle groups.

Questions

1. What is the likely diagnosis? 2. What is the most appropriate imaging modality?

Assessment and Planning

The differential diagnosis is broad, and it includes cervical spondylotic myelopathy, carpal tunnel syndrome, subacute combined degeneration, transverse myelitis, and spinal cord tumor. The clinical history and physical examination results for this patient indicate that the most likely diagnosis is cervical spondylotic myelopathy. Cervical spondylotic myelopathy is compression of the cervical spinal cord secondary to degenerative changes. Symptoms, which include gait disturbance, upper extremity paresthesia, weakness, and loss of dexterity, tend to progress gradually. A rapid onset of symptoms would be unusual for spondylotic myelopathy and would likely be secondary to transverse myelitis, multiple sclerosis, or cervical abscess. Electromyography and nerve conduction studies cannot confirm the diagnosis of cervical myelopathy. However, they are useful for excluding disorders such as carpal tunnel syndrome and diabetic neuropathy that present with similar features.

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Figure 7.1  Sagittal T-​2 weighted magnetic resonance imaging of the cervical spine demonstrates circumferential stenosis at the levels of the C3–​C4, C4–​C5, and C5–​C6 disc spaces. (Reproduced with permission from Barrow Neurological Institute, Phoenix, Arizona.)

The diagnosis of cervical spondylotic myelopathy cannot be made without imaging. Magnetic resonance imaging (MRI) is the most useful imaging modality in that it provides clear resolution of the neural elements. T2-​weighted MRI allows for careful inspection of the spinal cord and can reveal hyperintensity that may represent myelomalacia secondary to chronic compression. However, if the hyperintensity is disproportionate to the degree of compression, then pathology such as primary spinal cord tumors and transverse myelitis should be carefully considered in the differential diagnosis and further workup may be warranted. Computed tomography (CT) myelography may be useful in patients for whom MRI is contraindicated. Although CT myelograms do not visualize the spinal cord very well, they provide excellent visualization of the bony anatomy. Thus, they facilitate analysis of the extent of cervical canal stenosis. Flexion and/​or extension cervical radiographs should be obtained for any patient who reports neck pain. Dynamic imaging should be used to evaluate for cervical instability and to aid in surgical planning. In the present case, MRI of the cervical spine revealed circumferential stenosis at the levels of the C3–​C4, C4–​C5, and C5–​C6 disc spaces with preserved cervical lordosis (Figure 7.1).

Questions

1. How do this patient’s clinical picture and MRI findings influence surgical planning? 2. What are the surgical options for this patient?

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Oral Boards Review: Diagnostic Pearls

1. A thorough physical examination is crucial to the diagnosis of cervical spondylotic myelopathy. Myelopathic signs include Hoffmann reflex, positive Babinski reflex, and Romberg sign. There may be both upper and lower motor neuron signs, depending on the level of the lesion (i.e., hyporeflexia in the upper extremities and hyperreflexia in the lower extremities). 2. Careful history-​taking is important because the timing of symptoms may lead to the consideration of another diagnosis. Acute onset of symptoms is atypical and may be secondary to transverse myelitis, cervical epidural abscess, or multiple sclerosis. 3. Cervical spondylosis is a common disease in the elderly. If physical examination findings are out of proportion to the severity of cervical spondylosis, then additional pathology may be present. Additional workup should be performed, including electromyograms and/​or nerve conduction studies to evaluate for demyelinating disorders. MRI with and without contrast may be helpful in evaluating for intraparenchymal tumors, especially when there is severe T2 hyperintensity in the spinal cord.

Decision-​Making

Surgery should be performed in patients with cervical spondylotic myelopathy to preserve the function of the spinal cord. The goals of surgery are to decompress the neural elements and to preserve or restore cervical sagittal alignment. Both anterior (cervical discectomy and fusion, cervical arthroplasty, and cervical corpectomy) and posterior (cervical laminectomy, cervical laminoplasty, and cervical laminectomy with fusion) surgical approaches have been developed to achieve these goals effectively. Cervical alignment may be the most important factor to consider when determining which approach is most appropriate. In patients with cervical lordosis, maintaining lordotic alignment is crucial to successful treatment. Maintaining lordotic alignment may be achieved with either an anterior or a posterior approach. An anterior approach may be favored when there are only one or two levels of stenosis at the disc space or when there is significant compression anteriorly with minimal posterior compression. Cervical stenosis involving more than two levels requires much more extensive anterior decompression and may demand a corpectomy if there is compression posterior to the vertebral body rather than at the level of the disc space. This approach is more technically demanding for diffuse pathology but may be necessary if the alignment is kyphotic. Factors that may favor a posterior approach include a congenitally narrow canal, compression greater than two levels, ossification of the posterior longitudinal ligament, circumferential compression, and multiple medical comorbidities. The theoretical benefit of posterior decompression is to remove the lamina and the ligamentum flavum, thus allowing the spinal cord to shift posteriorly away from any anterior compressive elements.Although laminectomy alone is effective in decompressing the neural elements,

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its main drawback is the potential for development of cervical kyphosis or instability, which occurs in 13–​41%, and 18% of patients, respectively.1,2 In patients with cervical myelopathy and lordotic sagittal alignment, the preference of the senior author is to perform a cervical laminectomy and fusion when there is multilevel circumferential compression.

Questions

1. What steps should be performed when there is a significant decrease in somatosensory evoked potentials (SSEPs) during the operation? 2. If the patient were to develop unilateral deltoid and biceps weakness on postoperative day 1, what would be the most likely diagnosis?

Surgical Procedure

During intubation of patients with cervical instability or severe cervical stenosis, hyperextension of the neck should be avoided because of the potential for spinal cord injury. Either awake fiber-​optic intubation or video-​assisted intubation with the GlideScope (Verathon, Inc.) video laryngoscope should be considered to limit hyperextension. Neurophysiological monitoring is performed by monitoring intraoperative changes in SSEPs and motor evoked potentials (MEPs). Baseline recordings are obtained before positioning the patient, and intraoperative monitoring is done continuously throughout the case. The patient is positioned prone, with all pressure points padded, on either a Jackson table with the face resting in a foam head support or on a flat table with the chest supported on a gel chest roll and the head rigidly fixed in a Mayfield clamp.The arms of the patient should be well padded and tucked close to the sides. Before initiation of surgery, it is imperative to assess the cervical alignment with fluoroscopy to ensure that it is optimal. Analysis of postpositioning SSEPs and MEPs ensures that spinal cord compression has not been exacerbated. If there is a significant decrease in SSEPs or MEPs after positioning, then common sources for alarm should be interrogated, including hypotension, hypothermia, anesthetic agents, verification of electrode integrity, arm positioning, and cervical alignment. MEPs are especially sensitive to inhalational agents, and their use should be limited to ensure that the monitoring is reliable. When the patient is adequately positioned and draped in a sterile fashion, a midline incision is performed and dissection is carried down through the avascular median raphe between the paraspinal musculature. If the dissection strays laterally, extensive bleeding may be encountered from the musculature and venous plexus. At the bony elements, the muscles are dissected off the spinous process and lamina in a subperiosteal fashion. The lateral masses are then carefully exposed to prevent violation of the facet joints above and below the operative segments. When the level has been confirmed with anatomical landmarks and fluoroscopy, the facet joints should be curetted to remove cartilaginous material and to prepare the joints for fusion. Doing so also allows the surgeon to place an

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instrument (e.g., a Penfield 4 dissector) into the facet joint to determine the facet angle and assist with screw trajectory. Lateral mass screws may be placed at C3–​C6 for fixation. The lateral mass of C7 is relatively thin and may not be amenable to a lateral mass screw, so pedicle screws may be required if fixation is necessary at this level. For fixation above the C3 level, the senior author prefers to use C2 pars screws and C1 lateral mass screws, but a discussion of these screws is beyond the scope of this chapter. A pilot hole is then created through the cortex of the lateral mass (2 mm medial to center) with a high-​speed drill. A manual twist drill is angled approximately 30 degrees laterally and then angled cephalad parallel to the slope of the facet to maximize screw length and to avoid the nerve root and vertebral artery.3 The lateral mass is drilled to a depth of either 12 or 14 mm, and a ball-​tipped probe is used to interrogate for any breach of the lateral mass. Before placement of the hardware, the laminectomy is initiated with a high-​speed drill at the junction of the lamina and the lateral mass. Care is taken to keep the drill perpendicular to the cortical surface and to copiously irrigate to prevent thermal injury to the nerves. After the bilateral troughs have been drilled down to the epidural space, the lamina is removed en bloc by placing towel clamps on the cranial and caudal-​most spinous processes. While lifting upward with the clamps, we use a curette to strip adhesions and ligamentum flavum from beneath the lamina. Any residual compressive ligamentum flavum or lamina may be removed with Kerrison rongeurs. After completion of the decompression, the lateral mass screws (typically 3.5 mm in diameter and 12 or 14 mm in length) are inserted. A lordotically curved rod is then seated in the screw heads and locking caps are provisionally tightened. Fluoroscopy is used to confirm proper alignment and screw placement. The locking caps are then finally tightened with an antitorque screwdriver. The lateral masses are then decorticated with a high-​speed drill, and autologous bone from the laminectomy and allograft is placed over the cancellous surface. After adequate hemostasis is achieved, the incision is closed in a standard multilayer fashion.

Oral Boards Review: Management Pearls

1. If posterior decompression is to be performed, then fixation and fusion must be strongly considered to prevent development of postlaminectomy kyphosis and instability. 2. Checking cervical alignment with lateral fluoroscopy after positioning is critical to ensure proper alignment. 3. Mean arterial pressures should be maintained at 80 mm Hg or higher to ensure adequate perfusion to the spinal cord during the entire operation.

Pivot Points

1. If the patient presents with a medical history and physical examination findings consistent with cervical myelopathy, then the next step is to order MRI of the cervical spine to assess for spinal cord compression.

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2. If the sagittal alignment is kyphotic, then an anterior approach would be favored both to decompress the spinal cord and to restore alignment. A posterior approach may not be effective because the kyphosis would prevent the posterior shift of the spinal cord, and the neural elements would remain draped over the anterior disc osteophyte complexes. 3. If the sagittal alignment is lordotic, then either an anterior approach or a posterior approach may be effective, and the surgery should be customized to each patient.

Aftercare

Postoperative pain may be severe secondary to the extensive muscle dissection. Thus, patients are typically placed on intravenous muscle relaxants and on intravenous patient-​ controlled analgesia. When the pain has been adequately controlled, a transition to oral pain medication should be attempted. Rigid cervical collars provide additional immobilization and may be especially useful in patients with poor bone quality. Patients are typically advised to wear a cervical collar for about 6–​12 weeks. Its use is discontinued when follow-​up radiographs reveal no evidence of hardware failure. Physical and occupational therapists evaluate the patient during the hospitalization. Their input assists with early mobilization and discharge recommendations. Radiographic follow-​up consists of anteroposterior and/​or lateral cervical radiographs at 6 weeks, 6 months, and 1 year after surgery. Additional diagnostic imaging is obtained if new symptoms develop. Complications and Management

Vertebral artery injury is a rare but potentially devastating complication of cervical laminectomy that can result in hemorrhage, stroke, and death. The vertebral artery is most vulnerable to injury during screw placement. Preoperative imaging should be studied meticulously to determine the course of the arteries and to evaluate for any aberrant anatomy. If injury to the artery occurs during screw placement, then the screw should be inserted for hemostasis and the contralateral instrumentation should be aborted if it has not been completed. Cerebrospinal fluid leak may occur during decompression of the spinal cord, and any dural violation may be repaired primarily with sutures. If the durotomy is not amenable to repair with sutures, then a piece of muscle may be placed over the defect and attached using fibrin sealant. The incidence of postoperative C5 palsy after a cervical laminectomy with fusion is about 11%.4 The etiology of C5 palsy is poorly understood, and proposed mechanisms in posterior cervical surgery include tethering of the nerve root secondary to posterior shift of the spinal cord and foraminal stenosis. C5 palsy is manifested by pain in the shoulder, sensory loss in the C5 distribution, and paresis of the deltoid and/​or biceps brachii. These symptoms may occur immediately after surgery or may be delayed. There is no established treatment for C5 palsy; however, most patients tend to recover spontaneously, with a mean time to recovery of 5.4 months.5 68

 

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Oral Boards Review: Complications Pearls

1. Careful preoperative assessment of the vertebral arteries for aberrant anatomy will reduce the risk of iatrogenic injury during screw placement. 2. Postoperative C5 palsy may occur either immediately after surgery or may be delayed.

Evidence and Outcomes

There is no Level 1 evidence regarding which approach (anterior vs. posterior) is more effective for treatment of multilevel cervical spondylotic myelopathy. A systematic review of retrospective studies demonstrated no clear advantage for anterior and posterior cervical approaches in terms of safety and effectiveness.6 The determination of which approach to use should be customized to each patient. References and Further Reading

1. Li Z, Xue Y, He D, et  al. Extensive laminectomy for multilevel cervical stenosis with ligamentum flavum hypertrophy:  More than 10  years follow-​ up. Eur Spine J. Aug 2015;24(8):1605–​1612. 2. Kato Y, Iwasaki M, Fuji T, Yonenobu K, Ochi T. Long-​term follow-​up results of laminectomy for cervical myelopathy caused by ossification of the posterior longitudinal ligament. J Neurosurg. Aug 1998;89(2):217–​223. 3. Kim HS, Suk KS, Moon SH, et  al. Safety evaluation of freehand lateral mass screw fixation in the subaxial cervical spine: Evaluation of 1256 screws. Spine (Phila Pa 1976). Jan 1 2015;40(1):2–​5. 4. Nakashima H, Imagama S,Yukawa Y, et al. Multivariate analysis of C-​5 palsy incidence after cervical posterior fusion with instrumentation. J Neurosurg Spine. Aug 2012;17(2):103–​110. 5. Dai L, Ni B,Yuan W, Jia L. Radiculopathy after laminectomy for cervical compression myelopathy. J Bone Joint Surg Br. Sep 1998;80(5):846–​849. 6. Lawrence BD, Jacobs WB, Norvell DC, Hermsmeyer JT, Chapman JR, Brodke DS. Anterior versus posterior approach for treatment of cervical spondylotic myelopathy: A systematic review. Spine (Phila Pa 1976). Oct 15 2013;38(22 Suppl 1):S173–​S182.

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Cervical Myelopathy Kyphosis Mario Ganau, So Kato, and Michael G. Fehlings

8 Case Presentation

A 72-​year-​old woman presents with rapid decline of neurological function evolving over three decades after an uneventful multilevel posterior cervical laminectomy performed for an intradural benign neoplasm (left C4 schwannoma). The patient had quit smoking when she was diagnosed with diabetes mellitus type 2, and she also suffers from poorly pharmacologically controlled high blood pressure. She has been wheelchair bound for the past few weeks and describes several months of urinary urgency, multiple mechanical falls due to gaze disturbances, and progressive weakness, scoring at best 3/​5 on the Medical Research Council (MRC) muscle scale, in the upper and lower limbs. Recently, her inability to grip/​hold objects in both hands has made her unable to eat independently and safely ambulate despite the aid of a walker. The physical examination reveals a short neck with reduced range of motion in both lateral rotation and flexion-​extension, bilateral loss of muscle tone in legs, brisk patellar reflexes, and ankle clonus. Given her incomplete tetraplegia American Spinal Injury Association (ASIA) C, the patient is admitted for further investigations.

Questions

1. Which are the most common causes of cervical kyphosis? 2. What further radiological and neurophysiological investigations can be helpful? 3. Which functional scales are used for degenerative cervical myelopathy (DCM), and what do they tell us about prognosis?

Assessment and Planning

The computer tomography (CT) and magnetic resonance imaging (MRI) (Figure 8.1) results disclose a severe multilevel cervical kyphotic deformity, likely related to the previous multilevel posterior cervical laminectomy. Other causes of kyphotic deformity include ankylosing spondylitis, Pott disease, and previous cervical trauma. Dropped head syndrome is in the differential diagnosis, and this has many causes such as Parkinson disease, scleroderma, neuromuscular diseases, inflammatory polymyositis (i.e., due to Zika virus), and secondary myopathies due to metabolic or endocrine dysfunction. 71

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Figure 8.1  Preoperative bone window computed tomography (CT; left) and T2-​ weighted magnetic resonance imaging (MRI; right) scans of the cervical spine with sagittal views showing multiple degenerative changes causing severe kyphosis (C2–​C7 Cobb angle: −46 degrees) and spinal stenosis.

A careful study of the radiological investigations demonstrates a C2 to C7 Cobb angle of −46 degrees with a sagittal vertical axis (SVA, the distance between the plumb line from the C2 centroid and that from the posterosuperior corner of C7) of 46 mm. The modified Japanese Orthopedic Association (mJOA) score is 7, which confirms severe nontraumatic DCM and therefore a poor prognosis.

Oral Boards Review: Diagnostic Pearls

1. Clinical assessment: a. In kyphotic patients, stretching of the posterior paravertebral muscles as a tension band frequently causes axial pain, which can be the primary physical complaint of these patients. b. Being unable to lift the skull upright, patients with kyphotic deformities compensate with a typical upward gaze. c. Dysphagia can also be a common symptom, usually caused by collapse of pharyngeal space and inefficient coordination of swallowing muscles. 2. Radiological assessment: a. Radiometric measures of cervical alignment provide information on spinal balance and should always be carried out on long, standing cassette x-​rays. As a general rule, cervical kyphosis is defined by a C2–​C7 Cobb of less than −10 degrees and/​or an SVA greater than 40 mm. b. Although at more advanced stages of DCM, conventional T1-​and T2-​ weighted 1.5 Tesla MR images are sensitive enough to confirm the

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presence of myelopathy, discrepancies between the actual clinical status and imaging findings can be found in early stages of this condition. c. Myelopathic changes can appear even without T2 signal alterations: decreased fractional anisotropy (FA) values and increased apparent diffusion coefficient (ADC) values found in stenotic segments can reflect the spinal cord condition and its reversibility. Diffusion tensor imaging (DTI) and microstructural MRI may be promising modalities to predict functional recovery after surgery. 3. Functional assessment: a. The recovery rate for the mJOA score can be calculated using Hirabayashi’s method; of note, mJOA well defines moderate and severe DCM but is relatively insensitive in predicting outcomes for mild DCM patients. b. Other general scales, such as Short Form 36 (SF36), as well as those specific for cervical spine pathologies, like the Neck Disability Index (NDI), have a role in the functional assessment of patients with DCM and kyphotic deformity. Their findings, however, should always be weighed in light of the minimally clinical important difference and substantial clinical benefit achievable after cervical spine fusion. The clinical findings were confirmed by electromyogram (EMG) and nerve conduction studies, which revealed an acute on chronic myelopathy with signs of bilateral denervation of the median and ulnar nerves. A careful study of the flexion/​extension films (Figure 8.2) and CT reconstructions revealed the persistence of some cervical spine motion and excluded fusion of the facets joints. Additional measurements performed on the long cassette x-​rays, such as the thoracic slope (TS; the angle made by the T1 upper endplate and a horizontal line) and its mismatch with the C2–​C7 Cobb angle, as well as on T2-​weighted MRI, such as the modified K line, were considered in evaluating the global spinal balance and the most suitable management options.

Figure 8.2  Preoperative static and dynamic lateral x-​rays of the cervical spine, with neutral (left), flexion (center), and extension (right) views ruling out fusion of the facet joints and showing some preserved motion of the cervical segments.

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Questions

1. How do clinical and radiological findings influence the management? 2. What is the optimal time of intervention in DCM? What are the goals of surgery? 3. Which kind of surgical approach would be more effective in this kyphotic deformity, and why?

Decision-​Making

Since the patient was showing myelopathic signs and symptoms associated with features related to her kyphotic deformity, such as the alteration in visual horizon, both pathological aspects required appropriate surgical management. The goals of surgery in patients with DCM are to timely decompress the spinal cord and prevent progression of the demyelination processes responsible for the progressive neurologic deterioration seen at later stages. The optimal timing of intervention is still an area of ongoing debate; however, experimental studies have shown that delays in decompression could increase the extent of ischemia-​reperfusion injury and astrogliosis, resulting in poorer neurological recovery. Realignment may be particularly important when spinal cord compression is associated with kyphosis as the distance between the anterior compressive factors and the spinal cord can be increased by restoring lordotic alignment. Whenever a cervical deformity is evident on preoperative scans, spinal osteotomies must be considered in the surgical plan as an adjuvant to standard decompression techniques. Osteotomies represent powerful techniques that enable deformity correction of the cervical spine, and they range from relatively limited facet joint releases to complete vertebrectomy. These complex procedures have evolved through generations of surgeons, with the most recent classification being composed of seven anatomical grades of resection (anterior, posterior, and combination of the two) representing progressive degrees of potential destabilization. Overall, the greatest advantages of anterior (A)  approaches are the possibility to address any anterior pathology, such as discs and bony spurs, allowing for a sufficient distraction that can unbuckle the ligamentum flavum and indirectly treat spinal cord compression. Key to the anterior correction is a wide anterior release including the uncovertebral joints and a hybrid construct making use of multiple osteotomies and inserting longer than normal (bicortical) screws. This method is generally sufficient for stabilization; however, if two or more corpectomies are done, a posterior instrumented fusion is usually advisable. Posterior (P) approaches, including laminectomies and laminoplasties, are technically easier and therefore more suitable for older and osteoporotic patients; they can address various posterior sources of compression directly, such as the ligamentum flavum, or indirectly, such as ossification of the posterior longitudinal ligament (OPLL). Combined approaches (A + P, P + A, A + P + A and P + A + P) offer a way to perform multilevel decompression and osteotomies to address complex rigid deformities;

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however, they are burdened by longer operation time, larger intraoperative blood loss, and delayed recovery that is associated with increased hospital costs.

Questions

1. What are the most important anesthesiological considerations in terms of premedication, intubation, and intraoperative monitoring? 2. What are the foreseeable surgical and medical complications? 3. What strategies can enhance the chances of fusion?

Surgical Procedure

Following fiberscopic intubation and induction of general anesthesia, the patient was positioned supine and Gardner-​Wells tongs were applied for perioperative traction. She underwent C3–​C4, C4–​C5, C5–​C6, and C6–​C7 anterior cervical discectomies, supplemented with C5 corpectomy for reduction of kyphotic deformity. The intraoperative realignment was obtained through traction performed under fluoroscopic imaging with continuous intraoperative multimodality electrophysiologic recordings (monitoring the motor and somatosensory evoked potentials as well as the segmental EMG activity). The anterior cervical reconstruction was performed through anterior cervical bone grafting with multilevel fibular strut and allografts combined with a local morselized vertebral body autograft followed by the insertion of a four-​level anterior cervical titanium plate fixation (C3 to C7). A postoperative anterior and posterior x-​ray (Figure 8.3) confirmed the satisfactory cervical alignment obtained.

Figure 8.3  Postoperative static x-​rays of the cervical spine, with lateral (left) and anteroposterior (right) views showing that satisfactory sagittal and coronal alignment was achieved.

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Oral Boards Review: Management Pearls

1. Setting for surgery: a. Correct positioning to maximize lordosis is fundamental to obtain a satisfactory intraoperative spine alignment; use Gardner-​Wells tongs for traction if needed. b. Consider steroids and tranexamic acid at induction. c. Use intraoperative somatosensory and motor evoked potential monitoring. d. Make careful use of intraoperative imaging or radiographic guidance. e. Avoid hypotension: during surgery maintain mean arterial pressure at greater than 85 mm Hg. 2. Surgical nuances: a. Magnification counts: use surgical loupes or microscope throughout the intervention. b. Place the Caspar distraction pins in a divergent fashion to guarantee a satisfactory working channel. c. Use diamond burr on the OPLL segment to avoid injuring spinal cord. d. Expect possible dural breach and anticipate its repair. e. Collect bone dust and use it along with morselized vertebral body to enhance fusion. f. Always obtain a final radiological check before closure to ensure adequate reconstruction of the cervical lordosis and rule out malpositioning of the instrumentation. g. Carefully check the hemostasis; plan to keep a surgical drain for 48 hours and ensure a good multilayer closure.

Pivot Points

1. The following strategies may be considered to achieve correction of kyphotic deformity and management of DCM: a. Anterior standalone approach: To obtain a good alignment, multiple anterior cervical discectomies with partial uncovertebral joint resection, also known as grade 1 osteotomy, require mobility (nonfusion) of the facet joints. They are usually performed in association with grade 3 or 4 osteotomies, which include partial or complete corpectomy with complete uncovertebral joint resection to transverse foramen. Overall, anterior osteotomies allow for substantial release and correction of deformity but also facilitate the decompression of the spinal canal and foramina, leading to successful management of DCM. The risk of subsidence can be reduced by adding autograft bone or bone morphogenic proteins (BMP) to the body and disc substitutes (cages or bone grafts). The screw–​plate interface can be used to facilitate reduction maneuvers, and adequate bending of the plate further helps to obtain a satisfactory postoperative cervical lordosis.

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b. Posterior standalone approach: Alternatively, a posterior standalone approach may be used, providing decompression of the spinal cord and room for deformity correction. Grade 2 osteotomy involves laminectomy with resection of both superior and inferior facets. A more complex deformity correction at the cervicothoracic junction can be obtained through grades 5 and 6 osteotomies: namely, complete posterior element resection with osteoclastic fracture and open or closing wedge creation. Posterior approaches require fixation with lateral mass screws or with pedicle screws; in this option, properly bent rods can effectively recreate the cervical lordosis. Furthermore, to increase the stability of the construct, attention should be focused toward both intraarticular and extraarticular fusion. To this extent, cartilage removal from the facet surface can be obtained by facet joint cauterization or decortication with a high-​speed drill; tightly pack them with bone dust or BMP after this process. c. Combined anterior and posterior approach: Patients with severe and rigid cervical kyphosis may require both anterior and posterior approaches or osteotomies. The anterior plating can be supplemented with lateral mass screws in the subaxial spine and pedicle screws beyond the junctional level (T1, T2, or lower, depending on the characteristics of the scapular cingulus and the need for additional point of fixation).

Aftercare

Following surgical intervention, patients do not need to wear a collar for any reason other than subjective comfort. Concerns regarding swelling of the respiratory tract due to long operative time or conditions like ankylosing spondylitis require admission to the intensive care unit for additional postoperative monitoring before extubation. Patients undergoing anterior approaches may demonstrate minimal dysphonia or dysphagia in the early postoperative period; however, these side effects are self-​limiting and usually improve within 48–​72 hours. Early postoperative mobilization should be encouraged to avoid complications related to vein thromboembolism.The wound should be kept dry until removal of sutures. A postoperative radiological study is always advisable; it may serve as a baseline for future comparisons during follow-​up. In the case presented here, the C2–​C7 Cobb angle showed a tenfold reduction: from −46 degrees to −4 degrees after surgical correction (Figure 8.4). The patient had a remarkable postoperative improvement; she regained normal power in upper and lower extremities, being able to ambulate independently with a stick. She is now in the fourth year of her follow-​up, and the latest mJOA score is 13. Complications and Management

In case of dural tears, a lumbar drain (LD) should always be considered, with its height being adjusted to allow for drainage of 10–​15 mL of cerebrospinal fluid (CSF) hourly for 5 postoperative days to ensure dural and wound healing without tension.

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Figure 8.4  Postoperative bone window computed tomography (CT; left) and T2-​weighted magnetic resonance imaging (MRI; right) scans of the cervical spine, with sagittal views confirming good correction of cervical kyphosis (C2–​C7 Cobb angle: –4 degrees) and decompression of the spinal cord.

Devascularization and secondary atrophy of paravertebral muscles can become a source of delayed complication, including infections and wound dehiscence, which may become dramatic whenever associated with the exposure of the hardware and its contamination.

Oral Boards Review: Complications Pearls

1. Complications related to surgery: a. Intraoperative: • Any anterior approach can be complicated by injury to the structures pertaining to the carotid triangle (carotid artery, jugular vein, vagus nerve) or prevertebral region (esophagus, trachea, recurrent laryngeal nerve). • Discectomy and corpectomy can lead to injury of the vertebral artery (V2 segment) or spinal cord, with edema and anterior or central cord syndrome. • The management of dural tears depends on the location of the breach and the type of surgical exposure; as a general rule, if the surgeon has a direct visualization of the CSF leak, an attempt to close it through microsuture should be pursued. However, this may be technically challenging, especially in cases of ventrally or laterally located

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dural tears. Dural sutures in these areas increase the risk of making the tear even larger; in those instances, it is therefore better to simply use dura substitutes and fibrin glue. A Valsalva maneuver should be finally carried out to confirm the good quality of the dural closure. b. Perioperative: • Spinal epidural hematoma or pseudomeningocele • Graft dislodgment c. Postoperative: • Screws/​plate subsidence or pullout • Delayed adjacent disc disease 2. Complications related to general anesthesia: a. Blood pressure should be maintained within the normal range, avoiding hypotension and the related risk of spinal cord infarction, as well as hypertension and related risk of bleeding in the surgical site. b. Lingering effect of paralytics or anesthetics should be monitored. 3. Complications related to medical conditions: a. Comorbidities such as osteoporosis, ankylosing spondylitis, rheumatoid arthritis, and diabetes mellitus are known to increase the risk of instrumentation failure. b. Active and passive smoking affect osteoinduction and increase the risk of nonfusion. c. The rate of nonfusion is similar in nonsmoking and in patients with a previous history of smoking. d. Pharmacological and mechanical prophylaxis should be considered to reduce the risk of deep vein thrombosis and pulmonary embolism. Evidence and Outcomes

Patients with cervical kyphotic deformity tend to have worse preoperative NDI scores and significantly lower physical component scores on SF-​36 than do patients with DCM alone. Despite the significant attention paid by several authors to the correction of kyphotic deformity, a recent subanalysis of two prospective international multicenter AO Spine studies failed to demonstrate significant differences in postoperative outcomes regardless of achievement of deformity correction. These findings suggest that an aggressive realignment in this cohort might not always be necessary, especially when the symptoms directly related to the kyphosis are not the primary complaint. A prospective randomized Patient-​Centered Outcome Research Institute (PCORI) sponsored trial (www.ClinicalTrials.gov identifier: NCT02076113) is currently under way to evaluate cervical and global sagittal imbalance as a predictor of outcome following surgery for CSM. References and Further Reading

Ames CP, Blondel B, Scheer JK, et al. Cervical radiographical alignment: Comprehensive assessment techniques and potential importance in cervical myelopathy. Spine (Phila Pa 1976).

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2013 Oct 15;38(22 Suppl 1):S149–​S160. doi:  10.1097/​BRS.0b013e3182a7f449. Review. https://​www.ncbi.nlm.nih.gov/​pubmed/​24113358 Ames CP, Smith JS, Scheer JK, et al.; International Spine Study Group. A standardized nomenclature for cervical spine soft-​tissue release and osteotomy for deformity correction: clinical article. J Neurosurg Spine. 2013 Sep;19(3):269–​278. doi: 10.3171/​2013.5.SPINE121067. Epub Jul 5, 2013. https://​www.ncbi.nlm.nih.gov/​pubmed/​23829287 Hirabayashi K, Miyakawa J, Satomi K, Maruyama T, Wakano K. Operative results and postoperative progression of ossification among patients with ossification of cervical posterior longitudinal ligament. Spine (Phila Pa 1976). 1981 Jul-​Aug;6(4):354–​364. https://​www.ncbi.nlm. nih.gov/​pubmed/​6792717 Kato S, Nouri A, Wu D, Nori S, Tetreault L, Fehlings MG. Impact of cervical spine deformity on pre-​operative disease severity and post-​operative outcomes following fusion surgery for degenerative cervical myelopathy: Sub-​analysis of AOSpine North America and international studies. Spine (Phila Pa 1976). 2017 Jun 27. doi: 10.1097/​BRS.0000000000002307. [Epub ahead of print] https://​www.ncbi.nlm.nih.gov/​pubmed/​28658043 Liu S, Lafage R, Smith JS, et al. Impact of dynamic alignment, motion, and center of rotation on myelopathy grade and regional disability in cervical spondylotic myelopathy. J Neurosurg Spine. 2015 Dec;23(6):690–​700. doi: 10.3171/​2015.2.SPINE14414. https://​www.ncbi.nlm. nih.gov/​pubmed/​26315953 Martin AR, De Leener B, Cohen-​Adad J, et al. Clinically feasible microstructural MRI to quantify cervical spinal cord tissue injury using DTI, MT, and T2*-​weighted imaging: Assessment of normative data and reliability. AJNR Am J Neuroradiol. 2017 Jun;38(6):1257–​ 1265. doi:  10.3174/​ ajnr.A5163. Epub Apr 20, 2017. https://​www.ncbi.nlm.nih.gov/​pubmed/​ 28428213 Martin AR, Reddy R, Fehlings MG. Dropped head syndrome: Diagnosis and management. Evid Based Spine Care J. 2011 May;2(2):41–​47. doi: 10.1055/​s-​0030-​1267104. https://​www.ncbi. nlm.nih.gov/​pubmed/​23637681 Roguski M, Benzel EC, Curran JN, et  al. Postoperative cervical sagittal imbalance negatively affects outcomes after surgery for cervical spondylotic myelopathy. Spine (Phila Pa 1976). 2014 Dec 1;39(25):2070–​2077. doi: 10.1097/​BRS.0000000000000641. https://​www.ncbi. nlm.nih.gov/​pubmed/​25419682 Taniyama T, Hirai T,Yoshii T, et al. Modified K-​line in magnetic resonance imaging predicts clinical outcome in patients with nonlordotic alignment after laminoplasty for cervical spondylotic myelopathy. Spine (Phila Pa 1976). 2014 Oct 1;39(21):E1261–​ E1268. doi:  10.1097/​ BRS.0000000000000531. https://​www.ncbi.nlm.nih.gov/​pubmed/​25077905 Tetreault L, Kopjar B, Nouri A, et  al. The modified Japanese Orthopaedic Association scale:  Establishing criteria for mild, moderate and severe impairment in patients with degenerative cervical myelopathy. Eur Spine J. 2017 Jan;26(1):78–​84. doi: 10.1007/​s00586-​016-​ 4660-​8. Epub Jun 24, 2016. https://​www.ncbi.nlm.nih.gov/​pubmed/​27342612 Tetreault L, Wilson JR, Kotter MR, et al. Predicting the minimum clinically important difference in patients undergoing surgery for the treatment of degenerative cervical myelopathy. Neurosurg Focus. 2016 Jun;40(6):E14. doi: 10.3171/​2016.3.FOCUS1665. https://​www.ncbi. nlm.nih.gov/​pubmed/​27246484

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Ossification of the Posterior Longitudinal Ligament Cervical Todd D. Vogel, Hansen Deng, and Praveen V. Mummaneni

9

Case Presentation

A right-​handed 61-​year-​old woman presents with a 2-​week history of progressive right leg weakness and left leg decreased sensation to pain and temperature exacerbated at presentation with a fall. She is now nonambulatory. She has numbness and tingling into her hands. She has noticed difficulty with her hands in doing fine motor tasks. She takes medications for hypertension and hyperlipidemia. She has a long-​standing history of right leg sciatica that has been treated conservatively. On exam, her cranial nerves are intact. Her bilateral upper extremities are full strength except for some mild grip strength and hand intrinsic weakness. She is unable to lift her right leg off the bed. Her left leg is full strength. She has a T3 sensory level on the left to pin prick and temperature. She is hyperreflexive throughout including bilateral Hoffman, clonus, and Babinski sign. She has normal rectal tone (Figures 9.1–​9.3).

Questions

1. What is the likely diagnosis? 2. What is the most appropriate imaging modality? What anatomical areas should be imaged?

Assessment and Planning

In this clinical case, consideration needs to be given to the possibility of cervical myelopathy aggravated by mild trauma. The differential diagnoses for etiologies of cervical myelopathy include degenerative cervical spondylosis, congenital stenosis, tumor, spinal epidural abscess, and ossification of the posterior longitudinal ligament (OPLL). OPLL is seen in 25% of patients presenting with cervical myelopathy in the United States.1 It is more common in males (2:1) than females. OPLL typically presents in the fifth and sixth decades of life. There is a higher prevalence in the Asian population. It is located in the cervical spine in 70% of cases, and the remaining 30% is split between the upper thoracic and upper lumbar spine.2

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Figure 9.1  Midline sagittal computed tomography (CT) scan from case presentation demonstrating extensive ossification of the posterior longitudinal ligament (OPLL) in the cervical and upper thoracic spine. This CT demonstrates the “continuous” type of ossification.

Figure 9.2  Axial computed tomography (CT) from case presentation at the cervicothoracic junction demonstrating a double-​layer sign. Note the hypodense layer between vertebral body and the intraspinal calcified mass representing intradural ossification of the posterior longitudinal ligament (OPLL).

 

Ossification of the Posterior Longitudinal Ligament: Cervical

Figure 9.3  Midline sagittal magnetic resonance imaging (MRI) from case presentation demonstrates hypodensity behind the vertebral bodies and across the disk spaces suggesting ossification of the posterior longitudinal ligament (OPLL). Note that the sagittal MRI at the cervicothoracic junction underrepresents the severe stenosis as demonstrated in Figure 9.2.

Oral Boards Review: Diagnostic Pearls

1. Careful history-​taking is important in the diagnosis of early myelopathy. Early symptoms may include a history of difficulty with buttoning buttons, a history of falls, imbalance ascending or descending stairs (i.e., need to use a handrail), numbness and tingling in the fingers, and difficulty with micturition. 2. Physical exam findings may include both radicular and myelopathic features. Gait assessment should be included in the physical exam. 3. Imaging studies include dynamic cervical x-​rays, cervical magnetic resonance imaging (MRI), and cervical computed tomography (CT). The diagnosis of OPLL is most accurately made on cervical CT. Clinical presentation is typically that of a progressive cervical radiculopathy and myelopathy over months to years, whereas 10% of patients will present with an immediate deterioration following minor trauma.3 Initial imaging studies for myelopathy include dynamic x-​rays and a cervical spine MRI. Normal cervical canal width on x-​rays is 17 mm in the anterior-​posterior dimension.There is stenosis of the cervical canal when this measures less than 10mm.4 OPLL may appear hypointense on T2-​weighted MRI studies. MRI may also demonstrate spinal cord edema, myelomalacia, and gliosis with hyperintense signal on T2-​weighted imaging, thus demonstrating spinal cord impingement.5 However, MRI does a poor job differentiating ossification and may underestimate the amount of canal stenosis, thus CT is the preferred imaging modality for

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Figure 9.4  Sagittal computed tomography (CT) with representative segmental variant ossification of the posterior longitudinal ligament (OPLL). This type of OPLL is located behind the vertebral bodies. Additional types include the continuous, as demonstrated in Figure 9.1; mixed type; and other. The mixed type is a combination of the segmental and continuous variants of OPLL. OPLL (Figure 9.3). Non-​contrast CT imaging with reconstructed sagittal images best demonstrate the location and extent of OPLL (Figures 9.4 and 9.5). Dural penetration can be assumed when there is a double-​layer sign characterized by a hyperdense line of OPLL behind the vertebra followed by a hypodense mass representing the dura and finally an intradural hyperdense mass.6 The single-​layer sign is seen with a large central mass of OPLL with extensions laterally along the dura on axial imaging. Patients with a single-​or double-​layer sign have a high correlation with absent dura and subsequent cerebrospinal fluid (CSF) fistulas if operated anteriorly.7

Questions

1. How do clinical and radiographic findings influence surgical planning? 2. What is the appropriate timing for surgical intervention? 3. How should surgery be approached if there is dural penetration on imaging?

Decision-​Making

Decisions regarding the type of treatment are based on clinical and radiological findings. Two major myelopathy scales are used worldwide and may be helpful in determining the timing of surgery.The Nurick myelopathy scale covers six grades of neurological classification based upon gait dysfunction (Box 9.1).8 The modified Japanese Orthopedic Association

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Figure 9.5  Axial computed tomography (CT) demonstrate the single-​layer sign for dural penetration. This type is characterized by a single mass of ossification of the posterior longitudinal ligament (OPLL) between the vertebral body and the dura. Note that as the calcification expands laterally along the dura, it forms a “C” shape within the canal that can help with identification. scale has four domains covering upper extremity motor dysfunction, lower extremity motor dysfunction, sensory deficits, and sphincter dysfunction (Box 9.2).9 In patients with mild radiculopathy, oral nonsteroidal antiinflammatory drugs (NSAIDs), conservative physical therapy, and bracing can be provided along with regular follow-​up for signs of growth. Patients with progressive symptoms or mild to moderate myelopathy may be offered surgery. Comorbidities in elderly patients need to be weighed with the surgical risks. Surgical decompression is advised for patients with severe cervical myelopathy. For patients younger than 65 years with marked radiographic evidence of canal compromise and minimal clinical

Box 9.1  Nurick’s Classification System for Myelopathy Based on Degree of Difficulty in Walking Grade 0: Signs or symptoms of root involvement but without evidence of spinal cord disease Grade 1: Signs of spinal cord disease but no difficulty in walking Grade 2: Slight difficulty in walking that does not prevent full-​time employment Grade 3: Difficulty in walking that prevented full-​time employment or the ability to do all housework, but which was not so severe as to require someone else’s help to walk Grade 4: Able to walk only with someone else’s help or with the aid of a frame Grade 5: Chairbound or bedridden

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Box 9.2  Modified Japanese Orthopedic Association Scale This scale has four domains measuring upper and lower motor dysfunction, sensory dysfunction, and bladder dysfunction.



I. Motor dysfunction score of the upper extremities • Inability to move hands (0 points) • Inability to eat with a spoon but able to move hands (1 point) • Inability to button a shirt but able to eat with a spoon (2 points) • Able to button shirt with great difficulty (3 points) • Able to button shirt with slight difficulty (4 points) • No dysfunction (5 points) II. Motor dysfunction score of the lower extremities • Complete loss of motor and sensory function (0 points) • Sensory preservation without ability to move legs (1 point) • Able to move legs but unable to walk (2 points) • Able to walk on flat floor with a walking aid (3 points) • Able to walk up and/​or down stairs with hand rail (4 points) • Moderate to significant lack of stability but able to walk up and/​or down stairs without hand rail (5 points) • Mild lack of stability but can walk unaided with smooth reciprocation (6 points) • No dysfunction (7 points) III. Sensation dysfunction score • Complete loss of hand sensation (0 points) • Severe sensory loss or pain (1 points) • Mild sensory loss (2 points) • No sensory loss (3 points) IV. Sphincter dysfunction score • Inability to micturate voluntarily (0 points) • Marked difficulty with micturition (1 point) • Mild to moderate difficulty with micturition (2 points) • Normal micturition (3 points)

symptoms, a prophylactic operative decompression is recommended in an attempt to avoid rapid neurological decline following minor trauma.3 Much controversy surrounds whether anterior or posterior surgical approaches are superior for managing cervical OPLL. Anterior approach techniques include the anterior cervical diskectomy with fusion (ACDF) and anterior cervical corpectomy with fusion (ACCF). Anterior approaches offer direct decompression of the spinal cord with removal of the OPLL mass. Anterior approaches should be avoided when dural calcification is suspected as a ventral CSF leak may occur in such patients. Posterior approach techniques indirectly decompress the spinal cord. These include laminectomy alone, laminoplasty, and laminectomy and fusion.The number of segments to be decompressed should be considered. Anterior techniques work well for one to three segments, but are 86

 

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limited beyond three segments without adding significant soft tissue morbidity. Posterior techniques are favored in longer segment decompressions. Baseline dysphagia or a prior history of an anterior neck surgery for lymph node dissection or thyroid cancer may offer a relative contraindication to an anterior approach. Relative contraindications to the posterior approach include a cervical kyphotic deformity. Finally, elderly patients older than 65 years may do better postoperatively from a posterior approach as they have less dysphagia postoperatively and can maintain a better nutritional status.

Questions

1. What are the particular intraoperative advantages and risks associated with each procedure? 2. What is the degree of OPLL progression and postoperative changes in cervical motion associated with each approach?

Surgical Procedure Anesthesia and Neuromonitoring

An awake, fiber-​optic intubation is preferred in patients with significant OPLL and myelopathic findings on exam. For patients undergoing anterior surgery, we may opt for a nasotracheal intubation over an orotracheal intubation. The nasotracheal route does not inferiorly extend the jaw, allowing for a slightly larger operative field in patients with more rostral OPLL. Additionally, this avoids hyperextension or hyperflexion of the cervical spine. We routinely use intraoperative multimodality neuromonitoring (IONM) during cervical surgeries. We believe IONM may assist the surgeon in taking corrective measures to reduce or prevent permanent neurological deficits.10 This includes free-​run electromyography (EMG), motor evoked potentials (MEPs), and somatosensory evoked potentials (SSEPs). Ideal anesthesia for neuromonitoring utilizes no paralytics during the procedure and uses total intravenous anesthetic (TIVA) with a combination of ketamine, propofol, and short-​acting narcotics (remifentanil or fentanyl) while avoiding the use of inhalation agents.11 Communication to the anesthesia team prior to surgery about anesthetic needs is of utmost importance when using IONM to prevent delays. Finally, we routinely obtain supine MEP and SSEP baselines prior to flipping a patient prone for final positioning. New MEP and SSEP results are compared to our baseline and adjustments made as needed to avoid spinal cord injury or nerve root injury during positioning.

Oral Boards Review: Management Pearls

1. Anterior or posterior decompression of the cervical spine is acceptable. The number of levels to be treated, patient age, history of dysphagia or prior anterior neck surgery, and degree of cervical lordosis may affect which approach is best suited for the patient. 2. Avoid anterior surgery if there is suspicion of dural calcification. 3. Mildly symptomatic patients younger than 65 years with a high degree of canal compromise may be candidates for prophylactic decompression.

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Anterior Approach

The anterior approach is used in cases in which there is only one to two levels of compression and the ventral dura does not appear to be involved on the CT with the absence of the single-​or double-​layer sign. Depending on the extent of OPLL at a single level or at two adjacent levels, we favor an ACCF over a two-​level ACDF. Anterior approaches greater than three segments are generally avoided secondary to high pseudarthrosis rates in the authors’ experience.While this approach in general provides a more direct decompression of the OPLL and reduction myelopathy scores, there is a significantly higher risk of durotomy with CSF fistula.12 Fessler et al. and Iwasaki et al. have demonstrated significant improvement in Nurick or Japanese Orthopedic Association scores when utilizing ACCF with direct ventral resection of the OPLL mass as compared to indirect decompression with a posterior approach.13,14 Fixation should be performed with a system that allows for subsidence of the bone–​graft interface to avoid pseudarthrosis. Using either variable-​angle screws or a dynamic plate has demonstrated decreased rates of pseudarthrosis as compared to fixed plating systems.15–​17 Posterior Approach

The posterior approach is favored in cases in which long segment (>3 levels) decompression is needed, for elderly patients (>65 years), and for patients with a history of dysphagia or a prior anterior neck approach. Posterior approaches may not adequately decompress the spinal canal if greater than 60% is occupied by the OPLL mass.18,19 Simple laminectomy is avoided as there is a concern for cervical kyphosis over time and worsening of neurological status 5–​10  years from the time of surgery.20 This may be remedied by performing a laminectomy and fusion at the time of surgery. This is indicated if there is documented instability, loss of lordosis, or partial swan-​neck deformity. Advantages of a laminectomy and fusion include decompression of bilateral foramina as well. We prefer the Magerl screw trajectory for lateral mass screws,21 pars screws over pedicle screws at the C2 level to avoid vertebral artery injury, and we avoid stopping our fusion at C7 above the cervicothoracic junction (Figure 9.6). Disadvantages include cost, increased blood loss, and removing motion from the cervical spine. An alternative is laminoplasty, which offers indirect dorsal decompression without the need for a traditional fusion.22–​24 An advantage of laminoplasty is that there is some preserved range of motion in cervical laminoplasty patients.25 About half the range of motion is lost following laminoplasty. One disadvantage of laminoplasty is that only unilateral foraminotomies can typically be safely performed on the open side of the construct, thus making it less than ideal for a patient with bilateral symptoms. Additionally, laminoplasty may not adequately decompress a patient with congenital stenosis.15 Additionally, there has not been significant improvement of visual analog scale neck scores for patients using laminoplasty.26 This posterior approach reduces the risks of cervical CSF fistulas, carotid/​vertebral vascular injuries, and esophageal compromise that may be encountered through the anterior surgery.

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Figure 9.6  Postoperative images from case presentation. This patient was operated for a C4 to T10 laminectomy and fusion over two different stages. She had extensive disease in both her cervical and thoracic canals.

Pivot Points

1. A change of MEP/​SSEP while positioning a patient prone should prompt further positioning changes, traction, or returning a patient back to the supine position. If a patient is unable to be positioned prone without IONM changes, an anterior decompression may need to be considered first. 2. Patients with greater than three levels of involvement should be considered for a posterior decompression. 3. Patients with greater than 60% canal compromise should be considered for an anterior decompression.

Aftercare

Patients presenting with an acute decline in neurological status following minor trauma are typically observed in the intensive care unit (ICU) with a goal mean arterial pressure (MAP) of greater than 85  mm Hg preoperatively and immediately postoperatively. Electively operated patients are typically admitted to the floor postoperatively. Physical and occupational therapy services are consulted for discharge assessment and to begin therapy on patients. Speech therapy is consulted if there is concern for dysphagia postoperatively. Antibiotics are given perioperatively for up to 24 hours. Surgical drains are left in place until less than 50 mL output per 12-​hour  shift.

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Complications and Management

If a CSF leak occurs, a primary repair will be attempted intraoperatively. A lumbar subarachnoid drain may be placed in the postoperative period for 3–​7 days. The head of bed is elevated at 30 degrees in the postoperative period. Surgical drains are taken off suction, placed to gravity, and left in place until adequate wound healing has been achieved to prevent CSF leaking through the incision. Neurological deterioration following the procedure will prompt imaging with CT and MRI to look for reversible causes of spinal cord compression including hematoma, graft migration, or misplaced instrumentation. If no immediately nonreversible cause of neurological compromise is found, we may consult our neurology colleagues to look for additional causes of neurological deterioration. This differential would include cord infarct, demyelination, and neurological decline from detethering the cord. Additionally, we will admit these patients to the ICU and maintain their MAP at greater than 85 mm Hg for a few days postoperatively. We do not give steroids to these patients. Postoperative C5 palsy occurs in 5–​20% of cases.27,28 There does not appear to be a significant difference between ACCF and posterior laminoplasty approaches.29 While this complication may be distinguished from C5 nerve root injury or impingement by its painless nature, the weakness of the deltoid and/​or biceps postoperatively can be quite distressing for the patient. Imaging is generally obtained to check for graft migration or malpositioned instrumentation that could be corrected. The vast majority of C5 palsies will improve with time and therapy, although the time course is difficult to predict. Counseling the patient about this complication and expected recovery is best done during the preoperative period.

Oral Boards Review: Complications Pearls

1. C5 palsy occurs in 5–​20% of cases. Imaging may be obtained to rule out graft migration or malpositioned instrumentation. 2. Attempts to repair CSF leaks should be made intraoperatively. Early CSF diversion with a lumbar subarachnoid drain may be considered for concerns of persistent CSF fistula.

Evidence and Outcomes

Prospectively controlled studies for conservative management as compared to surgical treatment do not exist to date. Multiple studies have looked at anterior compared posterior decompression and demonstrated statistically significant neurological improvement with an anterior approach.13,14 However, the Fessler et al. study is limited by the fact that they compared an anterior approach to a laminectomy alone, a technique that has fallen out of favor. Iwasaki et al. demonstrated a better neurological outcome for anterior approaches in patients who had an OPLL mass occupying greater than 60% of the canal. However, their study is tempered by the fact that they had graft migration in 15% and reoperation in 26% of cases.

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References and Further Reading

1. Epstein NE. Ossification of the posterior longitudinal ligament in evolution in 12 patients. Spine (Phila Pa 1976). 1994;19(6):673–​601. 2. Kim TJ, Bae KW, Uhm WS, Kim TH, Joo KB, Jun JB. Prevalence of ossification of the posterior longitudinal ligament of the cervical spine. Joint Bone Spine. 2008;75(4):471–​474. 3. Katoh S, Ikata T, Hirai N, Okada Y, Nakauchi K. Influence of minor trauma to the neck on the neurological outcome in patients with ossification of the posterior longitudinal ligament (OPLL) of the cervical spine. Paraplegia. 1995;33(6):330–​333. 4. Miyasaka H. Consideration on pathophysiology of OPLL. Clin. Orthop. Relat. Res. 1975;10:1091–​1096. 5. Mummaneni PV, Kaiser MG, Matz PG, et al. Preoperative patient selection with magnetic resonance imaging, computed tomography, and electroencephalography: does the test predict outcome after cervical surgery? J. Neurosurg. Spine. 2009;11(2):119–​129. 6. Epstein NE. Identification of ossification of the posterior longitudinal ligament extending through the dura on preoperative computed tomographic examinations of the cervical spine. Spine (Phila Pa 1976). 2001;26(2):182–​186. 7. Min JH, Jang JS, Lee SH. Significance of the double-​layer and single-​layer signs in the ossification of the posterior longitudinal ligament of the cervical spine. J. Neurosurg. Spine. 2007;6(4):309–​312. 8. Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain. 1972;95(1):87–​100. 9. Benzel EC, Lancon J, Kesterson L, Hadden T. Cervical laminectomy and dentate ligament section for cervical spondylotic myelopathy. J. Spinal Disord. 1991;4(3):286–​295. 10. Clark AJ, Ziewacz JE, Safaee M, et al. Intraoperative neuromonitoring with MEPs and prediction of postoperative neurological deficits in patients undergoing surgery for cervical and cervicothoracic myelopathy. Neurosurg. Focus. 2013;35(1):E7. 11. Ziewacz JE, Berven SH, Mummaneni VP, et al.The design, development, and implementation of a checklist for intraoperative neuromonitoring changes. Neurosurg. Focus. 2012;33(5):E11. 12. Epstein NE, Hollingsworth R. Anterior cervical micro-​dural repair of cerebrospinal fluid fistula after surgery for ossification of the posterior longitudinal ligament. Technical note. Surg. Neurol. 1999;52(5):511–​514. 13. Fessler RG, Steck JC, Giovanini MA. Anterior cervical corpectomy for cervical spondylotic myelopathy. Neurosurgery. 1998;43(2):257–​265; discussion 265–​257. 14. Iwasaki M, Okuda S, Miyauchi A, et al. Surgical strategy for cervical myelopathy due to ossification of the posterior longitudinal ligament: Part 2: Advantages of anterior decompression and fusion over laminoplasty. Spine (Phila Pa 1976). 2007;32(6):654–​660. 15. Epstein NE. The management of one-​level anterior cervical corpectomy with fusion using Atlantis hybrid plates: preliminary experience. J. Spinal Disord. 2000;13(4):324–​328. 16. Epstein NE. Evaluation and treatment of clinical instability associated with pseudoarthrosis after anterior cervical surgery for ossification of the posterior longitudinal ligament. Surg. Neurol. 1998;49(3):246–​252. 17. Mummaneni PV, Haid RW, Rodts GE, Jr. Combined ventral and dorsal surgery for myelopathy and myeloradiculopathy. Neurosurgery. 2007;60(1 Supp1 1):S82–​S89.

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18. Iwasaki M, Okuda S, Miyauchi A, et al. Surgical strategy for cervical myelopathy due to ossification of the posterior longitudinal ligament:  Part  1:  Clinical results and limitations of laminoplasty. Spine (Phila Pa 1976). 2007;32(6):647–​653. 19. IshidaY, Ohmori K, Suzuki K, Inoue H.Analysis of dural configuration for evaluation of posterior decompression in cervical myelopathy. Neurosurgery. 1999;44(1):91–​95; discussion  95–​96. 20. Kato Y, Iwasaki M, Fuji T, Yonenobu K, Ochi T. Long-​term follow-​up results of laminectomy for cervical myelopathy caused by ossification of the posterior longitudinal ligament. J. Neurosurg. 1998;89(2):217–​223. 21. Jeanneret B, Magerl F, Ward EH, Ward JC. Posterior stabilization of the cervical spine with hook plates. Spine (Phila Pa 1976). 1991;16(3 Suppl):S56–​S63. 22. Morimoto T, Matsuyama T, Hirabayashi H, Sakaki T, Yabuno T. Expansive laminoplasty for multilevel cervical OPLL. J. Spinal Disord. 1997;10(4):296–​298. 23. Sodeyama T, Goto S, Mochizuki M, Takahashi J, Moriya H. Effect of decompression enlargement laminoplasty for posterior shifting of the spinal cord. Spine (Phila Pa 1976). 1999;24(15):1527–​1531; discussion 1531–​1522. 24. Deutsch H, Mummaneni PV, Rodts GE, Haid RW. Posterior cervical laminoplasty using a new plating system: Technical note. J Spinal Disord Tech. 2004;17(4):317–​320. 25. Fujimori T, Le H, Ziewacz JE, Chou D, Mummaneni PV. Is there a difference in range of motion, neck pain, and outcomes in patients with ossification of posterior longitudinal ligament versus those with cervical spondylosis, treated with plated laminoplasty? Neurosurg. Focus. 2013;35(1):E9. 26. Meyer SA, Wu JC, Mummaneni PV. Laminoplasty outcomes: Is there a difference between patients with degenerative stenosis and those with ossification of the posterior longitudinal ligament? Neurosurg. Focus. 2011;30(3):E9. 27. Sakaura H, Hosono N, Mukai Y, Ishii T, Yoshikawa H. C5 palsy after decompres sion surgery for cervical myelopathy:  Review of the literature. Spine (Phila Pa 1976). 2003;28(21):2447–​2451. 28. Chen Y, Chen D, Wang X, Guo Y, He Z. C5 palsy after laminectomy and posterior cervical fixation for ossification of posterior longitudinal ligament. J Spinal Disord Tech. 2007;20(7):533–​535. 29. Gandhoke G, Wu JC, Rowland NC, Meyer SA, Gupta C, Mummaneni PV. Anterior corpectomy versus posterior laminoplasty: Is the risk of postoperative C-​5 palsy different? Neurosurg. Focus. 2011;31(4):E12.

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Cervical Radiculopathy Due to Central Disc ACDF/​Arthroplasty Mazda K. Turel and Vincent C. Traynelis

10 Case Presentation

A 37-​year-​old women presented with neck pain radiating to her right arm and right middle finger for 6 months. Physical therapy increased the pain. On examination she had a positive right Spurling maneuver, 4/​5 strength in her right triceps, and hypesthesia in the right C7 dermatome.

Questions

1. What is the most likely clinical and radiological diagnosis? 2. What are the differential diagnoses in a case like this? 3. What are the various imaging modalities you would use confirm your diagnosis and plan your management? 4. Describe the radiological findings seen in Figure 10.1. Assessment and Planning

This woman has a right C7 radiculopathy that has failed to respond to a course of nonoperative therapy. Disc herniation usually occurs in patients with mild to moderate degenerative changes. The initial evaluation includes a careful history, which is important for distinguishing between vascular, infectious, neoplastic, and traumatic etiologies of the symptoms. Magnetic resonance imaging (MRI) allows direct visualization of neural structures and provides the greatest soft tissue detail. Because herniated discs can be found in about 20% of asymptomatic individual between the ages of 20 and 40, MRI findings must be strictly correlated with the clinical presentation, which remains the cornerstone of decision-​making. The MRI in this patient shows a very large right C6–​C7 lateral disc extrusion with extension into the neural foramen. There is indentation of the cord and narrowing of the foramen (Figure 10.1,A–​C). Plain and dynamic radiographs evaluate alignment, stability, bony anatomy, and degenerative disc disease. Cervical alignment parameters are important. In this patient, the neutral lateral cervical radiograph shows a C2–​C7 sagittal vertical angle (SVA) of 18.1 mm, C2–​C7 lordosis is 15.5 degrees, C1–​C7 lordosis is 57.6 degrees, and the T1 slope is 39.2 degrees. On flexion and extension views, there is no significant instability (Figure 10.1,D–​F).

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Figure 10.1 T2-​weighted axial (A, B) and sagittal (C) magnetic resonance images (MRI) of the cervical spine showing a large right C6–​C7 lateral disc extrusion with extension into the neural foramen. There is indentation of the cord and narrowing of the foramen. On flexion and extension and neutral lateral radiographs of the cervical spine there is no significant instability. (D–​F) The computed tomography (CT) scan in this case was done to rule out any associated fractures due to her previous trauma and to ascertain of there was evidence of posterior osteophytes or facetal hypertrophy  (G–​I).

 

Cervical Radiculopathy Due to Central Disc

Computed tomography (CT) provides optimal visualization of bony detail and has a high sensitivity in terms of detecting bony foraminal stenosis.The addition of myelography to CT provides an excellent adjunctive study to further delineate specific anatomy, such as the lateral recess, or to reconcile against an MRI study in which the etiology of clinical symptoms is not demonstrated. The CT scan in this case was done to rule out any associated fractures due to her previous trauma and to assess facet arthrosis (Figure 10.1,G–​I).

Oral Boards Review: Diagnostic Pearls

Neutral and lateral flexion and extension radiographs should be obtained to assess alignment, motion, and stability. An MRI scan or CT myelogram is needed to determine whether there is impingement of any neural structures. The axial MRI or CT scan should be carefully reviewed for the vertebral artery position, and any anomalies should be carefully noted. Decision-​Making

Since this patient has failed nonoperative therapy, surgery is a reasonable option. The goal of surgical decompression is symptom relief. She could be treated with an anterior cervical discectomy and fusion (ACDF) or cervical disc replacement (CDR). An anterior approach allows for direct decompression which will alleviate the symptoms, and the reconstruction can be with either a fusion or a total disc replacement. Arthrodesis can enlarge the neural foramina, maintain or restore proper alignment, and provide solid stabilization. It can be effective in the presence of facet arthropathy. Factors to consider when selecting suitable candidates for arthroplasty include the degree of segmental pathology,stability,and overall segmental motion.CDR is contraindicated in the setting of significant segmental or global deformity. Similarly, patients without preexisting motion or spinal instability should not be treated with a CDR. Currently, in the United States, CDR is approved by the Food and Drug Administration (FDA) for intractable neck pain with radiculopathy or myelopathy at a single level or two levels between C3 and C7 in a patient who has failed a minimum of 6 weeks of conservative treatment. Surgical Procedure

The timing of surgical intervention for symptomatic disc disease depends on the clinical situation. Emergent surgical intervention is indicated for patients with severe or rapidly progressive motor radiculopathy, myelopathy, or bowel or bladder dysfunction. Patients without evidence of spinal instability who present with pain, sensory disturbances, and mild or fixed motor deficits or those exhibiting neurological improvement should not be considered for emergent surgical decompression. Instead, these patients should be treated with nonoperative modalities. If they fail to improve, then elective surgical intervention should be considered. ACDF has been a successful surgical strategy for more than 60 years. The patient is positioned supine with the head resting on a doughnut and with an axillary roll below the shoulder. The ventral approach to the cervical spine is performed sharply through a

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plane between the sternocleidomastoid muscle and the carotid sheath laterally and the strap muscles and tracheoesophageal viscera medially. The omohyoid muscle crossing at C5–​C6 may be tagged, divided, and reapproximated at the time of closure. Caudal exposure at C6–​C7, C7–​T1 is facilitated by dividing the inferior thyroid artery, while at C2–​C3 or C3–​C4 it is important to carefully fully isolate the superior thyroid artery prior to dividing it to minimize the potential of injuring the superior laryngeal nerve. The disc space is identified using intraoperative fluoroscopy, and the medial attachments of the longus colli muscle are released with cautery. The exposure is maintained with a retractor system.The disc annulus is incised, and disc removal is done using a combination of curettes and pituitary forceps until the posterior longitudinal ligament is seen.The disc space may be distracted to improve visualization. The endplates are prepared for grafting, and then the operating microscope is brought into the field to complete the rest of the discectomy, expose the dura from one uncovertebral joint to the other to achieve an adequate lateral decompression, and visualize the origin of the nerve roots. The posterior osteophytes and posterior portion of the uncinate are removed. The reconstruction can be performed with allograft, autograft, or a cage. An anterior plate decreases subsidence, increases the fusion rate, and often eliminates the need for a rigid orthosis. The wound is thoroughly irrigated, hemostasis is achieved, and the closure is done in layers. The procedure for an arthroplasty remains the same up until completion of the discectomy, when a CDR is placed instead of the graft and plate with the aim to preserve motion. The CDR should be implanted with strict adherence to the recommendations of the manufacturer, which will vary depending on the implant selected. Figure 10.2 demonstrates an intraoperative radiograph of this patient who underwent a CDR. The dorsal approach is discussed in detail in the next chapter.

Figure 10.2  Lateral cervical intraoperative radiograph of the patient after cervical disc replacement.

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Oral Boards Review: Surgical Technique Pearls

1. The head and neck are stabilized and held in a neutral position or slightly extended for all procedures. The vertebral endplates at the operative level should be maintained in as close to a neutral position as possible. 2. On the left side, the recurrent laryngeal nerve loops under the arch of the aorta and is protected in the left tracheoesophageal groove; hence, we prefer the left-​sided approach. On the right side, however, it travels around the subclavian artery, passing dorsomedially to the side of the trachea and esophagus. The nerve is vulnerable as it passes from the subclavian artery to the right tracheoesophageal groove. 3. The vertebral artery is usually 5 mm lateral to the uncovertebral joint and is not covered by bone between two transverse foramina. There can be significant variations in its position, though, and it should be examined preoperatively on every MRI scan prior to the procedure. 4. The plate should not be near the adjacent disc space because this has been shown to accelerate disc degeneration. The utmost care should be taken to ensure the adjunct disc space is not violated by a screw as this will hasten degeneration at the adjacent level.

Pivot Points

1. The main objectives of treatment of cervical radiculopathy are to relieve pain, improve neurologic function, and prevent recurrences. 2. The indications for cervical arthroplasty are not synonymous with those for cervical fusion, and this technique should not be assumed to be appropriate for all patients who may benefit from an ACDF. 3. ACDF has the advantage of improving cervical lordosis and is the most appropriate option in patients with severe spondylosis, facet joint degeneration, and loss of motion at the pathological level, all of which are contraindications for arthroplasty. 4. Patients receiving a CDR should have normal cervical alignment and mobility. If one wishes to replicate the results from the prospective disc studies, then one should adhere to the entry criteria.

Aftercare

Patients are observed overnight in the hospital with a continuous pulse oximeter to watch for airway compromise from postoperative hematoma/​seroma. Diet and activity are allowed as tolerated. Drains, if placed, are typically removed on postoperative day 1. We do not prescribe any restriction of activity with the exception of carrying heavy loads on the head. Patients are seen in the clinic at 6 weeks and at progressively regular intervals up to 12 months.

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Complications and Management

Complications of anterior cervical spine surgery at a single level are extremely infrequent. Dysphagia is the most common complication and varies in incidence from 5% to 50%. However, less than 1% is permanent. Neurological deterioration can result from direct injury to the cord and is also very unlikely. Injury to the cervical sympathetic chain leads to Horner syndrome but is very rare. Injury to the esophagus and the carotid and vertebral arteries has been reported, and the incidence of these complications is less than 1%. Airway compromise is the most dreaded complication and can occur due to a postoperative hematoma, soft tissue swelling, or implant/​graft dislodgement. Prompt intubation before the development of stridor and reexploration can be life-​saving. Dural tear and cerebrospinal fluid leak occur exceedingly rarely and are treated with Gelfoam, tissue glue, and, in selected cases, a lumbar subarachnoid drain. Some patients may experience posterior interscapular pain, which can be severe but should resolve with time. Delayed complications include nonunion (pseudoarthrosis) and adjacent segment disease, both of which require revision surgery in symptomatic patients. Implant migration or subsidence, though rare, remains a potential complication following CDR. Postcervical kyphosis is another complication following CDR. Heterotopic ossification, defined as formation of bone outside the skeletal system has been reported following arthroplasty with variable incidence among different studies.

Oral Boards Review: Complications Pearls

1. Intermittent release of the retractor and deflating the cuff of the endotracheal tube may reduce the incidence of recurrent laryngeal nerve injury. 2. An adequate fascial dissection minimizes retraction and reduces postoperative soft tissue swelling and airway compromise. 3. Meticulous hemostasis of every layer of soft tissue within the neck before wound closure will ensure that the patient does not develop a postoperative hematoma. 4. The incidence of heterotopic ossification in patients treated with a CDR may be decreased by copious irrigation intraoperatively, limited muscle retraction, and nonsteroidal antiinflammatory drugs (NSAIDs) during the perioperative period.

Evidence and Outcomes

Postoperative neurological outcome is related to the type, duration, acuteness, and severity of the preoperative deficit. Data from prospective observational studies indicate that 2 years after surgery for cervical radiculopathy caused by soft cervical disc herniation (without myelopathy), 85% of patients have substantial pain relief from radicular symptoms. Radicular symptoms are more likely to improve with surgical decompression compared with myelopathy; however, several small reports note significant improvement in myelopathic patients if surgery is performed early. Overall quality of life as assessed by the Short-​Form 36 inventory and Oswestry Disability Index (ODI) also show significant improvement. Patients with deficits from acute disc herniations have a more favorable surgical outcome compared with those with deficits from spondylotic disease. Patients 98

 

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who present with severe or long-​standing symptoms and signs have a poorer functional outcome than those with only a short clinical history and minor neurological deficits. In an analysis of outpatient versus overnight-​admitted patients, a total of 7,288 ACDF cases were identified (outpatient = 1,168, inpatient = 6,120). Unadjusted rates of major morbidity (0.94% vs. 4.5%) and return to the operating room (OR) within 30 days (0.3% vs. 2.0%) were significantly lower in outpatient versus inpatient ACDF. After propensity matching, 1,442 cases (outpatient  =  792, inpatient  =  650) based on baseline 32 covariates, rates of major morbidity (1.4% vs. 3.1%, p = 0.03), and return to the OR (0.34% vs. 1.4%, p = 0.04) remained significantly lower after outpatient ACDF. Multivariate logistic regression demonstrated that ACDF performed in the outpatient setting had 58% lower odds of having a major morbidity and 80% lower odds of return to the OR within 30 days. It should be recognized that those treated as an outpatient represent an extremely select group in which one would expect minimal complications. In a recently concluded meta-​analysis comparing more than 1,000 patients each for ACDF versus CDR, the latter had a higher rate of overall success and better NDI scores with lower rates of secondary surgery and adverse events.The reoperation rate at 10 years following arthroplasty was around 10%, while it was 30% following ACDF. Fusion rates are greater than 95% for a single-​level ACDF and 85% for two levels. Although prevention of adjacent segment disease has been a compelling rationale for CDR, there is no conclusive supporting clinical evidence for this hypothesis at this point. Reference and Further Reading

Burkus JK, Traynelis VC, Haid RW Jr, Mummaneni PV. Clinical and radiographic analysis of an artificial cervical disc: 7-​year follow-​up from the Prestige prospective randomized controlled clinical trial:  Clinical article. J Neurosurg Spine. 2014 Oct;21(4):516–​ 528. doi:  10.3171/​ 2014.6.SPINE13996. Epub Jul 18, 2014. Engquist M, Löfgren H, Öberg B, et al. Factors affecting the outcome of surgical versus nonsurgical treatment of cervical radiculopathy: A randomized, controlled study. Spine (Phila Pa 1976). 2015 Oct 15;40(20):1553–​1563. doi: 10.1097/​BRS.0000000000001064. Gornet MF, Burkus JK, Shaffrey ME, Argires PJ, Nian H, Harrell FE Jr. Cervical disc arthroplasty with PRESTIGE LP disc versus anterior cervical discectomy and fusion:  A prospective, multicenter investigational device exemption study. J Neurosurg Spine. 2015 Jul 31:1–​16. [Epub ahead of print]. Loumeau TP, Darden BV, Kesman TJ, Odum SM,Van Doren BA, Laxer EB, Murrey DB. A RCT comparing 7-​year clinical outcomes of one level symptomatic cervical disc disease (SCDD) following ProDisc-​C total disc arthroplasty (TDA) versus anterior cervical discectomy and fusion (ACDF). Eur Spine J. 2016 Jul;25(7):2263–​2270. doi:  10.1007/​s00586-​016-​4431-​6. Epub Feb 11, 2016. McGirt MJ, Godil SS, Asher AL, Parker SL, Devin CJ. Quality analysis of anterior cervical discectomy and fusion in the outpatient versus inpatient setting: Analysis of 7288 patients from the NSQIP database. Neurosurg Focus. 2015 Dec;39(6):E9. doi: 10.3171/​2015.9.FOCUS15335.

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Cervical Radiculopathy Lateral Disc Foramintomy Michael Karsy, Ilyas Eli, and Andrew Dailey

11 Case Presentation

A 53-​year-​old woman presents to clinic with the chief complaint of right shoulder pain of 3 months’ duration. She describes a sharp pain emanating from the right lateral aspect of her neck into her trapezius and then down across the deltoid. She describes the intensity of the pain as a 6/​10 in her right shoulder. The pain worsens as the day progresses. Her symptoms are most notably worse in her right shoulder, and, as a result, she has become less active. She unsuccessfully tried treating the pain with nonsteroidal antiinflammatory drugs (NSAIDs) and physical therapy. She subsequently underwent a right C5 selective nerve root block; however, she reports having no pain relief with the injection and no resolution of her symptoms. She otherwise denies any clumsiness or weakness in her right upper extremity. A neurological examination reveals a motor strength of 5/​5 in the deltoid, biceps, triceps, wrist extension, wrist flexion, dorsal interosseous, flexor digitorum profundus, and abductor pollicis brevis. On sensory examination, there is diffuse decreased sensation throughout the patient’s right upper extremity that is not in a dermatomal pattern. The reflex examination reveals 2+ biceps bilaterally with a 1+ triceps reflex seen on the right. She has no evidence of Hoffman sign or gait abnormality. Magnetic resonance imaging (MRI) of the cervical spine without contrast demonstrates diffuse cervical disc degeneration from C3 to C7 (Figure 11.1). The most notable finding is a severe neural foraminal stenosis at the C4–​C5 level eccentric to the right side. Questions

1. What is the differential diagnosis of this patient? 2. What is the initial conservative management of this patient, and when should this patient be referred for surgical treatment? 3. What imaging should be completed to evaluate this patient?

Assessment and Planning

On the basis of the patient’s presentation, physical examination, and imaging findings, the diagnosis is cervical radiculopathy. Cervical radiculopathy results from direct compression and inflammation of a cervical nerve root, often because of disc herniation or

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Figure 11.1  (A) Axial T2-​weighted magnetic resonance imaging (MRI) without gadolinium demonstrates foraminal stenosis on the right C5 nerve root. An oblique cut (line) is shown in B. (B) Oblique T2-​weighted MRI without gadolinium demonstrates disc herniation causing compression of the exiting C5 nerve root. (C) Sagittal cervical spine x-​ray shows normal cervical lordosis with multilevel loss of disc height most pronounced at C4–​C5. osteophyte formation. Patients with cervical radiculopathy present with complaints of sharp, numbing, shooting, or lancinating pain attributable in a dermatomal distribution. Physical examination is notable for a depressed reflex arc in the affected nerve root. Additionally, the Spurling test, which involves head turn toward the symptomatic side and placement of downward axial pressure, can reproduce the radicular pain. Conversely, axial traction reduces the pain. Subtle changes in sensation and strength are not uncommon; however, a detailed neurological examination should be performed to rule out myelopathy. An initial workup to confirm the diagnosis includes obtaining cervical lateral x-​rays to evaluate the cervical spine curvature and identify degenerative changes such as osteophyte formation or disc collapse (Figure 11.1). Flexion and extension radiographs are also helpful in evaluating cervical spine stability prior to selecting patients for cervical foraminotomy versus arthroplasty or arthrodesis. Computed tomography (CT) imaging allows for visualization of the cervical bony anatomy, which is helpful in determining the etiology of the cervical root compression. Oblique reconstructions will depict foraminal narrowing. MRI is currently the standard imaging modality used for clear visualization of soft tissue, enabling the identification of disc herniation and impingement of nerve roots. In some situations, a CT myelogram may be helpful for patients with contraindications to an MRI to assess cervical stenosis and disc bulges.The direction and degree of disc herniation, course of the vertebral arteries, and trajectory to the symptomatic level should be assessed on preoperative imaging.

Oral Boards Review: Diagnostic Pearls

1. Management of patients with cervical radiculopathy requires a complete assessment, including history and physical examination. Findings that suggest cervical radiculopathy include pain radiating down the arm along a particular dermatomal distribution. The presence of upper motor neuron signs, such as

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Cervical Radiculopathy: Lateral Disc Foramintomy

hyperreflexia and the Hoffman sign, which could suggest the presence of myelopathy, should be ruled out. 2. MRI should be utilized to look for disc herniation or osteophytes as causes for nerve root compression. The course of the vertebral artery should be assessed as well as the presence of anatomic variants. 3. Cervical radiculopathy is initially managed conservatively with physical therapy, medication, and spinal injection. Most patients obtain adequate pain relief with nonsurgical management. Only after these measures fail to provide the patient with pain relief is surgery then indicated. 4. Laminoforaminotomy is contraindicated in patients with myelopathy and cervical spine instability.

Nonoperative management is recommended for most patients who have cervical radiculopathy. Conservative measures include physical therapy, activity modification, use of NSAIDs, and spinal injections. Most patients notice improvement and pain relief with conservative treatment; however, patients who continue to suffer despite such measures should consider surgery. Surgical intervention is thus reserved for patients who continue to have severe pain despite 6 weeks of conservative management.

Questions

1. What features of imaging modalities should be evaluated in the management of this disease? 2. What are the indications for surgery? 3. What are the contraindications to surgery? 4. What anatomical features limit use of this surgical approach?

Decision-​Making

Indications for cervical foraminotomy include radiographic documentation, with either CT or MRI, of foraminal stenosis caused by either an osteophyte or disc herniation and symptoms that correlate to the affected nerve root. Contraindications to performing cervical foraminotomy include the presence of kyphosis or cervical spine instability, symptoms of cervical myelopathy, and signs of spinal cord compression on imaging modalities. Among the advantages of a cervical foraminotomy are that the disc space is not destabilized, cervical fusion is avoided, and direct decompression of the foramen is achieved. Anterior and posterior approaches have been explored in the treatment of lateral disc herniation. Anterior discectomy was described by Robinson and Smith in 1955 and Cloward in 1958; it involves direct access to the ventral cervical root where compression was most often noted. Anterior microforaminotomy was described by Jho to avoid removal of the lateral disc and preserve the functional integrity of the spine.1,2 Candidates 103

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for anterior or posterior cervical foraminotomy approaches have clear unilateral cervical radiculopathy and foraminal stenosis caused by either an osteophyte or a disc herniation with symptoms that correlate to the affected nerve root; minimal neck pain; no prior cervical spine surgery; and no significant cervical kyphosis, stenosis, or instability. These two approaches minimize complete disc removal. This is an advantage because disc removal necessitates arthrodesis, which can be associated with complications including longer operative times and greater blood loss, adjacent segment disease, and hardware failure, as well as pseudarthrosis. Complications Management

1. What anatomical features favor an anterior versus posterior approach for cervical foraminotomy? 2. What are the critical structures in this approach? How can an injury to those structures be managed intraoperatively and postoperatively?

Surgical Procedure Anterior Approach

After the patient is positioned supine, an incision is localized to the uncovertebral junction of the symptomatic level, medial to the border of the sternocleidomastoid and perpendicular to the disc space (Figure 11.2A). A standard anterior cervical dissection to the level of the longus colli is performed. A knife is used to remove a rectangular area of the longus colli muscle at the area of the uncovertebral joint, with bipolar electrocautery used for hemostasis. The sympathetic trunk runs along the longus colli above the transverse foramen and lateral to the uncovertebral joint. A long, thin, malleable retractor is placed between the uncinate process and the vertebral artery to protect the transforaminal segment of the artery. The uncinate process is partially removed by creating a hole 5 mm in diameter in the medial wall of the neural foramen with a 2 mm drill bit followed by curettes and Kerrison rongeurs. Ruptured and migrated disc fragments commonly lie in the axillary region of the nerve root and can be identified on MRI. Opening the posterior longitudinal ligament can be useful in identifying fragments. Posterior Approach

The patient is placed prone in the reverse Trendelenburg position with 30 degrees of tilt to reduce cervical venous pressure or in a sitting position (Figure 11.2B).The advantages of the sitting position can include use of gravity to remove blood from the surgical field, but this position increases the risk of air embolism and is a less familiar approach to most surgeons. The neck should be maintained in a slightly flexed position, and a Mayfield skull clamp can reduce intraoperative movement. An incision is localized over the laminar interspace in the midline. A standard posterior cervical dissection is performed with the goal to localize to the lamina–​facet interface of the superior and inferior cervical level where the exiting nerve root is found. Drilling is centered at the lamina–​facet junction to expose the lateral border of the thecal sac, the exiting nerve root, and the disc

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Figure 11.2  Anterior and posterior approaches for cervical foraminotomy. (A) Artist’s illustration showing an anterior foraminotomy approach, outlining the location of a herniated disc fragment (dotted circle). The lateral retractor is placed to protect the exiting nerve root and vertebral artery. The longus colli has been split to allow access to the disc. (B) Artist’s illustration showing a posterior foraminotomy approach. The lamina–​facet junction has been drilled to give access to the exiting nerve root. A nerve hook is shown retracting the exiting nerve root. space. Localization of the depth and lateral extent of neural structures from the incision can be ensured by identifying the lateral border of the facet. The medial third of the facet and lateral third of the superior and inferior lamina are thinned using a high-​speed drill. Curettes and the Kerrison rongeur are used to remove the remaining bone. The ligamentum flavum is identified medially and incised to allow access to the nerve root and disc space. Disc material superior or inferior to the exiting nerve root is removed depending on the extent of disc herniation. A cruciate incision into the posterior longitudinal ligament and annulus is made to decompress disc extrusion. Use of endoscopic assistance to improve illumination of the working area has also been well described for these approaches.

Oral Boards Review: Management Pearls

1. Anterior or posterior approaches can be planned based on preoperative imaging. Attention should be paid to the exiting nerve root and vertebral artery with both approaches. The extent and direction of disc herniation causing foraminal stenosis should be identified. The artery will be lateral to the

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uncovertebral joint in a soft tissue plane not visualized during surgery. The most common entry for the vertebral artery is at the C6 cervical level. 2. The open and endoscopic approaches have shown equivalent efficacy.

Pivot Points

1. If the patient has preoperative neck pain, spine instability, stenosis or compression, or myelopathy, a larger anterior discectomy and fusion procedure may be needed. Arthroplasty may also be an option. 2. Anterior and posterior foraminotomy approaches can be used equivalently and based on individual patient characteristics

Aftercare

A cervical orthosis is not required postoperatively, and patients who have undergone an anterior approach can usually be discharged same day. Posterior approaches may involve more pain than anterior approaches, and most patients require 1 day in the hospital prior to discharge. Complications and Management

Complications during anterior or posterior approaches can include bleeding from injury to the vertebral artery or perivertebral venous plexus. The vertebral artery runs lateral to the uncinate process within the transverse foramen and most often enters the foramen at the C6 level. After injury, packing of the wound with hemostatic agents should be attempted to assess whether the injury is controllable. Primary repair of the vertebral artery is difficult given the narrow corridor but has been described. Immediate postoperative angiography is recommended to evaluate the degree and type of injury as well as whether there is adequate flow to the posterior circulation. Endovascular consultation can be helpful in further management. As with standard anterior cervical approaches, neck hematoma may be a significant comorbidity warranting urgent reexploration. Hematomas are most likely to occur within the first few hours postoperatively. Minimizing agitation and coughing during extubation can reduce postoperative hematoma risk but requires close communication with the anesthesia team. Air embolism is possible during cases performed with the patient in a sitting position. The most sensitive monitoring for air embolism is a precordial ultrasound monitor, but a decrease in end tidal CO2 is another common sign. Placement of a central line before the case can be a strategy to draw air bubbles if they occur. Immediate treatments include flooding the field with irrigation, lowering the head of bed below the heart, and positioning the patient in the left lateral position to trap air in the right heart. Lack of pain resolution postoperatively is possible; it is related to inadequate nerve root decompression or additional cervical spondylotic disease, which may require a wider decompression and fusion procedure. Injury to the thecal sac or nerve roots can occur during overzealous dissection. Other complications during dissection can 106

 

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include Horner syndrome from injury of the sympathetic chain. Attention to minimize longus colli dissection lateral to the uncinate process can aid in reducing injury risk. Cerebrospinal fluid leak is a possibility in both anterior and posterior approaches but can usually be managed conservatively, with a combination of primary closure, Gelfoam and/​or fibrin-​thrombin surgical glue along with instructing the patient to keep his or her head elevated. With anterior approaches, the patient’s airway and any swallowing dysfunction (e.g., dysphagia) should be evaluated postoperatively. Postoperative dysphagia can be managed conservatively in most cases. Postoperative C5 myeloradiculopathy can be a rare complication related to mobilization of the thecal sac and traction on the C5 nerve root.While more common in anterior cervical discectomies, C5 radiculopathy can be distressing to patients and can usually be managed conservatively with observation or a short course of steroids.

Oral Boards Review: Complications Pearls

1. Vertebral artery injury can occur with anterior or posterior approaches. 2. Postoperative dysphagia or C5 distribution myeloradiculopathy are rare complications and can be usually managed conservatively.

Evidence and Outcomes

Overall success rates and complication rates with anterior or posterior cervical foraminotomy and disc decompression are good in properly selected patients.1,3–​6 A  meta-​analysis of 20 studies showed very good clinical outcomes with both open foraminotomy (92.7% [95% confidence interval (CI):  88.9, 95.3]) and minimally invasive (94.9% [95% CI:  90.5, 97.4]) approaches.4 One limitation of this analysis was that long-​term follow-​up and standardized quality-​of-​life metrics varied depending on study. A  more recent analysis of 26 studies comparing open foraminotomy and microendoscopic foraminotomy showed that microsurgical approaches showed lower blood loss (by 100.1 mL), shorter operating times (by 24.9 minutes), and shorter hospital stays (by 3.0 days) compared with open approaches.7 The pooled clinical success rate was 89.7% (95% confidence interval [CI]: 87.7, 91.6) for open approaches and 92.5% (95% CI: 89.9, 95.5) for microsurgical approaches. Overall complication rates were not significantly different between microsurgery and open approaches; complications included dural tears (1.07 vs. 0.27%), infections (0.4 vs. 0.54%), root injury (0.8 vs. 1.48%), and revision surgery (2.32 vs. 3.35%). Improvement in visual analog scale for arm pain was 75% (95% CI: 66.0, 84.0) for open approaches and 87.1% (95% CI: 76.7, 97.5) for microsurgical approaches, which were not significantly different. Similarly, improvement in neurological function was not significantly different between groups, at 55.3% (95% CI: 18.6, 91.9) in open surgery and 64.9% (95% CI: 34.6, 95.2) in microsurgery. Risk of future need for surgical intervention has ranged from 1% to 24.3% at the index level or adjacent level depending on study type and follow-​up.6,8–​10 One study of 151 patients who underwent posterior cervical foraminotomy showed a reoperation rate of 9.9% (6.6% same level, 3.3% other level) over a mean time of 2.4 years8; however,

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reoperation rates increased to 18.3% and 24.3% at follow-​up greater than 2 and 10 years, respectively. Most patients (80%) who underwent reoperation had an anterior cervical discectomy and fusion. Preoperative neck pain was a significant predictor of revision surgery. Another study using propensity-​matched scoring of anterior cervical discectomy with fusion and posterior cervical foraminotomy showed reoperation rates of 4.8% and 6.4% within 2 years of index surgery, which were not significantly different.9 Another study suggested that patients older than 60 years at time of initial surgery and presence of preoperative cervical lordosis less than 10 degrees predicted later surgical correction.6 One limitation of comparing patients who underwent fusion and those who had decompression alone is the lack of randomized data supporting clinical decision-​making, making it possible for bias to select patients for one procedure or another despite possible clinical equipoise. References and Further Reading

1. Jho HD. Microsurgical anterior cervical foraminotomy for radiculopathy: A new approach to cervical disc herniation. J Neurosurg. 1996;84(2):155–​160. 2. Epstein NE. A review of laminoforaminotomy for the management of lateral and foraminal cervical disc herniations or spurs. Surg Neurol. 2002;57(4):226–​233; discussion 233–​224. 3. Johnson JP, Filler AG, McBride DQ, Batzdorf U. Anterior cervical foraminotomy for unilateral radicular disease. Spine (Phila Pa 1976). 2000;25(8):905–​909. 4. McAnany SJ, Kim JS, Overley SC, Baird EO, Anderson PA, Qureshi SA. A meta-​ analysis of cervical foraminotomy:  Open versus minimally-​invasive techniques. Spine J. 2015;15(5):849–​856. 5. Burke TG, Caputy A. Microendoscopic posterior cervical foraminotomy: A cadaveric model and clinical application for cervical radiculopathy. J Neurosurg. 2000;93(1 Suppl):126–​129. 6. Jagannathan J, Sherman JH, Szabo T, Shaffrey CI, Jane JA. The posterior cervical foraminotomy in the treatment of cervical disc/​osteophyte disease: A single-​surgeon experience with a minimum of 5  years’ clinical and radiographic follow-​up. J Neurosurg Spine. 2009;10(4):347–​356. 7. Song Z, Zhang Z, Hao J, et al. Microsurgery or open cervical foraminotomy for cervical radiculopathy? A systematic review. Int Orthop. 2016. 8. Bydon M, Mathios D, Macki M, et al. Long-​term patient outcomes after posterior cervical foraminotomy: An analysis of 151 cases. J Neurosurg Spine. 2014;21(5):727–​731. 9. Lubelski D, Healy AT, Silverstein MP, et al. Reoperation rates after anterior cervical discectomy and fusion versus posterior cervical foraminotomy: A propensity-​matched analysis. Spine J. 2015;15(6):1277–​1283. 10. Wang TY, Lubelski D, Abdullah KG, Steinmetz MP, Benzel EC, Mroz TE. Rates of anterior cervical discectomy and fusion after initial posterior cervical foraminotomy. Spine J. 2015;15(5):971–​976.

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Case Presentation

A 52-​year-​old Caucasian man presents with chronic mid back pain and bilateral lower extremity weakness. The patient notes the weakness began more than a year ago and has been progressive. He drags the left leg when walking and complains of stumbling with loss of balance. The patient also complains of shooting pain down the left leg. He denies any urinary incontinence or retention. He has no bowel dysfunction. On physical exam, the patient is unable to stand without assistance. He has a spastic gait, clonus of the left foot, weakness of all left lower extremity muscles, and decreased sensation to all modalities in his bilateral lower extremities.There is no obvious sensory level and the remainder of the physical exam was normal. Questions

1. What is the likely clinical diagnosis? 2. Where does the pathology localize anatomically? 3. What are the most appropriate imaging modalities for further evaluation?

Differential Diagnosis

The symptoms and physical signs here suggest myelopathy and more strongly fit with thoracic cord pathology than cervical cord pathology given the lack of upper extremity involvement. With suspicion of thoracic myelopathy, a broad differential diagnosis should be considered to guide the selection of the most appropriate diagnostic studies. The differential diagnosis can be divided into compressive and non-compressive thoracic pathologies.

Differential Diagnosis with Diagnostic Pearls Compressive Pathologies

1. Degenerative: a. Spondylosis is common as patients age, but is more typically seen in the more mobile cervical and lumbar regions. Nevertheless, it occurs in the thoracic spine, too, and often presents with axial mid-​back pain,

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pseudoclaudication, and unsteadiness of gait (Brown et al., 1992). The exam can range from grossly normal to hyperreflexia, presence of pathological reflexes, paraplegia, and loss of proprioception. The loss of sphincter function and pain/​temperature sensation tends to occur later in the disease course. Magnetic resonance imaging (MRI) with T2-​weighted sequences is usually sufficient to make the diagnosis (Blumenkopf, 1988). b. Disc herniations of the thoracic spine comprise less than 1% of all herniated discs and less than 4% of all herniated disc operations (Chen et al., 2012). Herniated thoracic discs (HTD) affect men more often than women, typically between the ages of 40 and 50 years. They occur more frequently in the lower thoracic spine (T8 and below) than the more rigid upper thoracic spine. Symptoms can be nonspecific, including pain, sensory changes, and weakness of the lower extremities, but, in approximately 15–​20% of cases, more specific symptoms like bowel and bladder dysfunction may occur (Brown et al., 1992). In most cases, physical exam plays a critical role in narrowing the diagnosis. Myelopathic signs involve proximal muscle weakness, mild paraparesis of the lower extremities, a wide-​based gait, positive Babinski, abnormal abdominal reflexes, and spasticity. To differentiate lower cervical from upper thoracic pathology, hyperreflexia of lower extremities with a negative Hoffman sign is indicative of thoracic involvement. Radiculopathic pain is in a band-​like distribution radiating anteriorly and inferiorly in associated dermatomes and can occasionally be reproduced with weight-​bearing, lateral bending, or palpation. In general, evaluation of sensory dermatomes is much more reliable than myotomes in thoracic pathology. MRI T2-​weighted sequences or a computed tomography (CT) myelogram are the best diagnostic imaging modalities for assessment of neurologic compression (Williams & Cherryman, 1988), and CT is best for assessment of disc calcification (Awwad et al., 1991). In some cases dynamic x-​rays and long scoliosis films can be useful for assessment of concomitant spinal instability or deformity. c. Arachnoid cysts are typically asymptomatic though rarely can be a cause of myelopathy (Santiago et al., 2004). Cysts typically occur in the thoracic spine and can be congenital or acquired. The best imaging modality is an MRI, but CT myelogram is also useful to distinguish arachnoid cysts from ventral cord herniations. Cysts demonstrate cerebrospinal fluid (CSF) signal (sometimes increased intensity on T2-​weighted sequences given less pulsation) with no enhancement or restricted diffusion. 2. Traumatic: This includes herniated discs, fractures, and ligamentous injury. The history should provide the nature of the injury and guide imaging studies. 3. Infectious: a. Epidural abscesses most commonly present in the thoracic spine, and they can present with thoracic radiculopathy or myelopathy (Fessler, 2006). Onset may be rapid or slowly progressive. Suspicion should be raised when there is severe local spine tenderness, systemic signs of infection, 110

 

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immunocompromised state, or recent invasive spinal or dental procedures. Fever, back pain, and tenderness to percussion is the classic triad but rarely do patients present with all three. MRI T1-​weighted sequences with and without gadolinium are best to evaluate the abscess, and T2-​weighted sequences are best for assessment of neurologic compression. Lab studies should include complete blood count (CBC) with differential, c-​reactive protein (CRP), erythrocyte sedimentation rate (ESR), and procalcitonin. 4. Neoplastic: a. Extradural and intradural masses: Most neoplastic spinal cord pathologies present initially with pain only (85%) that may be radicular (20%) or generalized, though myelopathy or radiculopathy can be seen later in the disease course (Vialle, 2014). The pain is typically worse at night, progressive, and unrelated to position. On exam, it can often be reproduced on palpation of the involved segments. Myelopathic signs are usually absent early in the disease, but 35% of benign and 55% of malignant tumors eventually progress to some degree of myelopathy. Diagnostic workup of the spinal pathology should include MRI with and without contrast (CT myelogram if patient is unable to undergo MRI) as well as CT without contrast if there is bone involvement. Additional workup will not be discussed in this chapter. 5. Vascular: a. Arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs) are lesions that shunt arterial blood directly to venous vasculature without resistance from capillary flow, and they typically occur in the midthoracic spine (Deshaies & Eddleman, 2011). Symptoms can be gradual with progressive myelopathy or acute due to subarachnoid or intramedullary hemorrhage. Up to 15% of patients present with Foix-​Alajouanine syndrome, which is a rapid decline in neurological function due to venous hypertension, thrombosis, and ultimately spinal cord infarction. Spinal subarachnoid hemorrhage (coup de poignard of Michon) may also occur leading to sudden-​onset back pain, rapid neurological decline, and meningismus. MRI without contrast is the modality of choice to localize the lesion and reveals signal voids on T1 and T2 sequences. Angiography is the gold standard of diagnosis and treatment planning. Noncompressive Pathologies

1. Demyelinating: a. Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that occurs most commonly in the corticospinal tracts and posterior columns (Sartor, 2002). Presentations can be confused with thoracic myelopathy due to commonality of spastic paraparesis, bladder disturbances, sensorimotor weakness, and gait ataxia. MRI with and without contrast is the imaging modality of choice and will show high 111

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signal on T2-​weighted sequences, +/​−enhancement on T1-​weighted images—​usually in the absence of cord compression. b. Transverse myelitis is an acute/​subacute motor, sensory, and autonomic spinal cord dysfunction caused by interruption of pathways in the transverse plane of the spinal cord. Demographic distribution is bimodal with peaks at 10–​19 years and 30–​39 years of age. Most causes are autoimmune, and patients often have a history of recent infection or vaccination (60%). Diagnostic criteria are specific and require bilateral (though not symmetric) sensorimotor and autonomic dysfunction with a clearly delineated sensory level deficit. MRI with gadolinium typically shows poorly delineated altered intensity in the cord with variable enhancement. Lumbar puncture demonstrates pleocytosis. 2. Vascular: a. Spinal arterial thrombosis patients present with acute onset of symptoms. Spinal artery syndromes include anterior spinal artery syndrome, posterior spinal artery syndrome, and Brown Séquard syndrome. MRI without contrast is the imaging modality to confirm the diagnosis and reveals altered T2 signal intensity in the area of the corresponding artery. Diffusion-​weighted imaging can be used but is limited by CSF flow artifact. 3. Metabolic: a. Vitamin B12 deficiency can lead to subacute combined degeneration of the spinal cord with symptoms and signs including loss of proprioception and vibration, hyperreflexia, ataxic gait, weakness, and positive Romberg sign (Botelho, 2017). CBC typically demonstrates anemia and elevated mean corpuscular volume (MCV). MRI can show symmetrically increased T2 signal in the posterolateral columns. In this case, our suspicion is highest for degenerative thoracic myelopathy, and therefore MRI without contrast or CT myelogram (if MRI is contraindicated) is most appropriate (Ghostine et al., 2011). As seen in Figure 12.1, MRI reveals a large central HTD compressing the cord. With this information, a CT without contrast is then appropriate to determine the presence and degree of disc calcification, which would influence management. We see in Figure 12.2 that the pathology is a giant central calcified disc. The term “giant” is applied when the disc occupies at least 40% of the spinal canal, and these are approached much differently than smaller noncalcified discs, which will be discussed later. Questions

1. For this case presentation, is surgical or nonsurgical management most appropriate? 2. If surgery is pursued, what is the most appropriate approach? 3. How does thoracic disc size and location and degree of calcification influence the surgical approach? 112

 

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A

B

Figure 12.1 T2 sequence of MRI of thoracic spine without contrast. Sagittal (A) and Axial (B) slices demonstrating HTD at T8-​9 level with severe spinal canal stenosis

Decision-​Making

Consensus in the literature supports surgery for severely symptomatic or disabling HTDs only, with all others requiring observation or nonsurgical intervention (Dietze et al., 1993). Specifically, patients with localized/​axial pain, radiculopathy alone, and even mild and stable myelopathy should be treated with close observation, physical therapy, or localized spinal injections/​nerve blocks for pain. For those patients requiring surgery, a variety of approaches are used depending on symptomatology, spinal level, disc size, disc location relative to the canal and to the neural elements, presence of calcification, and overall health status of the patient. Of note, single-​level laminectomy alone is not an appropriate treatment for HTDs as the literature has shown that this treatment can cause spinal cord kinking and devastating neurologic consequences, including paralysis (Chen, 2000). Appropriate surgical options can be divided based on the approach angle and working corridor to the spine and include dorsolateral/​lateral, ventrolateral, and ventral approaches. A

B

Figure 12.2  CT thoracic spine. Sagittal (A) and axial (B) slices demonstrating large calcified thoracic disc at T8-​9 level.

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Dorsolateral/​lateral approaches include transpedicular, transfacet pedicle-​ sparing, costotransversectomy, extracavitary, and parascapular approaches (Aizawa et al., 2007). The transpedicular approach is most appropriate for lateral soft discs but can also be used for other soft discs, small lateral calcified discs, and for patients with medical risk factors (Chen et al., 2012). This approach involves exposure of the facet, drilling of the caudal pedicle until flush with the body, and usually an ipsilateral hemilaminectomy to expose the lateral dura. Gentle medial retraction of the thecal sac is usually required to expose the disc space and the herniated disc. Soft extruded fragments can be mobilized away from the ventral thecal sac with microinstruments and removed with pituitary rongeurs. An annulotomy may also be required if the disc is not sequestered. Small calcified discs may require drilling to achieve adequate decompression of the thecal sac. Shorter operating time and hospital stay, less blood loss, and earlier return to activity are advantages of the transpedicular approach when compared to the more invasive approaches to be discussed later. Given the lack of visualization of the ventral dura and risks associated with thoracic cord manipulation, the transpedicular approach is limited for giant discs and central discs, particularly those with intradural extension of the HTD or those with dense calcifications. Endoscopic technique can help with visualization, though use of the endoscope can have a steep learning curve. Another disadvantage of the transpedicular approach is localized back pain, which occurs commonly. A transfacet pedicle-​sparing approach compares favorably to the transpedicular approach in terms of back pain (Chen et al., 2012). The positioning and exposure for the transfacet pedicle-​sparing approach is similar to the transpedicular approach. Instead of marking the pedicle, the facet is localized using fluoroscopy in relationship to the disc space. A partial facetectomy is then performed with preservation of the lateral facet. The rostral nerve root may be seen in the upper thoracic spine, although it is not typically exposed or seen below the upper thoracic levels. After completion of the bony drilling and cauterization of the epidural fat, the annulus should be evident. Microdiscectomy is then performed in the usual fashion.The main disadvantage is that the working corridor is smaller with less bone removal.This smaller corridor may not be an issue for certain favorable disc herniations, but the key is adequate exposure to the disc herniation with minimal spinal cord manipulation. If this cannot be achieved, then more bone removal is necessary. The costotransversectomy is a more lateral approach that provides greater access to the ventral spine at the expense of more invasiveness and surgical morbidity (Stillerman et al., 1991). The patient is typically placed in the prone position similar to the two aforementioned approaches. Skin incisions vary and include midline, paramedian, and semilunar. Depending on the skin incision used, the fascial flap will then be retracted medially or laterally to expose the posterior spinal elements and the appropriate rib and rib head. Fluoroscopy is used to confirm the appropriate rib that articulates with the disc space of interest, realizing that the correct rib level corresponds to the caudal vertebral body (e.g., T10 rib head articulates at the T9–​T10 disc space). A  laminectomy is performed in the usual fashion. The transverse process is resected with rongeurs. Approximately 8  cm of rib are partially drilled down. The intercostal nerve is then identified and traced into the neuroforamen. The caudal pedicle is then resected. The exiting nerve root is then ligated and divided near its exit from the neuroforamen. The lateral disc space is entered and disc material is removed, leaving the dorsal aspect of disc and posterior longitudinal ligament (PLL) intact. Partial corpectomies are drilled above

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and below the disc space including both endplates and subjacent bone. This maneuver creates a defect into which the disc can be delivered, away from the spinal cord.The ventral dura can be palpated with a probe or inspected with an endoscope or dental mirrors to ensure adequate decompression. The main advantages of this approach are greater visualization and access to the ventral canal compared to more dorsal procedures and less rib resection compared to more lateral approaches, with possible decreased perioperative pain. Disadvantages include less visualization when compared to more lateral and ventral approaches, which becomes a problem in the case of discs that are adherent to or transgress the dura.These cases may be better approached with a ventrolateral technique. The lateral extracavitary approach is very similar to the costotransversectomy, except that the entire rib head is removed, allowing for a more lateral approach to the ventral spinal elements and canal (Maiman et al., 1984). A midline, paramedian, or hockey-​stick incision can be used, and the surgery proceeds as described for the costotransversectomy. The rib head is disarticulated at the superior and inferior costal facets, which preserves anatomic planes and exposes the lateral disc space and the lateral wall of the rostral and caudal endplates and subjacent bodies. Care should be taken not to violate the parietal pleura during this maneuver. Partial corpectomies can then be performed as needed to deliver the disc into the corpectomy defect, away from the cord. Advantages of this approach over the other dorsal and dorsolateral approaches is that greater visualization of the ventral dura and disc space lead to less need for spinal cord manipulation and its attendant hazards. On the other hand, it is the most invasive of the dorsolateral approaches and therefore comes with greater morbidity and pain. It is less invasive than most ventral approaches though, and it avoids their known pulmonary complications. The primary disadvantage compared to ventral approaches is relatively less ventral cord visualization and relatively more cord manipulation. This is primarily an issue concerning giant calcified discs, which can be approached by lateral extracavitary or ventral techniques. If the calcified disc is fused to or transgresses the dura, which is common in this disc type, adequate decompression from dorsolateral approaches is a significant challenge. A variation of the lateral extracavitary approach in the upper thoracic spine is called the lateral parascapular extrapleural approach (Fessler et al., 1991). This approach mobilizes the rhomboid and trapezius muscles laterally toward the medial border of the scapula. The caudal fibers of the trapezius are cut and the scapula is rotated laterally to increase exposure. The remainder of the procedure is carried out similarly to the lateral extracavitary approach. Advantages of this approach are similar to the lateral extracavitary approach and also include avoidance of damage to mediastinal structures associated with a ventral approach and avoidance of recurrent laryngeal nerve injury. Disadvantages include shoulder-​and scapular-​ related problems,T1 nerve injury, Horner syndrome, and intercostal neuralgia. Ventrolateral approaches include transthoracic thoracotomy, transthoracic thoracoscopy, and retropleural thoracotomy approaches (Stillerman et al., 1998; Vollmer & Simmons, 2000). The transthoracic thoracotomy is a transpleural approach that provides an excellent anterolateral view of the thoracic spine, particularly of the anterior and middle columns (Chen et al., 2012). It is used primarily for giant calcified disc herniations, and it requires special considerations and preoperative planning not typical of posterior spinal approaches. First, it requires intubation with a double-​lumen endotracheal tube for lung deflation and manipulation. Next, patient positioning is in lateral decubitus, with the up-​side arm resting in an airplane arm rest. During positioning,

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the surgeon must consider that his working station will be at the patient’s abdominal side working toward the spine and ensure that there is adequate space. In addition, localization in the thoracic spine from ventral approaches is a particular challenge. Careful study of the patient’s spine and rib anatomy on preoperative imaging is essential. Preoperative marking of the index level with intrapedicular gold beads or other radiopaque markers can be quite helpful. A side-​on approach is usually selected ipsilateral to the side of the disc herniation. For central discs in the upper thoracic spine, a right-​side approach is typically used to avoid the heart and major vessels that can be obstructive on the left side. In the mid and lower thoracic spine, a left-​side approach is used to avoid damage to the vena cava, which is challenging to repair. A  cardiothoracic approach surgeon for the thoracotomy is recommended but not required. The rib overlying the disc space is identified, and an incision is made along the rib from the lateral edge of the paraspinal muscles to the sternocostal margin. The muscles are incised off the rib, and the level is confirmed once again with fluoroscopy. The periosteum is dissected from the rib using a Doyen elevator. The proximal and distal portions of the rib are cut and the edges are waxed. Careful attention should be paid to any defects in the endothoracic fascia or pleura, which will need to be closed primarily. Adjacent ribs can be removed as needed for exposure. Next, a rib retractor is placed, and the parietal pleura is incised in-​line with the rib. The lung is covered with a moist laparotomy pad, collapsed, and retracted ventromedially. The parietal pleura overlying the vertebral bodies is then incised and stripped from the vertebral surface with a Cobb elevator. The sympathetic chain running over the midportion of the bodies should be preserved, and injury to the segmental vessels should be avoided, though they may be ligated or clipped if needed. The radiate ligament is incised and the rib head is drilled to expose the working window. It is of supreme importance that normal dura is identified above and below the disc herniation in order to define the extent of the disc herniation and to limit cord manipulation. At a minimum, this requires drilling down the ipsilateral caudal pedicle to access the ventrolateral canal, and it may require drilling of the rostral pedicle as well. Partial corpectomies above and below the disc space are drilled down at the posterior wall, and the remaining thinned posterior wall is back fractured into this defect with curettes, thus exposing the ventral canal. The disc herniation can then be dissected away from the thecal sac with minimal manipulation. Transdural transgression or dural adhesion may require excision of dura and dural repair. Packing the dural defect with dural substitute and fibrin glue and backstopping with a sewn pleural patch are usually adequate to prevent dreaded CSF–​pleural fistulae. Typically, spinal stabilization or reconstruction at the site of the corpectomy is not required as less than 50% of the body is usually taken. The defects can be packed with the resected rib head removed earlier. To close, the lung is expanded, a chest tube placed, and the parietal pleura closed. The main advantage of this approach is the visualization of the ventral dura for resection of densely calcified or intradural giant HTDs. Disadvantages of this approach are mainly related to postoperative pain, pulmonary complications, need for a chest tube, the lack of surgeon familiarity with the anatomy from this view, and the usual need for an approach surgeon.

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Transthoracic thoracoscopy is another approach to the ventral canal with the same approach angle as the transthoracic thoracotomy (Ghostine et al., 2011). Though also transpleural, work is done through three to four small endoscopic ports, which minimizes the exposure, pain, and morbidity. It is ideally suited for small disc herniations, and it is not appropriate for giant calcified discs. Aside from less invasiveness, its other advantage compared to the thoracotomy is that an approach surgeon is not needed. Unfortunately, the main disadvantage of this method is the steep learning curve and need for costly specialized equipment. For the retropleural thoracotomy approach, the patient is positioned similar to the transthoracic thoracotomy approach. The incision is centered more posteriorly than the transthoracic approach and the proximal 4 cm of rib connected to the vertebral body is left in place. Once the endothoracic fascia is incised, the parietal pleura is bluntly dissected ventrally. The rib head is removed, and the remainder of the surgery proceeds similarly to the transthoracic approach. Advantages of this procedure include a shorter working distance to the spine as the approach is more posterior and lateral to that of the standard thoracotomy and does not traverse the entire chest cavity, avoidance of complications associated with entering the pleural space, less soft tissue dissection, easier mobilization of the diaphragm, and less need for intercostal nerve ligation. The main disadvantage is that the view of the ventral thecal sac is more tangential compared to the thoracotomy and the muscle dissection and retraction needed for exposure. Ventral approaches include transsternal and manubrial window (Chen et al., 2012). The ventral approaches are typically reserved for HTDs from T2–​T4 that cannot be approached from one of the lateral or dorsal approaches. High thoracic disc herniations are rare, and ventral approaches to the spine are associated with significant risks. Fortunately, most of these discs can be accessed using one of the aforementioned approaches. When needed, these approaches typically require an approach surgeon. Minimally invasive approaches include transpedicular, extracavitary, and transthoracic approaches. These procedures involve tubular retractor systems and endoscope (Sheikh et al., 2007). The main limitation of these procedures is the additional equipment and steep learning curve. Surgical Procedure

For the patient described in this case presentation, an open dorsolateral extracavitary approach was selected to address the giant central calcified disc herniation at T8–​T9. More specifically, a T8–​T9 costotransversectomy, T8–​T9 partial corpectomies, and T7–​T10 laminectomies were performed.The patient underwent general endotracheal anaesthesia and Foley catheter placement and was positioned prone on an open Jackson table. MEPs, SSEPs, and electromyography (EMG) were used during the procedure, and the mean arterial blood pressure was sustained at 85 mm Hg. A midline incision spanning T7 to T10 was marked using the C-​arm. A standard subperiosteal takedown of the paraspinal muscles was performed exposing the T7 to T10 laminae. The rib head attachments were exposed bilaterally for anatomical orientation. Pedicle screws were then placed at T7 and T10 in the standard fashion using a high-​ speed drill, a pedicle finder, a ball-​tipped probe, a tap, and finally the screws measuring

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5.5 × 45 mm at T7 and T10 bilaterally.Anteroposterior (AP) and lateral fluoroscopic shots of the fusion were obtained demonstrating correct positioning of the instrumentation. Laminectomies were performed from T7–​T10 bilaterally. This was extended laterally to the left, exposing the T8 and T9 pedicles.The left T8 nerve root was identified, ligated with 4-​0 Nurolon, injected with 1 cc of lidocaine and then sharply transected. The ligature was then used for gentle retraction and rotation of the thecal sac. The T8 and T9 rib heads were then exposed laterally and transected with Leksell rongeurs, exposing the thoracic pleura at this level. The T8 pedicle was then partially removed by drilling it with a matchstick burr, and the T9 pedicle was removed in its entirety. At this point, the microscope was brought into the field for microdissection. Gentle retraction was then applied to the thoracic cord, and its lateral ventral aspect was exposed. The bone window was further expanded by drilling the T8 and T9 vertebral bodies and removing the intervertebral disc at T8–​T9. This was a partial corpectomy yielding one-​third removal of each vertebral body and creating an anterior bone window into which the osteophyte could be collapsed. The osteophyte was then carefully dissected away from the dura using microsurgical technique and gradually pushed inferiorly and laterally with curettes. The mass showed dense calcification and ossification and was densely adherent to the dura. At this point in the case, there was significant improvement in bilateral lower extremity SSEPs on neuromonitoring. The remainder of the dissection was carried out, and the calcified disc was removed in its entirety. Posterolateral instrumentation was then completed with placement of pedicle screws on the right at T8 and T9 followed by contouring and placement of titanium rods, screw caps, and crosslink (Figure 12.3). Thorough irrigation, decortication, laying down bone substitute and graft, and drain placement were then performed. Multilayer wound closure was completed, and the patient was transferred to PACU.

A

B

Figure 12.3  Sagittal (A) and axial (B) images of post-​operative CT of thoracic spine status post T7-​T10 posterior instrumentation and T8-​9 costotransversectomy. Pedicle screws were placed from T7-​10 on the right. No screws were placed at T8 or T9 on the left where the costotransversectomy was performed. The calcified HTD has been removed in its entirety and troughs (partial corpectomies) were performed at the caudal posterior edge of T8 and rostral posterior edge of T9 to assist in ventral depression of the HTD away from the dura.

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The most important decision regarding this case is which technique is best to access a giant central calcified disc. As mentioned earlier, giant central calcified discs are best approached by lateral extracavitary approaches, as done here, or by thoracotomy/​ retropleural thoracotomy. There are pros and cons to each, and, with equipoise, the decision should be based on surgeon comfort and experience.

Oral Boards Review: Management Pearls

1. There are multiple reasonable approaches to address thoracic disc herniations, and the selection is driven largely by the morphology and location of the disc with respect to the canal and the neural elements. 2. The overarching surgical principle in all cases is to perform the least invasive procedure that allows adequate visualization and, most importantly, requires the least degree of spinal cord manipulation.

Aftercare

Postoperative care for surgery on an HTD depends on the technique used, patient’s comorbidities, intraoperative complications, and blood loss. Typically, patients can be monitored on a floor or step-​down unit. The exception for this are those with intraoperative complications such as those with significant decreases in the neuromonitoring parameters, those patients with significant blood loss, patients with a chest tube, and, last, those with significant cardiac or pulmonary comorbidities. Complications and Management

Benzel compared a review of 13 contemporary series of HTD surgeries with Stillerman et  al.’s series and found the following (Chen et al., 2012; McCormick et al., 2000). Stillerman et al. (1998) reported a major complication rate of 3.6% while the review noted a rate of 6.1%. No deaths were reported in the review group. Minor complications were found to be 11% by Stillerman et al. and 8.7% in the review group, with a total complication rate of 14.6% and 14.8%, respectively.There were no significant difference when comparing the series and the review group. As reported by Stillerman et al., the most common complications were superficial wound infection and pneumonia. Loss of spinal integrity and new transient and new permanent weakness each occurred at a rate of less than 2%. Evidence and Outcomes

Based on a study by Stillerman et al. (1998), the authors created a management algorithm for HTD that divides patients into three groups based on symptoms: localized/​ axial pain, radiculopathy, and myelopathy.Treatment arms exist for each group, which are further divided based on medical risks, location of the HTD, and degree of calcification. This can be seen in Figure 12.4. Advances in the management of HTD are continually being made with less invasive approaches and with the emergence of computer navigation and robotic technology that are allowing improved visualization and navigation.

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Myelopathy

Localized/T-L spinal pain Improving

Radiculopathy

Static

No functional impairment Pain tolerable

Progressive deterioration

Severe myelopathy and pain

Conservative treatment

Conservative treatment

Intractable symptoms Consider surgery

Low medical risk

High medical risk

Densely calcified centrolateral disc

Static myelopathy

All except densely calcified centrolateral disc

Progressive deterioration

Centrolateral disc

Lateral disc

Soft

Mildly calcified

Densely calcified

• Dorsolateral (thoracoscopy?)

• Dorsolateral • Lateral (anterolateral) • Anterior

• Lateral • Ventrolateral

Conservative treatment

Refractory symptoms

• Thorascopic (thoracotomy) • Retropleural

• Dorsolateral

• Dorsolateral

Figure 12.4  Management algorithm for treating symptomatic HTD’s. Printed with permission from Stillerman CB.

References

Aizawa T, Sato T, Sasaki H, et al.: Results of surgical treatment for thoracic myelopathy: minimum 2-​year follow-​up study in 132 patients. J Neurosurg Spine. 7:13–​20 2007. Awwad EE, Martin DS, Smith KR, et  al.:  Asymptomatic versus symptomatic herniated thoracic discs:  their frequency and characteristics as detected by computed tomography after myelography. Neurosurgery. 28:180–​186 1991. Blumenkopf B: Thoracic intervertebral disc herniations: Diagnostic value of magnetic resonance imaging. Neurosurgery. 23:36–​40 1988. Botelho R, De Oliveira M, Kuntz C: “Chapter 280: Differential Diagnosis of Spinal Disease.” Neurological Surgery, edited by Youmans and Winn, 7th ed., Elsevier/Sauders, 2017, pp. 2322–2336.

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Brown CW, Deffer PA, Akmakjian J, et al.: The natural history of thoracic disc herniation. Spine (Phila Pa 1976). 17:S97–​S102 1992. Chen TC:  Surgical outcome for thoracic disc surgery in the postlaminectomy era. Neurosurg Focus. 9 (4):e12 2000. Chen,Thomas C, et al. “Chapter 77: Thoracic Discectomy.” Spine Surgery: Techniques, Complication Avoidance, and Management, edited by Edward C. Benzel and Todd B. Francis, 3rd ed., Elsevier/​Saunders, 2012, pp. 741–​756. Deshaies E, Eddleman C: “Chapter 20: Spinal Arteriovenous Malformations.” Handbook of Neuroendovascular Surgery, edited by A Boulos, 1st ed.,Thieme, 2011. doi:10.1055/b-002-85450. Dietze DD, Fessler RG: Thoracic disc herniations. Neurosurg Clin N Am. 4:75–​90 1993. Fessler R: “Chapter 61: Thoracic Epidural Abscess.” Atlas of Neurosurgical Techniques, edited by L Sekhar, 1st ed., Thieme, 2006. doi:10.1055/b-006-149694. Fessler RG, Dietze DD, MacMillan M, et al.: Lateral parascapular extrapleural approach to the upper thoracic spine. J Neurosurg. 75:349–​355 1991. Ghostine, Samer, et  al. “Chapter  283:  Treatment of Thoracic Disk Herniation.” Youmans Neurological Surgery, edited by Julian R. Youmans and H. Richard Winn, 6th ed., vol. 3, Elsevier/​Saunders,  2011. Maiman DJ, Larson SJ, Luck E, El-​Ghatit A: Lateral extracavitary approach to the spine for thoracic disc herniation: report of 23 cases. Neurosurgery. 14:178–​182 1984. McCormick WE, Will SF, Benzel EC:  Surgery for thoracic disc disease. Complication avoidance: overview and management. Neurosurg Focus. 9(4):13 2000. Santiago P, Fine AD, Shafron D, et al.: Benign extradural lesions of the dorsal spine. Winn RH Youmans Neurological Surgery. 5th ed., 2004. Saunders Philadelphia 4491–​4506. Sartor K, ed. “Demyelinating and Degenerative Diseases of the Spinal Cord.” Diagnostic and Interventional Neuroradiology, 1st ed., Thieme, 2002. doi:10.1055/b-002-52047. Sheikh H, Samartizis D, Perez-​Cruet MJ: Techniques for the operative management of thoracic disc herniation:  minimally invasive thoracic microdiscectomy. Orthop Clin North Am.38 (3):351–​361  2007. Stillerman CB, Chen TC, Couldwell WT, et  al.:  Surgical experience in the operative management of 82 symptomatic herniated thoracic discs and review of the literature. J Neurosurg. 88:623–​633 1998. Stillerman CB,Weiss MH: Management of thoracic disc disease. Clin Neurosurg. 38:325–​352  1991. Vialle, L, ed. “Evaluation and Decision Making.” AOSpine Masters Series,Volume 2: Primary Spinal Tumors, 1st ed., Thieme, 2014. doi:10.1055/b-002-98011. Vollmer DG, Simmons NE:  Transthoracic approaches to thoracic disc herniations. Neurosurg Focus. 9 (4):E8 2000. Williams MP, Cherryman GR:  Thoracic disk herniation:  MR imaging. Radiology. 167:874–​875  1988.

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Thoracolumbar Burst Fractures Omaditya Khanna, Geoffrey P. Stricsek, and James S. Harrop

13

Case Presentation

A 32-​year-​old man presents to the emergency room after sustaining a fall from four stories while attempting to escape a building during a fire.The patient reports he landed on his feet and then fell backward onto his buttocks. He states that he hit his head, but denies any loss of consciousness. Emergency medical services (EMS) immobilizes the patient using a rigid cervical collar and backboard in the field prior to transport to the emergency room. Questions

1. What is involved in the initial evaluation of patients presenting with acute trauma? 2. What imaging studies are indicated? 3. What are the various classification systems of thoracolumbar burst fractures?

Assessment and Planning

The initial evaluation of the trauma patient is conducted using the advanced trauma life support (ATLS) ABCDE framework (Airway, Breathing, Circulation, Deficit, Exposure). This provides a standardized pathway for identifying injuries and establishing treatment priorities to guide resuscitation efforts. All suspected spinal trauma patients should remain in a rigid cervical collar until a thorough neurological evaluation and appropriate imaging can be performed, even in the absence of any overt reported focal neurologic deficits. The primary survey for the patient identifies the following:  despite having facial abrasions and a gross deformity of his nose, his airway and breathing are intact, evidenced by fluent, nonlabored conversation and unremarkable chest auscultation. His cardiovascular system is also stable with a blood pressure of 112/​82 mm Hg and heart rate of 88 bpm. On neurological exam, the patient is found to have full strength in his bilateral upper and lower extremities; he notes ankle pain while assessing dorsiflexion and plantar-​flexion, but there is no weakness. He describes numbness and tingling spreading into the right leg, but sensation to light touch is intact and symmetric between all extremities. Biceps, Achilles, and patellar reflexes are all 1+ and symmetric; there is no clonus or Hoffman sign; he has a negative Babinski bilaterally. There is tenderness to palpation over his low thoracic and upper lumbar spine. His rectal examination reveals normal tone, sensation, and volitional push.

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Following completion of the primary survey, the patient had imaging obtained including a computed tomography (CT) scan of the brain and cervical, thoracic, and lumbar spine, given that he hit his head during the fall and also had severe back pain. CT imaging of the thoracic and lumbar spine was significant for a T12 spinous process fracture and a sagittally oriented fracture through the L1 vertebral body with fracture of the L1 lamina, as well as a burst fracture of the L2 vertebral body with retropulsion of fragments into the spinal canal and an L2 laminar fracture. Magnetic resonance imaging (MRI) was obtained after CT evidence of lumbar fracture. MRI demonstrated compression of the thecal sac and the conus medullaris at L1–​L2 secondary to the bony retropulsion; there was associated epidural blood surrounding the thecal sac. MRI also showed a signal abnormality at T12–​L1 extending from the intradural to the extradural space, which could represent dural laceration (Figure 13.1). CT scans of the brain and cervical spine were unremarkable.

Figure 13.1  Sagittal (A) and axial (B) computed tomography (CT) scans demonstrate a burst fracture of the L2 vertebral body with retropulsion of bony fragments into the spinal canal. T2-​weighted magnetic resonance image (MRI) (C) demonstrates compression of the thecal sac and the conus medullaris at L1–​L2 and disruption of the posterior ligamentous complex secondary to the bony retropulsion, associated with epidural blood surrounding the thecal sac. The patient underwent posterior pedicle screw fusion from T11 through L4 (C) on hospital day 1.

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Fractures in the thoracic and lumbar spine are more common than in the cervical spine. The majority of thoracolumbar spine fractures occur in the transition zone between the lower thoracic and upper lumbar spine (between T11 and L2), accounting for approximately 20% of all spine fractures. This region is particularly susceptible to injury owing to the fact that it is a junction between the fixed, kyphotic thoracic spine and the more mobile lordotic lumbar spine, causing a concentration of stress forces upon the ventral thoracolumbar vertebral column. The majority of thoracolumbar fractures are caused by high-​energy mechanisms, which could result in concomitant injuries to other nearby organ and soft tissues. Ten to twenty percent of all thoracolumbar spine fractures are burst fractures. Burst fractures are typically a result of an axial-​loading mechanism, such as from jumping or a fall from height. Axial load injuries can also result in both thoracolumbar and calcaneal fractures. On imaging, burst fractures are characterized by fracture of the vertebral body with retropulsion of fractured vertebral body fragments into the spinal canal. The displacement of bony fragments into the vertebral canal can cause significant neurologic compromise. As such, it is imperative to promptly recognize these injuries in order to guide further management. There are several systems in place to evaluate thoracolumbar fracture:  the Denis three-​column concept, the Arbeitsgemeinschaft für Osteosynthesefragen (AO) Spine thoracolumbar classification, and the Thoracolumbar Injury Classification and Severity (TLICS) Scale. Denis, in 1984, proposed a three-​column classification scheme to describe the thoracolumbar spine. The first column extends from the anterior longitudinal ligament (ALL) to the midpoint of the vertebral body; the second column is from the midpoint of the vertebral body to the posterior longitudinal ligament (PLL); and the third column spreads from the PLL through the posterior elements, including the pedicles and facet joints. The AO Spine thoracolumbar classification system, proposed in 2013, would assign the patient an A4 fracture of the L1 and L2 vertebral bodies, since both levels have disruption of the superior and inferior endplates, as well as the posterior wall of the vertebral body. Additionally, edema in the L1–​L2 interspinous ligament and the T12 spinous process fracture suggests disruption of the posterior tension band, which would further classify this injury as B2 with an N0 modifier given that he was neurologically intact. In 2005, the Spine Trauma Study Group proposed a novel grading criteria for evaluation of thoracolumbar fractures: the Thoracolumbar Injury Classification and Severity Score (TLICS). Injuries are defined according to insult morphology (compression: 1 point; burst: 2 points; translational/​rotational: 3 points; distraction: 4 points), patient’s neurologic status (intact: 0 points; nerve root injury: 2 points; cord or conus medullaris incomplete injury: 2 points; cord or conus medullaris complete injury: 3 points; cauda equina syndrome: 3 points), and integrity of the posterior ligamentous complex (intact: 0 points; injury suspected/​indeterminate: 2 points; injured: 3 points). Under the TLICS classification scheme, a summation of point values from the categories of 3 or less can be treated with nonoperative management, scores of 4 may be treated either operatively or nonoperatively, and a cumulative score of 5 or above usually warrants surgical decompression and stabilization. This patient has a TLICS score of 5 (2 points for burst morphology and 3 points for posterior ligamentous complex injury).

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Oral Boards Review: Diagnostic Pearls

1. The initial imaging evaluation of patients with suspected spine fractures can include anteroposterior (AP) and lateral x-​rays. Plain films are useful in assessing for loss of vertebral body height, pedicle fractures, and malalignment of the spine. 2. CT imaging provides a more comprehensive evaluation of bony anatomy by providing coronal, sagittal, and axial plane reformatted images. In the presence of a known vertebral body fracture, the entire spinal axis should be imaged due to the high prevalence (5–​20%) of noncontiguous fractures. 3. MRI aids in the physician’s ability to visualize the spinous ligaments, surrounding soft tissues, intervertebral discs, and the underlying neural elements. MRI is especially important for evaluation of thoracolumbar pathology because of the variable level of the conus medullaris. 4. The AOSpine Thoracolumbar Classification System: Type A (Compression injuries) A0: Minor, nonstructural fractures A1: Wedge compression A2: Split fracture A3: Incomplete burst A4: Complete burst 5. TLICSS: a. Morphology: i. Compression (1 point) ii. Burst (2 points) iii. Translational/​rotational (3 points) iv. Distraction (4 points) b. Neurological status: i. Intact (0 points) ii. Nerve root or cord/​conus (complete) (2 points) iii. Cord/​conus (incomplete) or cauda equina (3 points) c. Posterior ligamentous complex: i. Intact (0 points) ii. Suspected injury/​indeterminate (2 points) iii. Injured (3 points) 6. The summation of the preceding categories helps guide management: a. Less than 4: Usually treated nonoperatively b. Equal to 4: May be treated operatively or nonoperatively c. More than 4: Usually considered for operative management Decision-​Making

Management of thoracolumbar burst fractures is based on neurological and structural considerations. Unless there are severe medical comorbidities precluding surgery, any patient with a neurological deficit in the presence of a burst fracture should be considered

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to undergo surgery for decompression of neurological elements. For patients without neurological deficit, mechanical stability of the spine should be evaluated to determine the need for surgical intervention. According to both the Denis’s classification and TLICS criteria, the patient’s injuries should be treated surgically if unstable. While some surgeons advocate intervention when burst fractures cause greater than 50% central canal narrowing, neurological recovery from burst fractures is not predicted by the amount of canal narrowing, and this should not be used as an indication for surgery in isolation. Surgical approaches for the treatment of thoracolumbar burst fractures include anterior, posterior, and lateral. For each approach, further options are available, including direct versus indirect compression, open versus percutaneous instrumentation, and short-​versus long-​segment constructs. A  review of prospectively collected data from 733 patients receiving care at German and Austrian hospitals suggests that the combined anterior-​posterior approach is the most commonly used at the thoracolumbar junction (47.3%), followed closely by a posterior alone (47%), and, infrequently, a stand-​alone anterior approach (5.7%). The choice of whether to pursue an anterior versus posterior approach depends on many factors, including the site of the pathology, degree of mechanical instability and kyphosis, the presence of other concomitant injuries incurred, and, last, surgeon preference. An anterior approach allows the surgeon to both effectively decompress the neural elements via removal retropulsed bone fragments and simultaneously reconstruct anterior and middle column support in patients with significant kyphotic deformity. However, adequate exposure of impacted vertebral bodies can be a challenge, particularly in the posttrauma setting and requires an experienced surgeon. In addition, in the acute setting, there can be a tremendous amount of bleeding from anterior epidural veins. From a posterior approach, decompression of the spinal cord is achieved by laminectomy or by the unilateral removal of the pedicle and facet joints, which allows reduction of fracture fragments. Dorsal decompression via laminectomy (without reduction or stabilization) alone has been shown to be an ineffective treatment strategy. Regardless of whether decompression is achieved via an anterior or posterior approach, segmental instrumentation is recommended for treatment of mechanical instability. The load-​sharing classification developed by McCormack can be used to help decide the number of levels requiring instrumentation and fusion. In the thoracolumbar junction, fractures tend to be more kyphogenic, which increases the corrective bending strain placed upon each pedicle screw. When looking at load-​ sharing, three characteristics are assessed, each on a three-​point scale: vertebral body comminution, fragment apposition, and the amount of kyphotic deformity correction. Fractures with load-​sharing classification (LSC) scores of 6 or less have been successfully treated via short-​segment instrumented fusion at two levels above and two levels below. LSC scores of 7 or more suggest poor load transfer through the vertebral body and often necessitates anterior instrumentation for restoration of alignment. In neurologically intact patients who do not have overt mechanical instability, nonoperative treatment is a viable management option. Tezer et  al. suggested that nonoperative treatment is appropriate when the PLL complex is intact, evidenced by

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anterior vertebral body height of greater than 50% of the posterior height and kyphotic angulation of less than 30 degrees. Questions

1. What are the treatment options for patients with thoracolumbar burst fractures? 2. What are the surgical indications for thoracolumbar burst fractures? 3. What are the various factors to take into consideration when determining whether to pursue an anterior versus posterior versus combined/​staged anterior-​posterior surgical approach (see Table 13.1)?

Surgical Procedure

This patient underwent a posterior thoracolumbar decompression and fusion for the treatment of his L1 and L2 burst fractures. Following induction of general anesthesia, a prepositioning baseline neurophysiological recording was obtained; the patient had monitorable signals, as was expected given his intact neurological exam. Iliac crest and chest pressure points were padded, and he was positioned prone on an open Jackson frame with his hips extended. Postpositioning neurophysiological monitoring confirmed there was no change in signals following the flip from supine to prone. Exposure with subperiosteal dissection was performed to expose from T11 to L4; the patient had a LSC score of 6 and it was decided to go two levels up and two levels down from his index levels. Pedicle screws were placed at T11, T12, L1, L3, and L4; the pedicles at L2 were not cannulated due to the extensive nature of the fracture. Laminectomies were performed at L1 and L2. A rod and caps were placed into the left-​sided instrumentation, and then the right L2 pedicle was removed so that fracture fragments from the L2 vertebral body could be tamped forward out of the spinal canal. The right-​sided rod was placed and secured with caps; AP and lateral x-​rays were obtained to confirm hardware trajectories and alignment; a surgical drain was placed, and the incision was subsequently closed. Aftercare

A postoperative neurological evaluation should be performed shortly after the patient returns to the recovery room. If the patient develops a delayed postoperative neurological deficit, CT or MRI is indicated to evaluate for epidural or subdural hematomas, nerve entrapment, or failure of instrumentation. Intermittent pneumatic compression Table 13.1. Indications for surgical intervention in patients presenting with thoracolumbar burst fractures

1. Anterior vertebral body height 20 degrees 3. Incomplete/​progressive neurologic injury 4. Spinal canal narrowing >50% (*relative indication) 5. Multiple noncontiguous spinal fractures

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devices should be continued in the immediate postoperative period, prophylactic anticoagulation should be started on postoperative day 1, and perioperative antibiosis is administered for 24 hours. Adequate pain control is also a point of emphasis in order to facilitate early mobilization and disposition planning. In both patients who have been managed conservatively or treated surgically, serial evaluation with AP and lateral flexion-​extension x-​rays for 4–​12 months is indicated to assess for any progressive kyphosis or other deformity. In patients who develop progressive neurologic deficits or who develop mechanical instability, surgical intervention may be necessary. Complications and Management

Possible complications in the thoracolumbar burst patient are similar to those in the elective patient population. Postoperative neurological deficit should be thoroughly investigated for reversible causes, which includes CT imaging to evaluate instrumentation placement and spinal alignment as well as MRI to assess spinal canal integrity and epidural hematoma formation. The surgeon should be prepared for the need to repair a traumatic dural laceration in the thoracolumbar burst patient including possible lumbar drain placement. Suspicion for cerebrospinal fluid leak may also guide preoperative decision making: if there is high clinical concern in the setting of a thoracic or high lumbar burst fracture, it may be advantageous to avoid a lateral approach given the need for chest tube placement. Medical complications can also disrupt the recovery in patients with thoracolumbar burst fractures. Deep venous thrombosis (DVT) is also a concern in this population given their decreased mobility secondary to pain, neurological deficit, or bed rest for dural healing. Vigilant prophylaxis is the best defense against DVT, but, in the patient where is arises, inferior vena cava filter should be considered to reduce the risk of pulmonary embolism if therapeutic anticoagulation is not a management option. Prolonged intubation and reduced ambulation also increase the risk of pneumonia; patients should have regular chest physiotherapy, and clinicians should have a low threshold for chest radiography if symptoms develop.

Oral Boards Review: Complications Pearls

1. Patients who are treated via conservative measures (brace, pain control, physical therapy) should be followed every few months in order to assess for any developing kyphosis or other deformity. 2. In patients who present neurologically intact and are treated via conservative measures, the rate of neurological worsening lies between 0% and 20%. 3. In patients who develop progressive neurologic deficits, mechanical instability, or worsening intractable back pain, prompt surgical intervention is necessary.

Evidence and Outcomes

The development of novel instrumentation techniques has improved the efficacy of surgical treatment of thoracolumbar burst fractures. However, there is no universal

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agreement in regards to the timing of surgery, extent of stabilization, or the preferred surgical approach that should be employed for the correction of deformity or decompression of neural elements. In a study by Mumford et al. evaluating the efficacy of nonoperative management of thoracolumbar burst fractures, 41 neurologically intact patients treated conservatively were followed for more than 2 years. The study found that 49% of patients reported excellent outcomes relative to pain and function at 2-​year follow-​up. Only one patient developed neurologic deterioration that prompted surgical intervention. Several other studies have corroborated the role of nonoperative treatment in neurologically intact patients. The TLICS score was proposed to aid surgeons in the decision-​making process for treating thoracolumbar burst fractures. Since its development, several studies have evaluated the TLICS’s reliability and validity in assessing and guiding treatment of thoracolumbar injuries. A study of 71 cases of thoracolumbar fractures graded independently by five separate spine surgeons found a 97% rate of agreement on the management. Other studies have validated the intraobserver reliability in grading of thoracolumbar fractures, which suggests it is a grading scale that can be readily taught and utilized to guide treatment. However, there have been scant prospective randomized studies that have investigated outcomes in surgically versus nonsurgically treated patients who present neurologically intact. In a study by Wood et al., 47 neurologically intact patients with thoracolumbar burst fractures were randomized into surgical versus nonsurgical treatment; operative treatment provided no major long-​term advantage compared with nonoperative treatment and was associated with a higher risk of complications. Several studies have corroborated the use of short-​segment posterior fixation for the treatment of thoracolumbar burst fractures. Parker et  al. showed that fractures with LSC scores of 6 or less can be treated via instrumented fusion with four screws at the level above and below, allowing sufficient mechanical stability in the interim while the bony fracture heals. In a study by Pellise et al., 86 patients with a mean LSC score of 6.3 who were treated with a six-​screw construct (one level above, one below, and one at the level of the fracture) were followed for more than 2  years postoperatively. The study revealed that short-​segment posterior fixation, including instrumentation insertion at the level of the fracture, was a viable treatment option that adequately restored alignment; none of the patients required repeat surgical intervention for postoperative complications. In a study by Park et al. in 2016, there was no difference in the long-​term outcomes in 45 patients with LSC scores of 7 or 8 treated with posterior short-​segment fixation at two versus three levels, thereby possibly obviating the need for anterior reconstruction. References and Further Reading

Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine. 1983;8(8):817–​831. Kaneda K, Abumi K, Jujiya M. Burst fractures with neurologic deficits of the thoracolumbar-​ lumbar spine. Results of anterior decompression and stabilization with anterior instrumentation. Spine. 1984;9:788–​795.

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Knight RQ, Stornelli DP, Chan DP, Devanny JR, Jackson KV. Comparison of operative versus nonoperative treatment of lumbar burst fractures. Clin Orthop. 1993;293:112–​121. Muller U, Berlemann U, Sledge J et al. Treatment of thoracolumbar burst fractures without neurological deficits by indirect reduction and posterior instrumentation: Bisegmental stabilization with monosegmental fusion. Eur Spine J. 1999;8:284–​289. Parker J, Lane JR, Karaikovic EE, Gaines RW. Successful short-​segment instrumentation and fusion for thoracolumbar spine fractures. A  consecutive 4 1⁄2  years series. Spine. 2000;25:1157–​1169. Patel AA, Dailey A, Brodke DS, et al. Spine trauma study group. Thoracolumbar spine trauma classification:  The thoracolumbar injury classification and severity score system and case examples. J Neurosurg Spine. 2009;10(3):201–​206. Reinhold M, Knop C, Beisse R, et al. Operative treatment of 733 patients with acute thoracolumbar spinal injuries: Comprehensive results from the second, prospective, internet-​based multicenter study of the Spine Study Group of the German Association of Trauma Surgery. Eur Spine J. 2010;19:1657–​1676. Verlaan et  al. Surgical treatment of traumatic fractures of the thoracic and lumbar spine: A systematic review of the literature on techniques, complications and outcome. Spine. 2004;29(7). Wood K, Buttermann G, Mehbod A, et al. Operative compared with nonoperative treatment of a thoracolumbar burst fracture without neurological deficit. A prospective, randomized study. J Bone Joint Surg Am. 2003;85A(5):773–​781.

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Thoracic Cord Compression Extradural Tumor Tej D. Azad, Anand Veeravagu, John K. Ratliff, and Atman Desai

14 Case Presentation

A 69-​ year-​ old man presents to an outside facility with concerns of an enlarging pigmented lesion on the bottom of his right foot. Punch biopsy reveals melanoma in situ, which is excised. Three years later, the patient develops new-​onset upper back pain and is referred to neurosurgery. The pain is reported as worst in the morning and relieved when in the supine position. The patient reports 7/​10 pain that localizes to the right shoulder blade, does not radiate, and worsens with upper arm movement. The patient denies any urinary incontinence, numbness, tingling, or weakness of the lower extremities. The patient has not fallen but endorses unsteady gait. No upper or lower extremity deficits in strength were elicited. Pin prick and light touch are normal in all extremities. Reflexes are 2+ and symmetric bilaterally. No clonus is elicited, and a negative Hoffman sign is observed. Questions

1. What is the most likely diagnosis? 2. What imaging modalities should be utilized? 3. What is the most likely etiology of the patient’s pain?

Assessment and Planning

The differential diagnosis for this presentation, shoulder pain with possible radiculopathy and mild myelopathy, includes musculoskeletal pathologies such as muscle spasm, rotator cuff injury, disc herniation, and spinal stenosis. Lesions such as metastases, primary spinal neoplasms, and vascular malformations need to be considered as well. Primary malignant spinal tumors include chondrosarcoma, chordoma, osteosarcoma, and Ewing’s sarcoma, while primary benign spinal neoplasms include osteoid osteoma, osteoblastoma, aneurysmal bone cyst, hemangioma, meningioma, schwannoma, and neurofibroma. Treatment is surgical, except for Ewing’s sarcoma, which is often chemosensitive. However, 90% of extradural spinal tumors are metastatic, and primary tumors necessitate a unique set of management considerations; therefore, this discussion will focus on metastatic neoplasms. Given the patient’s oncologic history, the neurosurgeon maintains a high degree of suspicion for metastatic melanoma. Spinal metastases occur in 1 out of 5 cancer patients and 5–​10% of patients with cancer develop spinal cord compression.1 Breast, prostate, and 133

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lung cancer are the most common primary tumors that are metastatic to the spine.2 Pain is the most common presentation of symptomatic spinal metastasis, reported in 83–​95% of patients,3 followed by motor dysfunction, sensory complaints, and urinary incontinence.4 Spinal instability pain in the thoracic spine can be elicited with extension. Upon extension, the patient will likely report constant pain while unstable kyphosis is straightened.

Oral Boards Review: Diagnostic Pearls

1. A detailed history and neurological examination are essential to understanding the clinical presentation of a patient with a spinal metastasis. 2. Neurological symptoms such as weakness, numbness, paraesthesias, imbalance, and urinary incontinence are suggestive of symptomatic spinal cord compression, as are objective motor and sensory deficits and abnormal reflexes and gait on clinical examination. 3. Pain worsened with movement and improved with recumbency is suggestive of a mechanical pain generator. This may be in the form of a compromised intervertebral disc, facet complex, or progressive spinal deformity induced by a pathological lesion. 4. A known history of a radiation-​sensitive tumor such as myeloma or small cell lung carcinoma may obviate the need for surgery. 5. Imaging should ideally include magnetic resonance imaging (MRI) predominantly for evaluation of the tumor and its relationship to the spinal cord and nerve roots. Computed tomography (CT) scan may give additional information including evaluation of bony lysis and involvement of anterior and posterior bony elements. Bony lysis, junctional location, vertebral body loss of height, and kyphotic deformity are all suggestive of spinal instability. MRI is the gold standard diagnostic imaging modality for assessment of a thoracic epidural tumor with spinal cord compression.5 The primary advantage of MRI, compared to other imaging modalities, is that MRI is noninvasive and provides precise spatial and contrast resolution, imperative for surgical planning. Moreover, MRI demonstrates significant utility in elucidating soft tissue structures, tumor margins, and neural elements. First, sagittal images of the entire spinal axis should be obtained to identify areas of metastatic involvement. Kyphotic pathology involving regions of transition, specifically the cervicothoracic and thoracolumbar segments, may function as a lever arm and therefore may induce more significant global sagittal malalignment. More focused studies, including alternative views, can then be obtained for further evaluation. Sagittal T2-​and T1-​weighted images, with and without intravenous contrast, are obtained. Axial images, both T2-​and T1-​weighted, can then be obtained to extend the preliminary assessment and provide details about adjacent structures and landmarks. A useful adjunct to MRI, CT details bony anatomy and extent of bony tumor involvement.This modality can be valuable distinguishing between cord compression secondary to tumor extension into the spinal canal and bony canal compromise.When used in combination with myelography, CT elucidates the bony anatomy and may provide significant insight into spinal reconstruction planning. A combination of MRI for tumor

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Figure 14.1  Preoperative sagittal T1 and postoperative T2 magnetic resonance images (A) reveal T3 spinal cord compression.

and soft tissue evaluation and CT for defining the osseous anatomy is the most effective method of assessing patients with extradural tumor and thoracic cord compression. In the present case, MRI demonstrated a destructive lesion of the T3 vertebral body and right pedicle, causing significant deformity and spinal compression, with no facet involvement (Figure 14.1). Questions

1. How do these clinical and radiological findings influence surgical planning? 2. What is the most appropriate timing for intervention in this patient? 3. How does the likely diagnosis and pathology of metastatic melanoma influence surgical planning?

Decision-​Making

The objectives of treatment in a patient with extradural thoracic tumor include recovery or preservation of neurologic function, pain relief, local oncologic control, maintenance of mechanical stability, and quality of life.6 Mainstay therapeutic options include corticosteroids, radiation therapy, and surgery. Corticosteroids may prevent short-​term neurological deterioration, mediate edema, and provide analgesia; however, this line of treatment is not definitive. A valuable decision-​making tool in approaching such a patient is the neurologic, oncologic, mechanical, and systemic (NOMS) paradigm. Consideration of the extent of epidural extension (neurologic) in conjunction with tumor sensitivity to

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Table 14.1. Epidural spinal cord compression scale.7 Grade

Definition

0 1a 1b 1c

Bone-​only disease Epidural impingement, without deformation of the thecal sac Deformation of the thecal sac, without spinal cord abutment Deformation of the thecal sac with spinal cord abutment, but without cord compression Spinal cord compression, but with CSF visible around the cord Spinal cord compression, no CSF visible around the cord.

2 3

radiation (oncologic) enables determination of a patient-​specific treatment algorithm. Stability of the spine (mechanical) and overall disease burden and health status considerations (systemic) further help determine the need and the feasibility of surgical intervention.1 The chief neurologic considerations are the degree of spinal canal compromise, evaluated through imaging and clinical assessment of myelopathy and/​ or radiculopathy. A  six-​point grading system, based on axial T2-​weighted images, has been proposed and validated to delineate the degree of epidural spinal cord compression (Table 14.1).7 Patients with manifestations of thoracic mechanical instability, irrespective of neurologic or oncologic evaluation, may require surgical stabilization because mechanical pain does not typically improve with steroids, bracing, and/​or radiation.2 An 18-​point Spinal Instability Neoplastic Score (SINS) has been developed and validated to guide assessment of neoplastic instability.The SINS covers six domains: location, pain, alignment, osteolysis, vertebral body collapse, and posterior elements involvement.8 Importantly, the patient’s overall health and comorbidities must be accounted for in treatment decisions. If surgical management is pursued, the approach should be tailored to the specific characteristics of the patient’s lesion with the goal of achieving circumferential spinal cord decompression. Traditionally, posterior decompressive laminectomy was the sole surgical treatment offered for neoplastic spinal cord compression. While laminectomy can be used for disease isolated to the posterior elements, transthoracic, transpedicular lateral extracavitary and retroperitoneal approaches provide more direct access to the anterior thoracic and thoracolumbar regions. Questions

1. What approaches can be taken to stabilize the spinal column in cases of instability (getting at, e.g., pedicle screws, rods and hooks, anterior struts and plates)? 2. What surgical approaches may be taken for ventral spinal cord decompression and spinal column reconstruction? 3. For anterior and anterolateral approaches to the spine, which factors influence laterality of approach?

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An additional decision-​making point arises if the lesion is highly vascular. Renal cell carcinoma, thyroid carcinoma, melanoma, and hepatocellular carcinoma are lesions which may warrant preoperative embolization to mediate intraoperative blood loss. Surgical Procedure

Resection of a thoracic extradural tumor is performed under general anesthesia. In this patient, a lateral extracavitary approach was employed to allow access to the anterior elements. Sensory and motor evoked potentials may be helpful to mediate risk of new-​onset postoperative neurologic deficits and ensure neurologic integrity during positioning and resection. Patients are placed prone on the operating room table and an x-​ray is taken to localize the appropriate skin incision. A  midline linear skin incision is made and taken down through the subcutaneous tissue. Electrocautery is used to perform subperiosteal dissection of the spinous processes, laminae, and transverse processes of T1 through T5. An x-​ray is taken to confirm the correct levels. The pedicles of T1, T2, T4, and T5 are bilaterally cannulated. This is done using a high-​speed drill, followed by a gearshift pedicle finder, a tap, and a ball-​tip probe. Pedicle screws are then placed at these levels bilaterally. Next, a laminectomy is performed one level above and one level below the compression. This is done using a combination of high-​speed drill and Kerrison rongeurs. Next, subperiosteal dissection of the T3 transverse process and the third rib on the right is performed, and the transverse process is removed with a combination of the high-​speed drill and rongeurs. A curette is used to develop a surgical plane between the rib and the surrounding pleura, and the rib head is removed. At this time, a combination of rongeurs is used to remove the pedicle—​in the present case, the pedicle was grossly infiltrated with tumor and epidural spinal cord compression was evident. After removal of the tumor-​infiltrated pedicle, corpectomy is pursued. The tumor is dissected from the dura using a Penfield dissector and resected using a combination of suction and rongeurs. Curettes are used to perform a discectomy at T2–​T3 and T3–​T4; the inferior endplate of T2 and the endplate of T4 are identified and decorticated. To complete the corpectomy and perform a decompression, transpedicular decompression is performed. This is done using a high-​speed drill to remove part of the transverse process and pituitary rongeurs to remove any tumor that has infiltrated the pedicles. The contralateral pedicle may also require removal if the cord is not adequately decompressed or if more tumor needs to be removed to decrease oncologic burden. If infiltration is identified, the pedicle is drilled down in its entirety and the corpectomy is completed. In the present case, more than 80% of the vertebral body was removed. An appropriately sized expandable cage is placed after packing it with cadaveric bone chips and demineralized bone matrix (DBM). The cage is cautiously expanded until a secure fit is achieved. X-​ray is taken to confirm proper instrumentation placement. Next, rods are placed in the tulip heads of the screws bilaterally. In the current case, we applied a compressive force from T2 to T4 to assist in correction of the kyphotic deformity. After compression, locking caps are placed and x-​ray is again taken to confirm the cage has not subsided or migrated, appropriate thoracic kyphosis is maintained, and all instrumentation has maintained integrity during final tightening. The wound is

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Figure 14.2  Postresection sagittal (A) and axial (B) T2 magnetic resonance images. Lateral x-​ray (C) depicts T3 cage. irrigated and bony surfaces are decorticated using the high-​speed drill. Cadaveric bone chips mixed with DBM are placed in the facet joints. In the present case, arthrodesis was performed from T1 through T5. Drains are placed in the epidural space and tunneled through separate skin incisions.The wound is closed in multiple anatomic layers, the skin is closed with staples, and sterile dressings are applied (Figure 14.2).

Oral Boards Review: Management Pearls

1. In a patient with mild or no neurological or mechanical compromise and a radiosensitive tumor, nonsurgical management only with radiation therapy and/​or chemotherapy can be considered. Radiation (either fractionated or stereotactic radiosurgery) may be also used as an adjuvant treatment after surgery for many tumors. 2. In cases of ventral spinal cord compression or deformity with instability, direct ventral decompression and anterior column stabilization in addition to posterior fixation will often provide optimal decompression and stabilization. Retraction of the dura from a posterior approach carries a high risk of neurological injury and must be avoided. 3. In all cases of possible surgery, extent of disease and patient life expectancy should be considered.

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Aftercare

If a cerebrospinal fluid (CSF) leak is detected or a durotomy identified, primary closure is ideal treatment. If repair of the CSF leak is watertight, patients are typically encouraged to ambulate approximately 36–​48 hours after surgery. During this time, thigh-​length graduated compression stockings and/​or intermittent pneumatic compression or foot impulse devices should be utilized to prevent formation of venous thromboemboli (VTE). Anticoagulant prophylaxis may also be considered. Bowel and bladder function should also be monitored postoperatively to ensure return of function and prevent delayed diagnosis of spinal cord injury. As pain improves, ambulation is encouraged. Pain management is often achieved through a multimodal approach involving physical therapy and pharmaceuticals.

Pivot Points

1. If a patient presents with acute neurological compromise from epidural spinal tumor that is not known to be radiation sensitive, then urgent surgical decompression is warranted. 2. For a patient presenting with mechanical pain, deformity, and radiographic characteristics of spinal instability from tumor, surgical stabilization should be strongly considered. 3. In patients with radiosensitive disease, widely disseminated disease, or poor life expectancy, then nonsurgical management may be most appropriate.

Complications and Management

Reported complication rates following surgical management of extradural spine tumors causing spinal cord compression range widely. In a recent prospective trial, 29.6% of patients experienced an adverse event within 30 days.9 Complications following resection and stabilization can be classified as surgical, instrumentation-​related, or medical. Commonly reported complications include wound infection, CSF leakage, and hematoma formation. Rarer adverse events include VTE, instrumentation complications, and new-​onset neurologic deficits. Reported risk factors for complications include morbid obesity, posterior approach, malnutrition, preoperative radiation, and steroid use.10

Oral Boards Review: Complications Pearls

1. Postoperative patients with metastatic cancer are at high risk for deep vein thrombosis (DVT) and thromboembolism. Early mobilization and use of prophylactic anticoagulation when considered safe from a surgical viewpoint should be encouraged. 2. Neurological injury intraoperatively may be minimized by taking great care to avoid any retraction of dura or excessive distraction of instrumentation. The use of intraoperative neuromonitoring may assist in this.

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Evidence and Outcomes

Management of metastatic epidural spinal cord compression was assessed in a randomized prospective clinical trial by Patchell et al.11 This trial compared direct decompressive surgical tumor resection plus radiation therapy versus radiation alone. The study included patients with displacement of the cord visible on imaging, compression restricted to a single area, and an expected survival of at least 3 months. This study concluded that patients with surgery and radiation retain the ability to ambulate longer and recover the ability to ambulate more frequently than those treated with radiation therapy alone. Improvement in survival was also noted for patients treated surgically. A more recent trial by Fehlings et al. enrolled 142 surgically managed patients with single metastatic epidural spinal cord compression tumors, including 116 patients (81.7%) with thoracic lesions.9 The investigators found that surgical intervention, adjunctive to chemotherapy and radiation, yields short-​and long-​term improvements in pain, neurologic functional, and health-​related quality of life outcomes. References and Further Reading

1. Laufer I, Rubin DG, Lis E, et al.The NOMS framework: approach to the treatment of spinal metastatic tumors. Oncologist. 2013;18(6):744–​751. 2. Sciubba DM, Baaj AA, Gokaslan ZL. Spinal cord compression. In: Abeloff’s Clinical Oncology. 5 ed. Philadelphia, PA: Elsevier; 2014:715–​725. 3. Bach F, Larsen BH, Rohde K, et  al. Metastatic spinal cord compression. Occurrence, symptoms, clinical presentations and prognosis in 398 patients with spinal cord compression. Acta Neurochirurgica. 1990;107(1-​2):37–​43. 4. Helweg-​Larsen S, Sorensen PS. Symptoms and signs in metastatic spinal cord compression: A study of progression from first symptom until diagnosis in 153 patients. Eur J Cancer. 1994;30A(3):396–​398. 5. Loblaw DA, Perry J, Chambers A, Laperriere NJ. Systematic review of the diagnosis and management of malignant extradural spinal cord compression:  The Cancer Care Ontario Practice Guidelines Initiative’s Neuro-​ Oncology Disease Site Group. J Clin Oncol. 2005;23(9):2028–​2037. 6. Witham TF, Khavkin YA, Gallia GL, Wolinsky JP, Gokaslan ZL. Surgery insight:  Current management of epidural spinal cord compression from metastatic spine disease. Nat Clin Pract Neurol. 2006;2(2):87–​94; quiz 116. 7. Bilsky MH, Laufer I, Fourney DR, et al. Reliability analysis of the epidural spinal cord compression scale. J Neurosurg Spine. 2010;13(3):324–​328. 8. Fisher CG, DiPaola CP, Ryken TC, et al. A novel classification system for spinal instability in neoplastic disease:  An evidence-​based approach and expert consensus from the Spine Oncology Study Group. Spine. 2010;35(22):E1221–​E1229. 9. Fehlings MG, Nater A, Tetreault L, et al. Survival and clinical outcomes in surgically treated patients with metastatic epidural spinal cord compression:  Results of the prospective Multicenter AOSpine Study. J Clin Oncol. 2016;34(3):268–​276. 10. Klimo P, Jr., Schmidt MH. Surgical management of spinal metastases. Oncologist. 2004;9(2):188–​196. 11. Patchell RA, Tibbs PA, Regine WF, et  al. Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: A randomised trial. Lancet. 2005;366(9486):643–​648.

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Spinal Cord Tumor Intramedullary Rajiv R. Iyer and George I. Jallo

15 Case Presentation

A 45-​year-​old woman presents to her primary care physician complaining of 1 month of intermittent bilateral hand numbness in addition to occasional sharp, shooting pain down her neck and spine when she flexes her neck. Bowel and bladder function is normal. She reports no medical problems, no cancer history, and no history of prior neck pain or arthritis. Due to suspicion for cervical spondylosis, magnetic resonance imaging (MRI) is obtained, which demonstrates an expansile lesion within the spinal cord at the level of C7–​T1 (Figure 15.1). She is referred to a neurosurgeon for evaluation. Neurological examination reveals normal muscle bulk and tone but slight weakness with handgrip bilaterally. Sensory examination is unremarkable. Patellar reflexes are 3+ and Babinski sign is positive bilaterally. Questions

1. What is the most likely diagnosis? 2. What are the common imaging findings associated with intramedullary spinal cord tumors (IMSCTs)? 3. What is a common classification system for spinal cord tumors?

Assessment and Planning

Based on the neurological examination and imaging findings, the neurosurgeon is concerned about the presence of an IMSCT. Spinal cord tumors can be subdivided into extradural, intradural-​extramedullary and intramedullary subtypes, the least common being the intramedullary group. The most common types of IMSCTs are ependymomas and astrocytomas, with ependymomas being more likely in adults and astrocytomas more commonly found in the pediatric population. Other lesions in the differential diagnosis for IMSCTs include hemangioblastomas, especially in cases of the inherited disorder von Hippel Lindau (vHL) disease, as well as gangliogliomas, cavernous malformations, subependymomas, and several other rare lesions. Clinical characteristics of patients with IMSCTs can range widely, with the most common complaint being axial back or neck pain. Other

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Figure 15.1  Cervicothoracic intramedullary spinal cord tumor (A–​F). T2-​weighted (A,B) and post-​contrast T1-​weighted preoperative (C,D) magnetic resonance imaging (MRI) demonstrating an expansile, T2-​hyperintense, rim-​enhancing lesion concerning for an intramedullary spinal cord tumor (IMSCT). A gross total resection was achieved through an osteoplastic laminoplasty (E,F).

features may include radicular pain, sensory disturbances, progressive motor deficit, and, in more severe cases, bowel or bladder dysfunction and myelopathy. MRI is the diagnostic modality of choice in the diagnosis of IMSCTs. The majority of lesions appear as expansile lesions within the spinal cord and are often hyperintense on T2-​weighted MR imaging. T1-​weighted post-​gadolinium imaging is variable and may demonstrate homogenous enhancement, especially in the case of ependymomas, or patchy enhancement, more commonly seen with spinal astrocytomas (Figure 15.2). Sharp, demarcated borders are more commonly seen in cases of ependymomas. In some cases, adjacent spinal cord edema may be obvious on T2-​weighted imaging, in addition to the presence of syringomyelia or tumor-​a ssociated  cysts.

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Figure 15.2  Spinal astrocytoma (A–​D). Magnetic resonance imaging (MRI) demonstrates a T2-​hyperintense lesion (A) centered at the level of C4–​C5 with irregular borders (B), concerning for an intramedullary astrocytoma. Postoperative imaging (C,D) is also shown following resection.

Oral Boards Review: Diagnostic Pearls

1. MRI is crucial to the diagnosis and localization of IMSCTs. a. IMSCTs typically appear as hyperintense intramedullary lesions on T2-​ weighted MRI. Enhancement post-​gadolinium administration varies—​for ependymomas, homogenous enhancement is common, while astrocytomas are more variable and may demonstrate a patchy enhancement pattern. b. Well-​demarcated borders on MRI are more characteristic of ependymomas, consistent with well-​defined dissection planes often discovered in the operating room. For astrocytomas, their infiltrating nature correlates with their poorly demarcated borders on MRI. A more eccentric location is characteristic of astrocytomas, while ependymomas are more centrally located. c. The third most common IMSCTs in adults are hemangioblastomas. Unique features on imaging include flow voids on T2-​weighted MRI, a contrast-​enhancing nodule within the spinal cord, and a syrinx out of proportion in size to the tumor bulk itself. Ancillary imaging with cerebral angiography may be useful in identifying hypertrophic feeding vessels that supply the tumor.

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2. The cervical and thoracic regions are the most common locations for IMSCTs. 3. Risk factors for developing IMSCTs are not well known, but inherited disorders including neurofibromatosis type 2 (NF2) predispose patients to developing spinal ependymomas, while vHL predisposes patients to the development of hemangioblastomas of the spinal cord.

Questions

1. What are some risk factors for the development of IMSCTs? 2. What are some favorable imaging features for surgical intervention? 3. Is there a benefit to performing an osteoplastic laminoplasty versus laminectomies for tumor resection?

Decision-​Making

Generally, ependymomas and astrocytomas of the spinal cord are low-​grade lesions that are amenable to surgical resection. Rarely, they are of a higher grade, which is associated with increased aggressiveness and invasion. Patients with high-​grade IMSCTs tend to fare poorly regardless of surgical intervention. In such cases, radiation therapy may be appropriate as an adjuvant treatment modality. If a patient presents with symptoms that are attributable to an IMSCT, surgical intervention is the mainstay of treatment. The goal of surgery is to obtain a diagnosis and to perform a maximal safe resection without causing a permanent neurological deficit. For ependymomas, gross total resection (GTR) is often achievable given the well-​defined dissection planes that allow the surgeon to carefully spare normal surrounding neural structures. On the other hand, astrocytomas of the spinal cord have irregular borders and an infiltrating pattern and thus discerning tumor tissue from normal neural parenchymal may be challenging. Intraoperative neurophysiological monitoring is critical in such cases as its use can prevent permanent iatrogenic deficits. Surgical Procedure

IMSCT resection is performed under general anesthesia using rigid skull fixation and prone positioning. Intraoperative electrophysiological monitoring includes motor evoked potentials (MEPs) and somatosensory evoked potentials (SSEPs). A  localizing x-​ray may be useful in guiding incision placement. A midline skin incision is made and electrocautery is used to expose the lamina at the level(s) of interest. Use of an ultrasonic bone-​cutting device can be used to perform an osteoplastic laminoplasty, which can be reaffixed following tumor resection and dural closure. Depending on surgeon preference, standard laminectomies may also be performed. During this stage, care must be taken to avoid facet joint entry or sacrifice so as to not destabilize the spinal column. There does not appear to be any significant difference in spinal deformity outcomes after IMSCT surgery regardless of the use of laminectomies compared to the osteoplastic laminoplasty. However, there is a trend toward a decreased cerebrospinal fluid (CSF) leak rate with

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the use of the osteoplastic laminoplasty. Once the laminae are removed, further tumor localization can be achieved with intraoperative ultrasound. The use of the ultrasound also allows one to determine whether there is sufficient bony exposure allowing for a large enough intradural exposure above and below the lesion of interest. Other features such as tumor-​cysts or syrinxes can be visualized during this step and aid in localization when compared to preoperative imaging. Once an adequate dural exposure is achieved, intraoperative epidural electrodes can be placed for electrophysiological monitoring of the D-​wave. This measure represents the number of functional units of the corticospinal tract above and below the lesion and provides real-​time feedback to the surgeon about graded motor function during tumor resection. While MEPs provide an all-​or-​none measure of motor function, D-​ wave monitoring can be used as a threshold at which a surgeon may pause or terminate tumor resection in order to avoid an iatrogenic, permanent neurologic deficit. Commonly, once the D-​wave threshold reaches 50%, tumor resection is halted as this represents a threshold predicting permanent rather than transient postoperative neurological dysfunction. Once the dura is opened, obvious surface abnormalities may be present on the spinal cord surface. A midline myelotomy is made, and, many times, SSEP function is compromised due to dorsal column manipulation. Identifying midline may be challenging due to cord rotation or asymmetric enlargement, but the presence of dorsal sulcal veins or identification of the midpoint between dorsal root entry zones can aid in this step. The myelotomy should extend the rostro-​caudal extent of the tumor in order to avoid harmful manipulation of normal structures. Once the tumor is encountered, careful microscopic dissection can proceed, freeing the tumor from surrounding normal neural tissue. Circumferential dissection is often utilized, especially when good dissection planes exist. Sometimes, tumor cysts or a syrinx will aid in the identification of these planes. If significant retraction is required to circumnavigate the tumor, internal debulking can be performed with a laser contact probe or an ultrasonic aspirator. The goal of surgery is maximal resection without causing a permanent neurological deficit. Especially in cases of infiltrating astrocytomas, subtotal resection may be necessary if a decline in electrophysiological monitoring occurs. Meticulous hemostasis is performed following tumor resection. After the tumor is removed, the dura is closed in a watertight fashion with a nonabsorbable suture such as a 5-​0 Prolene. In some cases, if the dura cannot be well opposed, a dural substitute patch may be necessary. Fibrin sealants may help in avoiding postoperative CSF leak. If a laminoplasty was performed, this is fixed in place with titanium miniplates. The fascia and superficial tissues are closed in a layered fashion in a tight, interrupted manner in order to minimize the risk of postoperative CSF leak.

Oral Boards Review: Management Pearls

1. Surgical resection is the mainstay in the management of IMSCTs with the goal of maximal safe resection. Dissection planes are usually clearer with ependymoma resection compared to astrocytomas, which have irregular borders due to their infiltrating nature.

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2. Surgical treatment often entails the use of an osteoplastic laminoplasty with care taken to avoid joint space disruption. Additional use of electrophysiological monitoring with MEPs, SSEPs, and D-​waves provides critical information to the surgeon during tumor resection. A greater than 50% reduction in epidural D-​wave monitoring is often a threshold used to pause or terminate tumor resection as this can be the difference between a transient versus permanent postoperative neurological deficit. 3. Watertight dural closure, the use of fibrin sealants, and an osteoplastic laminoplasty, as well as meticulous fascial and skin closure, all help to prevent postoperative CSF leak.

Pivot Points

1. If during IMSCT resection, changes or loss of SSEPs occur, postoperative sensory disturbances can be expected due to manipulation of the dorsal columns. These may be transient or long-​term. If MEPs are unchanged and D-​wave monitoring decreases by less than 50%, the patient’s motor abilities are expected to be unchanged. If MEPs are lost and D-​wave monitoring decreases by less than 50%, a transient motor deficit can be expected postoperatively. If bilateral MEP loss occurs in addition to greater than 50% loss of D-​wave monitoring, a prolonged motor deficit can be expected postoperatively. 2. Postoperative functional status is highly dependent on preoperative functional status, and maximal safe resection is performed in an attempt to preserve existing preoperative function. Functional status pre-​and postoperatively can be measured with the McCormick grading scale, which takes into account motor and sensory function, as well as the patient’s functional independence.

Aftercare

Following surgery for IMSCT resection, it is common practice to keep the patient in a recumbent position initially to minimize the chance of a postoperative CSF leak. Elevation can normally start 24 hours postoperatively, with special attention paid to the wound to monitor for signs or symptoms of CSF leak. Generally, a postoperative MRI is obtained that aids in determining the extent of surgical resection. While some patients present with minimal symptomatology associated with their IMSCT, others are discovered only after significant, progressive neurologic deficit has occurred. In these situations, symptoms may be exacerbated initially by surgery, with transient postoperative motor or sensory disturbances. The purpose of intraoperative electrophysiological monitoring is to prevent permanent neurologic deficits. However, transient changes may occur in the postoperative period, and patients should be counseled regarding this possibility. Thus, physical therapy and rehabilitation play a significant role in the recovery period following surgery.

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Spinal Cord Tumor: Intramedullary

Serial monitoring with gadolinium-​enhanced MRI allows the surgeon to monitor for tumor recurrence or progression following surgical resection of IMSCTs. For symptomatic tumor recurrence, repeat surgical resection can be considered, but the risks and benefits of re-​resection must be weighed against factors including preoperative functional status, tumor location, and multiplicity and extent of disease, as well as medical comorbidities. Generally, radiation therapy is reserved for cases of multifocal or aggressive tumors that are not amenable. Complications and Management

Postoperative CSF leak and pseudomeningocele are some of the potential complications of IMSCT surgery. During initial surgery, several methods can be undertaken to avoid these phenomena. For example, watertight dural closure and a multilayered soft tissue closure with special attention to the muscular fascia is critical. The use of a laminoplasty in addition to dural substitutes and fibrin sealants can also help to avoid this complication. If CSF leak occurs, the use of a lumbar drain and recumbent positioning can be attempting to heal the source of the leak. If the leak persists, re-​exploration may be necessary to avoid the risk of meningitis. Exploration can involve the use of a dural patch or buttressing dural sutures, as well as a subfascial drain placed to straight drainage. If further CSF accumulation occurs, a drain allows for diversionary fistula formation that can be subsequently closed with a figure-​of-​eight suture after the wound has been given sufficient time to heal. Postlaminectomy kyphosis and spinal deformity can also occur, more frequently in children and especially when there is violation of the facet joints during bony exposure for intradural tumor resection. Large tumors spanning several segments may harbor a higher risk for the development of deformity postoperatively. Typically, if spinal fixation is required for a destabilized segment, it occurs after recovery has occurred from the initial tumor resection.

Oral Boards Review: Complications Pearls

1. The use of osteoplastic laminoplasty compared to laminectomies for IMSCT resection is not a definitive measure to prevent postoperative kyphosis and spinal deformity. 2. Pseudomeningocele formation or CSF leak can be managed with lumbar drainage and recumbency, but may require re-​exploration for attempted primary repair in order to avoid open communication between the intradural space and the atmosphere, which can lead to meningitis.

Evidence and Outcomes

In the majority of reports, excellent outcomes have been reported for patients undergoing surgical resection of low-​grade IMSCTs. While there is no concrete data to suggest that extent of resection affects progression-​free survival or overall survival, several groups maintain that maximal safe resection should be performed at the time of first surgery. Previously, open biopsy followed by radiation was posed as an alternative

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to aggressive resection. However, excellent outcomes have been reported for patients undergoing aggressive resection, regardless of age, and this should be attempted to avoid the need for repeat surgery for tumor recurrence. The largest predictor of postoperative function following IMSCT surgery is preoperative functional status. Generally, transient motor deficits postoperatively can improve with physical therapy up to 6–​12 months postoperatively. References and Further Reading

Hanbali F, Fourney DR, Marmor E, et al. Spinal cord ependymoma: Radical surgical resection and outcome. Neurosurgery. 2002;51:1162–​1172; discussion 1172–​1164. Jallo GI, Danish S, Velasquez L, Epstein F. Intramedullary low-​g rade astrocytomas:  Long-​term outcome following radical surgery. J Neurooncol. 2001;53:61–​66. Jallo GI, Kothbauer KF, Epstein FJ. Intrinsic spinal cord tumor resection. Neurosurgery. 2001;49:1124–​1128/​ McGirt MJ, Garces-​Ambrossi GL, Parker SL, et al. Short-​term progressive spinal deformity following laminoplasty versus laminectomy for resection of intradural spinal tumors: analysis of 238 patients. Neurosurgery. 2010;66:1005–​1012.

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Spinal Cord Tumor Intradural Extramedullary Michael A. Galgano, Jared Fridley, and Ziya Gokaslan

16 Case Presentation

A 52-​ year-​ old woman presented to the emergency department with progressively worsening mid-​back pain, bilateral leg weakness and numbness, urinary retention, and balance dysfunction over the course of a few weeks. She had no significant past medical or surgical history and denied any recent trauma, travel, or fever. Detailed neurological examination revealed a well-​developed middle-​aged female with appropriate mentation and cognitive function. She was found to have 4+/​5 motor strength in all major muscle groups of the bilateral lower extremities, a mid-​upper chest sensory level, brisk patellar and ankle reflexes, and bilateral clonus. Upper extremity sensorimotor exam was unremarkable. Hoffman sign was negative in both hands, and upper extremity reflexes were within normal limits. Basic laboratory studies were unremarkable. Questions

1. To what part of the neuroaxis can the patient’s neurological signs and symptoms be localized? 2. What are some differential diagnoses based on the patient’s history and physical exam? 3. What would be the most appropriate imaging modality now? 4. What is the urgency of the diagnostic workup given the patient’s progressive neurological decline?

Assessment and Planning

This patient has signs and symptoms consistent with thoracic myelopathy. Differential diagnoses include thoracic disc herniation, spinal tumor, spinal epidural abscess, and spinal arteriovenous malformation. Although thoracic disc herniations can certainly cause thoracic myelopathy, their clinical course tends to be drawn out over a period of many months. Spinal vascular malformations are incredibly rare entities that can cause symptoms in a progressive fashion or acutely from an intradural hemorrhage. Spinal vascular pathology should be kept in mind with any myelopathy that is unexplained by radiographic imaging, as the findings on magnetic resonance imaging (MRI) may be missed due to their subtleness. Patients harboring infectious etiologies generally have

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more systemic signs and symptoms, often coupled with abnormal inflammatory markers and leukocytosis. The current patient was afebrile and did not have an elevated white blood cell count; however, if there is a strong clinical suspicion for a spinal infection, c-​reactive protein (CRP) and erythrocyte sedimentation rate (ESR) should both be ordered. Neoplastic processes leading to thoracic myelopathy have significant variability. If a tumor is suspected, it cannot be determined whether the lesion is intradural or extradural based solely on history and physical examination. Imaging is needed for further differentiation. When dealing with progressively worsening myelopathy, it is important to obtain the proper imaging in a timely fashion. An MRI with and without contrast of the thoracic spine is warranted on an urgent basis. If the thoracic spine MRI is suggestive of a neoplasm or infection, the whole spine should be imaged to look for additional lesions because this might affect patient treatment. If a spinal fusion is being considered to supplement the decompression en route to the site pathology, a computed tomography (CT) scan may be warranted to plan out instrumentation trajectories and for purposes of measuring screw lengths. An MRI of the cervical and thoracic spine with and without contrast was completed revealing a dorsolateral, intradural, extramedullary mass at the level of T2 measuring 1.9 × 0.7 × 0.9 cm.There is homogenous contrast enhancement with evidence of a “dural tail.” The mass causes cord displacement and severe central canal stenosis. T2 hyperintensity within the cord is consistent with edema versus myelomalacia (Figure 16.1). The most common intradural extramedullary neoplasms of the thoracic spine are meningiomas and peripheral nerve sheath tumors such as schwannomas and neurofibromas. Less common lesions found in this compartment are metastases, paragangliomas, extramedullary cavernomas, neuroenteric cysts, ependymomas, and arachnoid cysts.

Figure 16.1  Preoperative T1-​weighted magnetic resonance image (MRI) with contrast revealing a dorsally located contrast enhancing mass at the level of T2–​T3, causing mass effect on the underlying spinal cord

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Based on history and physical examination as well as imaging findings, the most likely diagnosis in this case is a thoracic spine meningioma. Meningiomas are histologically benign tumors that arise from arachnoid cap cells. There are more aggressive subtypes, although these are quite rare in the spine. There is a female preponderance, likely because of hormonal receptor types that are common in women.

Oral Boards Review: Diagnostic Pearls

Neurological presentation in the patient with an intradural extramedullary tumor: 1. Cervical: Cervical spine intradural extramedullary lesions often present with features of cervical myelopathy, including gait/​balance disturbance and difficulty with manual dexterity. If the tumor causes compression of a nerve root, there may be a significant radiculopathic component causing pain or sensorimotor deficits in the affected nerve distribution. Neck pain is a common symptom in these patients. Depending on the size of the lesion, these patients may have brisk reflexes and positive Hoffman and Babinski signs, as well as myo-​/​dermatomal weakness and numbness, respectively. Dorsal column tracts in the cord may be affected, causing imbalance and discoordination. 2. Thoracic: Thoracic spine intradural extramedullary lesions often present with myelopathic features. Back pain with recumbency is often a complaint of the patient. Thoracic radiculopathy as a band-​like pain may be manifested. Gait disturbance may be present, as well as varying degrees of lower extremity weakness, depending on the level of the lesion and chronicity of symptoms. A thoracic sensory level is often discovered on neurological assessment. Clonus, brisk lower extremity reflexes, and positive Babinski sign are often found as well. The thoracic corticospinal tracts are particularly vulnerable and sensitive to mass effect from ventrally located lesions. Lesions situated more dorsally may cause a sensory ataxia. Bowel and bladder involvement may be a late finding. 3. Lumbar: Lumbar spine intradural extramedullary lesions may also present with back pain brought on by recumbency. If a tumor is located at the level of the conus medullaris, bowel and bladder symptoms may be present. However, lesions distal to this will often cause nerve root symptoms, such as weakness and numbness. The degree of weakness depends on the size of the mass and amount of canal compromise. Nerve sheath tumors often cause isolated sensory symptoms as these tumors usually arise from the dorsal root. MRI with and without contrast is the imaging modality of choice for differentiating intradural and extradural lesions because it can delineate in detail the relationship of the tumor to its surroundings. Meningiomas are often iso-​or hypointense on T1 and iso-​or hyperintense on T2. They typically display avid homogenous enhancement with contrast. An enhancing dural tail is also characteristic of meningiomas. CT scan may demonstrate calcifications within the tumor. It is important to differentiate meningiomas from peripheral nerve sheath tumors, such as schwannoma, as both are contrast-​enhancing

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and both can cause cord compression. Schwannomas are iso-​or hypointense on T1 and hyperintense on T2. Some schwannomas display markedly increased regions of T2 intensity, often indicating a cystic component (Figure 16.2). Areas of T2 hypointensity can be representative of hemorrhage or collagen formation. Unlike meningiomas, schwannomas arise from the nerve sheath and therefore a significant tumor component can be seen in the neural foramen, often with dilation and thinning of the surrounding bone. Dural tails are not associated with schwannomas, unlike meningiomas. The MRI appearance of neurofibromas is similar to that of schwannomas, although neurofibromas do not typically harbor cystic changes. Spinal radiographs and CT may reveal thinning of the pedicles (Figure 16.2), increased interpedicular distance, scalloping of the posterior vertebral bodies (especially with schwannomas and neurofibromas), and enlarged neural foramina. Questions

1. To maximize surgical resection of this lesion, what steps can be taken to ensure the dural attachment is excised along with the tumor? 2. What modifications to the surgical approach would need to be made if the lesion was situated ventral to the spinal cord? 3. Why should a distinction be made between an intradural tumor with outward extension through the nerve root sleeve into the neural foramen and an extradural tumor with inward extension into the neural foramen?

Figure 16.2  Axial computed tomography (CT) scan at the level of the conus, showing an intradural partially calcified tumor causing thinning of the pedicles bilaterally.

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Decision-​Making

Most intradural extramedullary tumors are histologically benign. Small, asymptomatic lesions in this compartment can often be watched radiographically over time. Many intradural extramedullary lesions are discovered, however, because they have become symptomatic. The patient in this case has had progressive worsening back pain, bilateral lower extremity weakness, numbness, urinary dysfunction, and difficulty ambulating. In addition to her lower extremity weakness, she is displaying signs and symptoms of sensory ataxia. Although this is likely a histologically benign lesion, the mass effect on the spinal cord is concerning. Progression of the tumor may cause further worsening of her existing deficits, potentially leading to paraplegia. Intervention to decompress her spinal cord and resect the mass would allow the best chance of neurological recovery. Barring medical contraindications to surgery, observation is not a good option. Additionally, surgical resection of the tumor is helpful in terms of tissue diagnosis. This may affect the patient’s prognosis, dictate whether adjuvant therapy may be needed, and determine the frequency of clinical and radiographic follow-​up. Questions

1. Unlike their intracranial counterparts, spinal meningiomas do not penetrate the pia. What two factors have been proposed to account for this? 2. Why is bony remodeling not seen in the spine with meningiomas, as opposed to intracranial meningiomas?

Surgical Procedure

A posterior approach is commonly utilized for most intradural extramedullary tumors, regardless of whether they are dorsal, lateral, or ventrally located. Large ventrolateral meningiomas commonly push the spinal cord toward the contralateral side. This gives the surgeon a reasonable working corridor without having to engage in additional retraction of the cord. If necessary, sacrifice of a noncritical thoracic nerve root or a division of a dentate ligament may be utilized to allow further safe manipulation of the spinal cord. A ventral or ventral-​lateral intradural extramedullary thoracic tumor can alternatively be accessed utilizing a costotransversectomy or lateral extracavitary approach. Utilizing a more lateral approach minimizes the need for retraction of the cord. A typical approach to a dorsal meningioma entails a standard posterior spinal subperiosteal dissection, followed by a laminectomy or laminoplasty at the levels of interest. The potential for postlaminectomy kyphosis must be discussed with the patient prior to performing surgical intervention. A preoperative loss of cervical lordosis, for example, can potentially place the patient at risk for postoperative kyphosis. A laminoplasty can be considered in such a situation to keep the dorsal supporting structures intact. In the thoracic spine, the risk of abnormal kyphosis after a laminectomy is less, likely in part to the further stability rendered by the rib cage. Another potential advantage of laminoplasty versus laminectomies is reduced epidural scarring, which can make surgery for tumor recurrences more challenging.

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The surgical approach utilized for the presenting patient was a posterior T1–​T3 laminectomy. Neuromonitoring of free running electromyogram (EMG) and somatosensory and motor evoked potentials (SSEPs and MEPs) was utilized. An alteration in neuromonitoring signals during the tumor resection may alert the surgeon that spinal cord perfusion needs to be optimized. Neuromonitoring also allows the surgeon to stimulate selected nerve rootlets during the tumor excision to preserve their functionality. The operative levels were localized with an anteroposterior (AP) x-​ray. The T1 through T3 pedicles should associate with their respective ribs at the same level. A midline incision was made and subperiosteal dissection performed, followed by the laminectomy. It is important to expose above and below the tumor to minimize risk of neural element injury and allow total tumor resection with excision of any dural attachments. Because the lesion was purely dorsal, there was no indication to perform a facetectomy and remove more bone laterally. Once the laminectomy was completed, an ultrasound was brought into the surgical field to confirm that the tumor is in fact beneath the exposed dura. The operating microscope was then draped and brought into the field. A split-​thickness durotomy was made using an 11-​blade scalpel. Care was taken to not violate the tumor capsule. The superficial dural layer was dissected from the inner dural layer. The superficial dural layer was then tacked up using appropriate-​sized sutures. Once the lateral margins of the meningioma were identified, the inner layer of the dura was opened sharply, followed by circumferential dissection around the capsule. Once the capsule was freed from the underlying cord and any attached nerve rootlets, it was removed en bloc with the inner dural attachment (Figure 16.3). If the tumor is too large to safely be removed in one piece, it can be cored out utilizing an ultrasonic aspirator and then folded in on itself prior to fully being excised. If an en bloc excision is not achieved, then the dural edges once attached to the tumor capsule should be cauterized

Figure 16.3  Postoperative T1-​weighted magnetic resonance image (MRI) with contrast revealing gross total resection of the previously enhancing mass at the level of  T2–​T3.

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with a bipolar device. Optimal hemostasis was achieved, followed by intradural irrigation. Dural sutures were then used to close the remaining superficial layer of dura. Alternatively, a dural substitute graft can be sewn to the native dura. A Valsalva maneuver was then done to ensure there is no cerebrospinal fluid (CSF) leak. Care was taken to close the fascial layer tightly to minimize risk of a CSF leak.

Oral Boards Review: Diagnostic Pearls

1. Excision of intradural meningiomas can be achieved via an en bloc fashion by utilizing a split-​thickness durotomy or by ultrasonic aspiration and piecemeal removal. 2. Osseous involvement is exceptionally uncommon with spinal meningiomas. This is likely due to the well-​defined epidural space in the spine. 3. Spinal meningiomas uncommonly penetrate the pia. One theory is that there is an “intermediate leptomeningeal layer.” The other concept that has been postulated to explain pial preservation is that spinal meningiomas often become symptomatic sooner than their intracranial counterparts. Patients often become symptomatic from spinal cord compression earlier than mass effect on the brain. Therefore, surgical resection may be undertaken before pial penetration occurs. 4. Neurofibromas commonly arise as a fusiform enlargement of the nerve, making it necessary to sacrifice the root during excision of the tumor. 5. Schwannomas arise from the nerve root of origin, which is usually a nonfunctional dorsal sensory root that can be sacrificed; there is always a corresponding nerve root, which is typically a functional ventral motor root, that needs to be dissected off the tumor.

Pivot Points

1. A traditional laminectomy or, alternatively, laminoplasty can be utilized to gain access to the dura. 2. Paying close attention to the patient’s spinal alignment is important. A patient with a kyphotic cervical spine prior to the intradural tumor excision may require supplemental instrumentation and fusion to ensure she does not develop further kyphosis after surgery. a. More lateral approaches to the spine for intradural tumors with a foraminal or very ventral component may require removal of the facet joints and potentially proximal ribs for optimal access 3. Three options exist for dural opening and closure with a dorsal spinal meningioma: a. Traditional two-​layer dural opening with coagulation of tumor attachments to the dura, followed by a primary dural closure b. Traditional two-​layer dural opening with excision of both dura layers overlying the tumor, followed by duraplasty

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c. Split-​thickness dural opening, followed by excision of the meningioma with the inner dural layer, followed by a primary superficial dural layer closure Aftercare

Most surgeons keep patients flat for 24–​48 hours after performing an intradural tumor resection. This is done to discourage a postoperative CSF leak or pseudomeningocele from forming. A bladder catheter is left in place so the patient does not need to use a bedpan repeatedly. After the first 24–​48 hours following surgery, it may be advisable to have physical therapy work with the patient for mobilization. We generally give 24 hours of prophylactic antibiotics after the operation. Steroids are usually not indicted unless there is concern for cord edema from manipulation during the surgery. Tylenol, narcotics, and muscle relaxants are generally given for the first few days after surgery. A postoperative MRI with and without contrast is obtained prior to discharge to ensure the desired degree of resection has taken place. Depending on the pathological grade of the tumor and degree of tumor resection, a repeat MRI is generally obtained within the first 6 months of surgery to ensure there has been no recurrence. Complications and Management

During an operation to resect an intradural extramedullary tumor, the adjacent neural elements are at risk of injury. Both nerve sheath tumors and meningiomas have very intimate anatomic relationships with surrounding nerve roots and the spinal cord, depending on the level. It is important to have a reliable neuromonitoring technician on hand during the case to stimulate surrounding nerve roots and ensure functional roots are not sacrificed. Obtaining MEPs periodically throughout the case ensures that the corticospinal tracts have not been compromised. Although an attempted watertight dural closure is undertaken after excision of the tumor, CSF can sometimes leak through the suture holes, leading to a pseudomeningocele. Most pseudomeningoceles will resolve with time on their own. However, if symptomatic, or if a CSF leak develops through the incision, placement of a lumbar drain or re-​exploration of the dural closure should be performed. Antibiotics are generally administered for a few days if CSF is noted to be draining through the skin after surgery. Immaculate hemostasis prior to both dural and soft tissue/​skin closure is necessary to prevent intradural and epidural clot formation. A good tumor resection can quickly be complicated by a compressive hematoma within the first days of surgery. It is advisable to ensure patients are kept off antiplatelet agents and therapeutic anticoagulation for up to 2 weeks after surgery. Postoperative infection is always a risk with any open surgery. Violation of the dura puts the patient at increased risk of meningitis after surgery. One dose of preoperative antibiotics is given within 1 hour of making incision, and 24 hours of postoperative antibiotics are generally administered. Urinary retention is a potential obstacle after the patient’s Foley catheter is removed. The risk for this is higher with increased narcotic usage and in men with benign prostatic hypertrophy. 156

 

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Delayed cervical postlaminectomy kyphosis may be seen in a small percentage of patients after the posterior tension band is removed along with the dorsal elements.This may require supplemental instrumented fusion if the patient is symptomatic.

Oral Boards Review: Complication Pearls

1. Intraoperative neuromonitoring can be a valuable tool, especially when excising tumors intimately involved with nerve roots. 2. Utilization of a postdural closure Valsalva maneuver may reveal sites of CSF leak which can be addressed prior to soft tissue closure. 3. Use of hemostatic agents with gentle cottonoid tamponade in the epidural space can keep a clear surgical field, diminishing the likelihood of blood leaking into the intradural space. 4. Once the dural closure has been performed, pulse irrigation with antibiotic-​impregnated saline can be utilized on the soft tissue prior to closure.

Evidence and Outcomes

There is an abundance of literature documenting a variety of surgical techniques and outcomes for resecting intradural extramedullary tumors. Due to their typical benign histological nature, patients harboring such tumors generally have a good oncological outcome following resection. References and Further Reading

Dickman C, Fehlings M, Gokaslan Z. Intradural extramedullary spinal tumors. In Spinal Cord and Spinal Column Tumors, Principles and Practice (­chapter 21). Stuttgart: Thieme; 2006. Galgano M, Beutler T, Brooking A, Deshaies E. Spinal meningiomas: A review. J Spine. 2014;3(1). doi: 10.4172/​2165-​7939. Hirabayashi H, Takahashi J, Kato H, Ebara S, Takahashi H. Surgical resection without dural reconstruction of a lumbar meningioma in an elderly woman. Eur Spine J. 2009 Jul; 18(Suppl 2): 232–​235. Levy WJ, Latchaw J, Hahn JF, Sawhny B, Bay J, Dohn DF. Spinal neurofibromas:  A report of 66 cases and a comparison with meningiomas. Neurosurgery. 1986; 8:331. Seppälä MT, Haltia MJ, Sankila RJ, Jääskeläinen JE, Heiskanen O. Long-​term outcome after removal of spinal neurofibroma. J Neurosurg. 1995;82:572.

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Radiation-​Sensitive Spine Tumor Adam M. Robin and Ilya Laufer

17

Case Presentation

A 71-​ year-​ old right-​ handed woman with a history of childhood asthma and hip arthroplasty presented to her primary care physician complaining of progressive back pain that radiated down her left leg. Her pain was initially attributed to deconditioning and compensation from her hip replacement, and she was treated with steroids and pain medication. After modest improvement initially she continued to worsen, developing difficulty sitting and sleeping at night. Referral was then made to the neurosurgeon. Cranial nerve evaluation is unremarkable, as is segmental muscle group testing of the upper extremities. She prefers to stand during her examination, but with effort is able to sit and participate with segmental muscle group testing in her lower extremities. She has mild pain limitation in her left hip flexors and extensors. Sensory examination for light touch and temperature sensation is within normal limits. Normal patellar reflex responses are found bilaterally; she has plantar flexor responses bilaterally without clonus. Although antalgic when rising from a chair, once under way, her gait is normal. She is unable to tolerate a fully supine position on the examining table and has significant leg pain and discomfort in an L3 dermatomal distribution when seated. Her Karnofsky Performance Scale (KPS) is 60. Questions

1. What is the likely diagnosis? 2. What is the next step in her evaluation? 3. What is the most likely anatomical region to be involved? 4. What is a reasonable differential diagnosis?

Assessment and Planning

Considering the history and physical exam findings, particularly the patient’s age, progressive back pain, and mechanical radiculopathy with axial loading, her findings are highly suggestive of a progressive process involving the spine near the left L3 nerve root.1,2 Other diagnostic considerations include osteoporotic compression fracture, spondylosis, spondylolisthesis, degenerative or isthmic pars fracture, and synovial cyst. A magnetic resonance imaging (MRI) scan is the next step in the evaluation of this patient. The scan should be ordered with gadolinium and can be requested with perfusion imaging if available when neoplastic disease is suspected. T1 sequences with

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gadolinium provide excellent anatomic detail of the spinal and neural anatomy and demonstrate well the enhancement characteristics of a lesion if identified. Note is made of the spinal sagittal alignment; involvement of anterior, middle, and posterior column structures; vertebral body morphology; cortical integrity; marrow signal; and presence of epidural disease within the central canal and neural foramen. Importantly, on the gadolinium-​enhanced images the reader should be certain to evaluate lumbar nerve roots for signs of leptomeningeal disease. This patient’s MRI revealed a T2 hyperintense lesion arising from within the marrow space of the L3 vertebral body and involving the bilateral pedicles. There is an associated pathologic compression-​burst fracture at this level with approximately 35% loss of vertebral body height and retropulsion associated with loss of integrity of the posterior vertebral body line/​cortical margin and roughly 50% canal compromise. There is no associated kyphotic deformity. Additionally, there is a ventral epidural soft tissue component suggestive of tumor extending along the cranio-​caudal axis from L3 to L5 and into bilateral L3 foramen causing nerve root compression on the left more so than the right (Figure 17.1).

Figure 17.1 T2 axial (A) magnetic resonance image (MRI) at the level of L3 demonstrating a vertebral compression burst fracture, increased intrapedicular distance, and cortical compromise/​retropulsion of the posterior vertebral body into the central canal causing stenosis and nerve root compression. Sagittal (B) T1 sequence demonstrating the hypointense bone marrow and pathologic compression fracture at L3. Panel C depicts the degree of hyperintense disease infiltration into the pedicle on sagittal short T1 inversion recovery (STIR) imaging at L3. Sagittal T2 (D) sequence demonstrating the L3 vertebral compression burst fracture and resultant degree of canal stenosis.

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Questions

1. Do these radiographic features explain the patient’s findings? 2. Is the patient mechanically unstable? 3. What is the significance of left L3 pedicle involvement? 4. Are there any additional studies that would aid in the assessment of this patient? 5. What is the differential diagnosis?

Oral Boards Review: Diagnostic Pearls

1. Patients with multiple so-​called red flags in association with complaints of back pain should be evaluated with MRI. In a recent systematic review advanced age, prolonged use of corticosteroids, severe trauma, and a prior history of malignancy were all associated with a higher post-​test probability of fracture or malignancy detection.3 In this case, the patient is advanced in age; had relatively insidious, progressive onset of back pain in conjunction with worsening radiculopathy on axial loading; and, on further questioning, was found to have a component of “biological,” tumor-​related pain unresponsive to standard conservative therapy. These are all factors that should prompt the clinician to evaluate the patient with MRI. 2. Owing to improving longevity in patients with metastatic cancer, up to 40% of patients will develop spinal metastases with epidural disease.2 It is often possible to predict disease severity based on the patient’s presenting symptoms, which often include pain and less often neurological deficit: a. Biologic or “tumor-​related” pain is more prominent at night and in the early morning, with resolution later in the day and is secondary to the diurnal variation in endogenous steroid secretion, which is diminished at night. It is an early symptom of bony metastasis and is responsive to radiation and steroid therapy. b. Mechanical pain is less common and is related to movement. In the cervical spine, mechanical pain worsens with rotation, flexion, and extension. In the thoracic spine, where the facets are oriented in the coronal plane and there is less mobility owing to the stability provided by the thorax, pain may be worse when lying down or worsen in the process of changing positions from lying down to sitting and vice versa. In the lumbar spine, the facets are arranged in the sagittal plane and often there is adjacent pedicle involvement. This patient has a classic presentation of a mechanically insufficient pedicle from invaded tumor within the pedicle itself and into the neural foramen space, manifested as severe radicular pain elicited by axial loading of the spine.1,2,4 3. Evaluation of spinal stability is an important consideration independent from both the cancer and neurological assessments. Pathological fracture from tumor and traumatic fracture represent different pathologies and thus have distinct biomechanical implications. The Spinal Oncology Research

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Group developed and tested a scoring system, the Spinal Instability in Neoplasia Score (SINS), to aid in determining the stability of the spine in neoplastic disease. This system uses six domains: location, pain, bone lesion character, radiographic spinal alignment, degree of vertebral body collapse, and the degree of posterolateral involvement of the spinal elements (Figure 17.2).5,6

Figure 17.2  SINS system: Spinal Instability Neoplastic Score. 4. If a neoplastic process is suspected based on initial non-​contrast lumbar MRI, then a gadolinium-​enhanced MRI of the complete spine should be

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obtained to rule out involvement of the spine at other locations. Additionally, a computed tomography (CT) scan of the chest/​abdomen/​pelvis or positron emission tomography-​CT (PET-​CT) can be obtained to assess systemic disease burden. 5. If multiple myeloma is suspected, serum and urine electrophoresis for assessment of a monoclonal hypergammaglobulinemia or urinary Bence-​ Jones protein can aid in diagnosis. IgG followed by IgA protein spikes are most commonly seen on electrophoresis, evident in up to 80% of patients. Hypercalcemia, hyperuricemia, and increased alkaline phosphatase can all be diagnostic clues.7 6. Metastatic lesions, multiple myeloma, and other lymphoproliferative tumors are the most common malignant tumors of the spine. The differential diagnosis of an enhancing soft tissue lesion arising from the bone marrow of a vertebral body and involving the pedicles, epidural, and paraspinal spaces include metastasis, hematopoietic neoplasia, chondrosarcoma, chordoma, osteosarcoma, and liposarcoma in order of decreasing frequency.8

Decision-​Making

In this case, a 71-​year-​old woman presents with an L3 pathologic burst fracture involving her pedicles, there exists epidural extension of the mass, and resultant thecal sac and nerve root compression manifests with mechanical back pain and radiculopathy. Further workup reveals positive Bence-​Jones urinary protein and an IgG spike on protein electrophoresis. CT of the chest, abdomen, and pelvis did not demonstrate additional disease. There are many factors to consider in the treatment of this patient with a spinal tumor. After initial radiographic diagnosis, a biopsy may be required in order to make a diagnosis, especially if a primary spinal tumor is suspected. In this case, the protein electrophoresis facilitated the diagnosis of multiple myeloma. A decision-​making framework called NOMS (Neurologic, Oncologic, Mechanical and Systemic) facilitates and guides therapeutic decisions for patients with spinal metastases. This decision-​making tool is designed for use in a multidisciplinary fashion by surgeons in conjunction with medical and neuro-​oncologists, interventionalists, pain physicians, and radiation oncologists (Figure 17.3).9 The neurologic assessment consists of evaluating the patient for evidence of myelopathy or cauda equina syndrome and the extent of radiographic epidural spinal cord compression (ESCC). The ESCC scale facilitates reporting of the degree of spinal cord compression (Figure 17.4).4 In our case, the patient had radiculopathy without signs of myelopathy or cauda equina syndrome. In general, the oncologic assessment within the NOMS framework consists of determining the histology-​ specific expected degree of tumor response to conventionally fractionated external beam radiation (cEBRT) and systemic therapy.9 In considering our patient’s oncologic status, she has laboratory and diagnostic testing suggestive of multiple myeloma, a tumor which is amenable to treatment with conventional radiotherapy (Figure 17.5).9 Radiation therapy effectively treats biologic pain. The mechanical assessment

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Figure 17.3 The NOMS framework: Neurologic, Oncologic, Mechanical and Systemic.

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3 0

1c 1b 1a

2

Schematic representation of the 6-point ESCC grading scale. Grade 0 Grade 1a Grade 1b Grade 1c Grade 2 Grade 3

Bone-only disease Epidural impingement, without deformation of thecal sac Deformation of thecal sac, without spinal cord abutment Deformation of thecal sac with spinal cord abutment, without cord compression Spinal cord compression, with cerebral spinal fluid (CSF) visible around the cord Spinal cord compression, no CSF visible around the cord

Figure 17.4  Epidural Spinal Cord Compression Grading Scale.

requires careful evaluation for the presence of movement-​associated pain and determination of tumor-​associated mechanical instability is facilitated by the SINS scoring system.5,6 Since radiotherapy and systemic therapy do not restore mechanical stability of the spine, patients with mechanical instability require stabilization. Assessment of mechanical instability as an independent factor in surgical decision-​ making even for radiosensitive tumors can be of great benefit to patients.1,2 SINS scoring for assessment of spinal stability in this patient yields a potentially unstable score of 12 (Location = 2 [mobile lumbar spine], Pain = 3 [mechanical], Lesion = 2 [lytic], radiographic spinal alignment  =  0 [minimal de novo deformity], vertebral body collapse = 2 [involvement of the vertebral body with less than 50% height loss], posterolateral involvement of spinal elements  =  3 [bilateral pedicle involvement]). A significant number of patients will score in the SINS 7–​12 range, indeterminate or potentially unstable, and that’s where additional information such as the character and circumstances of the patient’s pain aid in the assessment of spinal stability and suitability for surgical intervention. Patients who have no radiculopathy at rest, but which is then invariably elicited on sitting or standing, or back pain that is most severe when changing position from lying to sitting and from sitting to standing make excellent candidates for surgical stabilization and are thought to have mechanical pain. In the authors’ single-​center study of patients with mechanical pain, nearly 98% of patients had improvement in their mechanical pain with spinal fixation.2 Radiographically, these tumors often manifest as burst fractures with some degree of posterior element involvement. The mechanical problem arises when a pedicle and/​ or facet complex is compromised by tumor infiltration rendering these structures unable to maintain the patency of the neural foramen with axial load stress. Hence,

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Figure 17.5  Summary of expected radiation response by histology.

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when patients load the facet when standing or sitting, there is foraminal collapse and impingement of the exiting nerve root.2,4 To summarize, this patient has spinal instability and mechanical radiculopathy as a result of a myelomatous L3 pathologic burst fracture with high-​grade epidural extension. Neurologically, she has back pain and radiculopathy without cauda equina syndrome and high-​grade epidural disease. Oncologically, her treatment will consist largely of radiation and systemic therapy. Independent of her oncologic treatment, on mechanical assessment, she has a SINS of 12 with mechanical radiculopathy, indicating she would benefit from surgical stabilization. Systemically, there are no major contraindications to surgery or immediate concerns about the durability of her disease control. There are multiple options for surgical stabilization including external orthosis alone, or kyphoplasty or vertebroplasty alone or in addition to short-​or long-​segment open or percutaneous posterior fixation with or without cement augmentation. Percutaneous cement augmentation represents an excellent stabilization option for fractures confined to the vertebral body.10 However, pathologic compression fractures that extend into the posterior elements (pedicle and joint) require stabilization of the posterior elements using posterior instrumentation.1 Surgical excision of the tumor is not required since durable local control is expected after cEBRT and systemic therapy. Therefore, the primary goal of surgical intervention is restoration of mechanical stability. Surgery should be designed to expedite systemic and radiation therapy. The patient in this case was offered cement-​augmented, short-​segment percutaneous transpedicular fixation with kyphoplasty for the symptomatic level at L3. Questions

1. What are the treatment options for this patient’s L3 pathologic burst fracture? 2. What are some of the considerations that might inform your decision-​making? 3. Is surgical fixation, kyphoplasty, or radiotherapy the superior treatment of this disease? 4. If radiotherapy is used, should it be conventional fractionated radiotherapy or stereotactic radiosurgery (SRS)?

Surgical Procedure

The patient is positioned prone on an open Jackson operating table or other table with a radiolucent frame. Care is taken to pad all pressure points. Leads for intraoperative free-​ running electromyography (EMG), somatosensory evoked potentials, and transcranial motor evoked potentials are placed. The patient is prepped and draped in the standard fashion. Fluoroscopy or neuronavigation may be used to guide the Jamshidi needles for the placement of the instrumentation and cement-​injection cannulas (Figure 17.6). Kirschner wires are then passed through L2 and L4 pedicles, dilators are utilized serially, and the cannulated pedicles are tapped. In general, 6.5  mm × 45  mm screws are used throughout the midlumbar spine. Cannulated pedicle screws are placed over the Kirschner wires and advanced to near the anterior vertebral body cortical margin.

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Figure 17.6  Intraoperative fluoroscopy for guidance of Jamshidi needle placement (A, anteroposterior [AP] view). Lateral fluoroscopic views of Kirschner wires (B) and cement cannulas (C) as they are passed through L2 and L4 pedicles. Balloon kyphoplasty (C) followed by cement injection (D) viewed via lateral fluoroscopy. Cannulated pedicle screws are placed over the Kirschner wires and advanced to near the anterior vertebral body cortical margin. Cement injection, in order to improve the bony purchase in patients with osteoporotic vertebrae, may be carried out prior to placement of the screws. The wires are removed and rods are placed percutaneously and secured to the pedicle screws using locking set screws (E).

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Cement injection, in order to improve the bony purchase in patients with osteoporotic vertebrae, may be carried out prior to placement of the screws. Fenestrated screws that permit cement injection after the screw is placed facilitate cement augmentation of the screws and decrease the risk of cement extravasation. The wires are removed (Figure 17.6). Care is taken not to overdrive the screw and to maintain the polyaxial nature of the tulip head. Cement augmentation of the vertebral body fracture may be carried out using balloon kyphoplasty or vertebroplasty technique (Figure 17.6). A series of fluoroscopic images aids in early identification of any cement extravasation. Approximately 2.5–​3.5 mL of cement is used to fill the fracture cleft and restore vertebral body integrity (Figure 17.6). Rods are placed percutaneously and secured to the pedicle screws using locking set screws. Meticulous hemostasis is obtained.The wounds are irrigated with antibiotic solution, and vancomycin powder is used at level of the hardware. The fascia and subcutaneous tissues are closed with 0 and 2-​0 absorbable suture in an interrupted fashion, and the subcuticular layer closed with interrupted 3-​0 absorbable suture. The skin is closed with 4-​0 Monocryl suture in a subcuticular fashion. In patients requiring longer constructs, a midline skin incision with multiple transfascial incisions may provide improved cosmesis and healing.

Oral Boards Review: Surgical Management Pearls

1. Cement augmentation of the pedicle screws provides improved pull-​ out strength and decreased screw subsidence in patients with cancer and osteoporosis. 2. Neurophysiological monitoring including free-​running EMG and nerve stimulation can help to avoid suboptimally placed instrumentation. 3. Ensuring optimal cement viscosity and serial fluoroscopy during cement augmentation of fenestrated transpedicular instrumentation and kyphoplasty can help avoid extravasation of cement into the central canal or neural foramen as well as embolization of cement material.

Aftercare

Postoperatively, patients undergo close neurologic observation. Steroids are continued in the perioperative period to reduce swelling and improve radicular pain. Postoperative films are obtained as a baseline for future comparison (Figure 17.7). Radiation oncology is involved early in the patient’s postoperative course so that conventional radiotherapy can begin shortly after surgery, often within 1–​2 weeks. In the case of more radioresistant histology, SRS can be given within 7–​10 days of surgery. Most importantly, care is taken to minimize undue delay in the initiation of systemic therapy. Surveillance MRI scans are obtained every 2 months following surgery and treatment.

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Figure 17.7  Lateral (A) and anteroposterior (AP) (B) plain films and T2 axial (C) and sagittal (D) magnetic resonance images (MRIs) through the index level approximately 3–​4 weeks after spinal instrumentation and conventional radiotherapy. ESCC, epidural spinal cord compression; SRS, stereotactic radiosurgery; SINS, Spinal Instability Neoplastic Score; NOMS, Neurologic, Oncologic, Mechanical, and Systemic scoring.

Complications and Management

Surgery for radiosensitive spinal tumors can be complicated by pseudarthrosis or wound dehiscence, both sequelae of postoperative radiation therapy. Often, a solid bony lion does not occur and the surgical construct should be strong enough to function on its own and not necessarily rely upon bone formation. Wound complications can be prevented by careful communication with the oncology team members regarding timing of adjuvant treatments and involvement of wound care specialists.

Oral Board Reviews: Complications Pearls

1. Bony fusion at the site of the tumor stabilization is a rare event since radiation therapy and systemic therapy severely impair arthrodesis. Therefore, spinal constructs should be designed to provide stand-​alone stabilization. Utilization of larger rod diameters (e.g., 6.5 mm) and cement reinforcement of the pedicle screws may improve the durability of spinal instrumentation in patients with metastatic spinal tumors. 2. Additional consideration should be made to wound closure techniques that minimize the risk of wound dehiscence or infection. In the setting

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of wound dehiscence or infection, early involvement of plastic surgeons is recommended. 3. Progression of disease can be managed with salvage open surgery and decompression with or without intraoperative brachytherapy followed by re-​ irradiation when applicable.

Evidence and Outcomes

The NOMS framework takes advantage of the increasingly multidisciplinary nature of the treatment of patients with neoplastic spine disease and allows for the incorporation of newer treatments and technologies as they become available, adapting as treatment paradigms shift. It is important to note that surgery for the treatment of spinal metastases is palliative. For solid cancers, 2-​year survival from the time of a cancer diagnosis for most patients is in the range of 10–​20%, although with immunologic and targeted therapies this may be improving.9 In the case of lymphoproliferative neoplastic disease like multiple myeloma, with current medical therapies including bone marrow transplant 10-​year survival approximates 30%. The primary indication for spinal surgery among patients with multiple myeloma is restoration of mechanical stability, which results in pain control and improvement in quality of life. Surgery for maintenance or improvement of neurological status and local disease control is rarely required in patients with radiosensitive tumors such as multiple myeloma.9 From a neurologic and oncology perspective, patients with multiple myeloma, even in the setting of spinal cord compression, respond readily to conventional fractionated radiotherapy, both clinically and radiographically. However, in the setting of progressive neurologic deterioration secondary to spinal cord compression, surgical decompression may be beneficial for rapid decompression of the spinal cord and optimization of neurologic function restoration. More often, patients with multiple myeloma are operated on for mechanical instability, as was the case with our patient. With respect to mechanically unstable patients with pathological vertebral compression fracture and radiosensitive histology, cement-​augmented, short-​segment percutaneous fixation with kyphoplasty has been shown to decrease the proportion of patients in severe pain from 86% to 0%, with as many 65% of patients reporting no pain referable to instability postoperativly.1 For pathologic vertebral compression fractures of all histologies associated with deformity or debilitating pain refractory to opioid analgesics and corticosteroids, there is class 1 data that demonstrate pain-​and back-​specific functional status is significantly improved at 1 month in those who undergo balloon kyphoplasty when compared to patients who are managed without intervention.10 In contrast, for patients with solid tumor metastases resulting in ESCC and/​or neurologic deficit, Roy Patchell et al. published class I evidence for direct surgical decompression.11 Patients in this study who were randomized to receive 30 Gy conventional radiotherapy in addition to direct surgical decompression fared better with respect to recovery and maintenance of ambulation and preservation of bladder and bowel function, as well as subsequent decreased need for corticosteroids and narcotic medications

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than patients who received 30 Gy conventional radiotherapy alone.11 Importantly, 70% of these patients had local recurrence at 1-​year postoperative evaluation. More recently, advancements in radiation technology, instrumentation, and surgical technique have led to the development of newer approaches for treatment of ESCC from metastatic disease, with a trend toward less surgical morbidity, less invasive surgery, and a greater reliance on radiosurgical therapy (SRS) for local disease control.With high enough single-​fraction or hypofractionated SRS, ablative doses of radiation may be delivered to cancer histologies previously thought of as radioresistant (Figure 17.5). SRS in the range of 18–​27 Gy provided in 1–​3 fractions have yielded radiographic progression-​free survival ranging from at least 84% at 2 years to potentially as high as 96% at 3 years in retrospectively reviewed large multi-​institutional series comprised of all solid tumor histologies.12,13 In another analysis of patients with ESCC and instability manifesting in mechanical radiculopathy, “separation” surgery followed by posterior instrumented fixation resulted in 98% of patients reporting improvement in pain and a 41% improvement in performance status as determined by Eastern Cooperative Oncology Group (ECOG) scoring.2 In so-​called separation surgery, a posterolateral approach is utilized to obtain ventrolateral access to nerve roots, the posterior longitudinal ligament, and, most importantly, ventral epidural disease. Circumferential decompression and reconstitution of the thecal sac is achieved such that high-​dose single-​fraction or hypofractionated radiosurgery can be given to remaining disease. “Separation” surgery followed by SRS within our institution yielded an 84% 1-​year progression-​free survival rate on evaluation of one of the earlier cohorts in our experience.14 Recent cohorts have demonstrated even higher progression-​free survival at 2 and 3 years and will be reported shortly (unpublished data). The NOMS framework is broadly applicable to spinal neoplastic disease of radiosensitive and radio-​resistant histology and is able to incorporate new technologies and shifting disease management paradigms. References and Further Reading

1. Moussazadeh N, Rubin DG, McLaughlin L, Lis E, Bilsky MH, Laufer I. Short-​segment percutaneous pedicle screw fixation with cement augmentation for tumor-​induced spinal instability. Spine J Off J North Am Spine Soc. 2015;15(7):1609–​1617. doi:10.1016/​j.spinee.2015.03.037. 2. Moliterno J,Veselis CA, Hershey MA, Lis E, Laufer I, Bilsky MH. Improvement in pain after lumbar surgery in cancer patients with mechanical radiculopathy. Spine J Off J North Am Spine Soc. 2014;14(10):2434–​2439. doi:10.1016/​j.spinee.2014.03.006. 3. Downie A, Williams CM, Henschke N, et al. Red flags to screen for malignancy and fracture in patients with low back pain: Systematic review. BMJ. 2013;347:f7095. 4. Bilsky M, Smith M. Surgical approach to epidural spinal cord compression. Hematol Oncol Clin North Am. 2006;20(6):1307–​1317. doi:10.1016/​j.hoc.2006.09.009. 5. Fourney DR, Frangou EM, Ryken TC, et al. Spinal instability neoplastic score: An analysis of reliability and validity from the spine oncology study group. J Clin Oncol Off J Am Soc Clin Oncol. 2011;29(22):3072–​3077. doi:10.1200/​JCO.2010.34.3897. 6. Fisher CG, DiPaola CP, Ryken TC, et al.A novel classification system for spinal instability in neoplastic disease: An evidence-​based approach and expert consensus from the Spine Oncology Study Group. Spine. 2010;35(22):E1221–​E1229. doi:10.1097/​BRS.0b013e3181e16ae2.

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7. Bilsky MH, Azeem S. Multiple myeloma: Primary bone tumor with systemic manifestations. Neurosurg Clin N Am. 2008;19(1):31–​40. doi:10.1016/​j.nec.2007.09.001. 8. Rodallec MH, Feydy A, Larousserie F, et al. Diagnostic imaging of solitary tumors of the spine: What to do and say. RadioGraphics. 2008;28(4):1019–​1041. doi:10.1148/​rg.284075156. 9. Laufer I, Rubin DG, Lis E, et al.The NOMS framework: Approach to the treatment of spinal metastatic tumors. Oncologist. 2013;18(6):744–​751. doi:10.1634/​theoncologist.2012-​0293. 10. Berenson J, Pflugmacher R, Jarzem P, et al. Balloon kyphoplasty versus non-​surgical fracture management for treatment of painful vertebral body compression fractures in patients with cancer: A multicentre, randomised controlled trial. Lancet Oncol. 2011;12(3):225–​235. doi:10.1016/​S1470-​2045(11)70008-​0. 11. Patchell RA, Tibbs PA, Regine WF, et  al. Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: A randomised trial. Lancet. 2005;366(9486):643–​648. doi:10.1016/​S0140-​6736(05)66954-​1. 12. Guckenberger M, Mantel F, Gerszten PC, et al. Safety and efficacy of stereotactic body radiotherapy as primary treatment for vertebral metastases: A multi-​institutional analysis. Radiat Oncol Lond Engl. 2014;9:226. doi:10.1186/​s13014-​014-​0226-​2. 13. Yamada Y, Lovelock DM,Yenice KM, et al. Multifractionated image-​guided and stereotactic intensity-​modulated radiotherapy of paraspinal tumors:  A preliminary report. Int J Radiat Oncol Biol Phys. 2005;62(1):53–​61. doi:10.1016/​j.ijrobp.2004.09.006. 14. Laufer I, Iorgulescu JB, Chapman T, et al. Local disease control for spinal metastases following “separation surgery” and adjuvant hypofractionated or high-​dose single-​fraction stereotactic radiosurgery: Outcome analysis in 186 patients. J Neurosurg Spine. 2013;18(3):207–​214. doi:10.3171/​2012.11.SPINE12111.

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Cauda Equina Syndrome Emily P. Sieg, Justin R. Davanzo, and John P. Kelleher

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Case Presentation

A 34-​year-​old woman with no past medical history presents to the emergency department with acute loss of motor function and significant radicular type pain in both lower extremities. In addition, she was noted to have significant urinary retention and loss of rectal tone with bowel incontinence. A detailed neurologic examination is performed which reveals 5/​5 motor strength in the bilateral upper extremities; 2/​5 motor strength in the bilateral iliopsoas, quadriceps, and hamstrings; and 0/​5 motor strength in the bilateral tibialis anterior, gastrocnemius, and extensor hallucis longus. Sensory examination reveals normal sensation in the bilateral upper extremities and decreased sensation to light touch and pin prick throughout the bilateral lower extremities. Testing of reflexes revealed 2+ reflexes in the bilateral upper extremities and absent patellar and ankle jerk reflexes bilaterally. A urinary catheter is placed with return of 1,000 mL of clear, yellow urine. A rectal exam reveals absence of rectal tone. Questions

1. What is the most likely diagnosis? 2. What imaging modality should be used to confirm this diagnosis? 3. What anatomic location should be imaged based on this constellation of symptoms? 4. What is the most appropriate timing of the diagnostic workup for this patient?

Assessment and Planning

This constellation of symptoms is most consistent with cauda equina syndrome. The cauda equina is a group of nerves in the lumbosacral spine that provide motor and sensory function to most of the lower extremities, pelvic floor musculature, and sphincters. Cauda equina syndrome (CES) arises secondary to compression of or injury to these roots.The signs and symptoms of this disease include lower extremity motor and sensory dysfunction, autonomic dysfunction (including loss of bowel and bladder control), and pain. While these symptoms are most consistent with CES, other pathologies must be on the differential diagnosis. Most importantly, compression of the cervical or thoracic spinal cord must be considered. Other pathologies such as multiple sclerosis, neoplasms, and vascular malformations should also be included in the differential.

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A multitude of pathologies can lead to CES, and distinguishing between these pathologies is important as it may lead to dramatically different treatment strategies. It is of paramount importance to determine if the etiology is compressive or noncompressive in nature as this is the primary determinant with regards to the need for surgical management. Compressive etiologies are far more commonly the cause of CES, the most common of which is a midline disc herniation. This can lead to either the acute or subacute development of CES. Spinal stenosis can lead to a more chronic development of CES. It is also important to note that, in the setting of significant spinal stenosis, even a small disc herniation can lead to the acute development of CES. Other compressive causes of CES include spinal fractures with retropulsion, hematomas, iatrogenic (i.e., hardware failure), vascular lesions (i.e., arteriovenous malformations), and neoplastic lesions (i.e., schwannomas, ependymomas, metastases). Noncompressive causes of CES include ischemic insults and inflammatory conditions. While these are much less common, it is important to keep them in mind as their treatment is often nonsurgical in nature. When a patient presents with acute loss of motor and sensory function in the lower extremities, the first step in diagnostic evaluation is often a computed tomography (CT) scan of the lumbar spine.While this will rule out any bony cause of compression, it does not have the resolution to show compression due to soft tissue, such as an intervertebral disc. Thus, any patient with this constellation of symptoms should undergo magnetic resonance imaging (MRI) of the lumbar spine. In a normal T2-​weighted axial image, the cauda equina appears as a number of hypointense circular structures, which are the nerve roots, within a large area of hyperintensity, the cerebrospinal fluid (CSF)-​filled thecal sac. Typically, areas of hyperintensity can be seen between each of the nerve roots. With compression significant enough to cause CES, there is usually a complete loss of this hyperintense CSF, especially between the nerve roots. When working up a patient with new onset of motor and sensory loss, it is important to consider imaging of the brain and cervical and thoracic spine as well. This is of greater significance if the lumbar spine MRI is unrevealing or if symptoms suggestive of cervical or thoracic myelopathy are present on exam. In the case at hand, MRI of the lumbar spine revealed an acute disc herniation at the L4–​L5 level with complete obliteration of the CSF space (Figure 18.1).

Oral Board Review: Diagnostic Pearls

1. Timely acquisition of the MRI of the lumbar spine is important in the setting of CES. Not only does this confirm the suspected diagnosis, but it also reveals the level of the disease if needed for surgical planning. 2. In patients who cannot undergo MRI, a CT myelogram should be obtained to confirm the diagnosis as well as the level of disease. 3. If the routine workup, including MRI of the rest of the neuroaxis, is negative, other diagnostic considerations should include lumbar puncture for acquisition of CSF and vascular imaging to rule out arteriovenous malformation.

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Figure 18.1  (A) Sagittal T2-​weighted magnetic resonance image (MRI) of the lumbosacral spine revealing a disc herniation at the L4–​L5 level causing significant mass effect on the thecal sac. (B) Axial T2-​weighted MRI of the lumbosacral spine at the L4–​L5 level showing an acute disc herniation with complete obliteration of the cerebrospinal fluid space and severe nerve root compression.

Questions

1. How do the findings on MRI and clinical exam influence surgical planning? 2. Based on the case presentation, what is the most appropriate timing for surgical intervention to optimize patient outcome? 3. In the setting of acute disc herniation, what consideration needs to be given to stabilization techniques?

Decision-​Making

In the setting of acute loss of motor, sensory, or autonomic function and a disc herniation noted on lumbar spine MRI, emergent decompression via laminectomy should be undertaken. Partial or incomplete CES, when patients have difficulty voiding or urinary frequency and resultant urinary retention, is often a precursor to complete CES. Since recovery is less certain once nerves have become extensively damaged, surgical intervention early in partial CES is recommended. While most would recommend that this decompression for both partial and complete CES be done as soon as possible, patients should never wait more than 48 hours from their presentation to undergo decompression in acute CES. By delaying decompression, the risk of permanent damage to the nerve roots is increased. This could lead to long-​term loss of motor, sensory, or autonomic function. The main surgical option in this case is lumbar laminectomy at the level of the disc herniation to decompress the nerve roots. In addition, with an acute disc herniation, a micro-​discectomy is typically performed. Consideration can be given to performing the decompression via a minimally invasive technique in which the primary goal becomes

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removal of the herniated disc fragment to decompress the nerve roots. However, in an emergent setting, most experts recommend performing this operation via a traditional open technique. Prior to surgery, the risk and benefit profile for this particular disease state and surgical procedure should be discussed with the patient.The risks of this procedure include bleeding, infection, damage to the nerve roots, CSF leak, and need for further surgical intervention. When discussing the need for future surgical intervention, consideration must be given to the need for spinal fusion. If the laminectomy performed at the time of surgery needs to be particularly wide, including removal of parts of the facet joints or pars interarticularis, over time, the patient may develop degeneration at this level requiring spinal fusion. Most often, spinal fusion is not required at the time of initial decompression for CES, especially when this is secondary to an acute disc herniation; however, there are situations where this should be considered, especially in neoplastic disease processes resulting in instability. Questions

1. What intraoperative techniques should be used to localize the appropriate level of operation? 2. If an acute disc herniation cannot be located, what steps should be taken to ensure an adequate decompression has been performed?

Surgical Procedure

Once CES is diagnosed based on both clinical examination and imaging, emergency surgical decompression within 48 hours is recommended. Several surgical options exist depending on patient pathology, including laminectomy with or without discectomy. The mainstay of treatment in patients presenting with CES due to lumbar stenosis or a lumbar disc is posterior laminectomy and decompression in order to relieve the pressure on the nerves. If CES is caused by a more complicated structural lesion, such as a retropulsed bone fragment in the setting of trauma, chronic inflammation, tumor invasion, or metabolic disease such as lipomatosis, the addition of concurrent instrumentation or an anterior staged procedure in the future should be considered. Premorbid conditions as well as age should be considered when determining the anesthetic plan. A lumbar laminectomy can be done either under general anesthesia or using a spinal epidural if patient is high risk for anesthesia. A urinary catheter should be placed preoperatively due to the high risk of urinary retention and bladder distention in the setting of CES. Fluoroscopy should be available for localization of level, and the need for neurophysiologic intraoperative monitoring should be considered. The patient should be positioned prone on a Wilson or Jackson table. The Wilson frame allows for flexion of the lumbar spine which opens the posterior elements, while the Jackson table maintains more normal lumbar lordosis. All pressure points should be carefully padded to prevent pressure sores and peripheral neuropathies. Pressure on the abdomen should be checked preoperatively after final positioning as excessive abdominal compression can make epidural bleeding more difficult to control due to venous congestion.

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A linear midline incision should be made after a spinal needle is used to obtain x-​ray verification that the level is appropriate. Subperiosteal dissection then removes the erector spinae muscles from the lamina. Care should be taken to remain in this subperiosteal plane to minimize bleeding. Dissection is then carried out laterally to the medial aspect of the facet joint complex and the bilateral pars are exposed. It is important not to violate the facet joint capsule as this significantly increases the risk of instability. A Leksell rongeur is then used to remove the spinous processes, and a high-​speed drill is used to thin out the lamina. A Kerrison rongeur can then be used to complete the remainder of the boney laminectomy as well as removal of the ligamentum flavum. The lateral recesses are then decompressed using a Woodson elevator and Kerrison rongeur. In the setting of a disc herniation leading to CES, the thecal sac should then be retracted medially using a nerve root retractor. An 11 blade is used to incise the posterior longitudinal ligament and the disc annulus, and an upgoing curette in combination with a pituitary rongeur is used to remove the disc material. The surgeon should always be aware of where the anterior longitudinal ligament is in order to prevent accidental injury to the retroperitoneal vessels. Once the disc has been removed, a nerve hook should be used to feel under the posterior longitudinal ligament (PLL) and a Woodson elevator should be passed over the dura to feel and for any residual fragments. Hemostasis should be obtained using bipolar electrocautery and hemostatic agents. Bone wax should be used to help obtain hemostasis at boney edges. Once immaculate hemostasis has been achieved, the wound should be copiously irrigated. A  subfascial drain may be used. It is more likely to be required if multiple levels are involved and can help with wound healing and prevention of postoperative epidural hematoma. Attention is then turned to closing. Tight fascial closure is important to minimize wound dehiscence and other postoperative wound complications. The fascia should be closed with 0 or 2-​0 absorbable sutures. The subcutaneous layer is closed with interrupted inverted 3-​0 absorbable sutures. The skin should then be closed in standard fashion.

Oral Boards Review: Management Pearls

1. If the patient has advanced degenerative disease, spondylolysis, or spondylolisthesis on flexion-​extension, imaging should be obtain preoperatively to rule out spinal instability. 2. Adequate hemostasis should always be obtained using hemostatic agents to prevent postoperative epidurals. If minor bleeding persists, a subfascial drain should be considered. 3. When using the 11 blade to incise the disc, always go medial to lateral thus incising away from the dura.

Pivot Points

1. Use caution to avoid decompression or dissection that is too lateral and leads to destruction of the facet, pars interarticularis, or facet capsule thus potentially causing instability requiring a spinal fusion.

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2. Due to severe compression of the thecal sac, these patients are at high risk for dural tear. Drilling the lamina to a thin shelf before carefully using a combination of a curette and Kerrison punch can help minimize this. 3. The ligamentum flavum ends at the superior aspect of the lamina, leaving the dura unprotected in this area and making the risk of durotomy higher at this location. Additional care should be taken to ensure the dura is protected.

Aftercare

Postoperatively, a detailed neurologic examination of both upper and lower extremity sensory and motor function should be done and documented as soon as possible. Many surgeons require that these patients remain in a horizontal position for the first 24 hours, to help prevent a CSF leak or pseudomeningocele if there was a known intraoperative durotomy. While flat, the urinary catheter is typically left in place. Patients without a CSF leak should be encouraged to ambulate as early as postoperative day 0. Early ambulation helps prevent atelectasis, pneumonia, deep venous thrombosis, and pulmonary embolus. Physical therapy and occupational therapy consults should be considered. Stool softeners should be used to prevent postoperative ileus. Once the urinary catheter has been removed, postvoid residuals should be followed and straight catheterization or catheter replacement used as needed to prevent bladder distension. Perioperative antibiotics are generally given and should not be continued beyond 24 hours in a routine case. Narcotic pain medications are often needed, as well as muscle relaxants. Tylenol as well as nonsteroidal antiinflammatory medications should be considered to decrease narcotic needs. Nonsteroidal antiinflammatory medications should not be used if a fusion is done. Although short-​term recovery of bladder function often lags behind reversal of lower extremity motor deficits, the function may continue to improve up to 18–​24 months after surgery. In the postoperative period, drug therapy combined with catheterization can help with a slow recovery of bladder and bowel function. Complications and Management

Potential complications range from structural damage intraoperatively to more general postsurgical complications and can occur intraoperatively or in a delayed fashion. Direct injury to nerve roots can lead to new or worsening neurologic deficits or neuropathic pain. A dural tear can lead to an immediate or delayed CSF leak requiring either primary repair or re-​exploration. If a durotomy is seen at the time of surgery and a primary repair is done, a Valsalva should be performed to assess for any continued leak. The need for postoperative flat bed rest should be considered at the discretion of the surgeon depending on the integrity of the repair. Poor surgical positioning can lead to compressive neuropathies or pressure sores. Postoperative complications can be related directly to the procedure or to general hospital complications. Wound infections, urinary tract infections, atelectasis, and pneumonia can all be the cause of postoperative fevers or leukocytosis. An epidural hematoma 180

 

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or CSF collection can lead to recompression requiring a surgical revision. Deep vein thrombosis is a potential complication that can be minimized by early ambulation if possible. Delayed complications seen in clinic range from continued pain to spinal instability. In the setting of radicular or neuropathic pain with no evidence of nerve compression on MRI, the addition of gabapentin or pregabalin (Lyrica) should be considered. If the patient presents with continued back pain, dynamic imaging should be obtained. Instability may warrant instrumentation and fusion.

Oral Boards Review: Complications Pearls

1. In the case of a CSF leak, use of a lumbar drain to remove tension on the wound should be considered. 2. If the patient develops new or worsening symptoms postoperatively, an immediate scan should be obtained to rule out a compressive hematoma or CSF collection. 3. If the patient complains of persistent or worsening back pain at postoperative visits, dynamic imaging should be obtained to rule out instability requiring instrumented fusion.

Evidence and Outcomes

CES is rare, and the evidence for the timing of surgical intervention is thus poor quality. It depends almost exclusively on retrospective observational studies that show a low level of evidence, grade III or IV. A logistic regression analysis of previously published studies by Ahn et al. in 2000 of 322 CES patients concluded that although there was a significant advantage to treating patients before versus after 48 hours from symptom onset, there was no difference in outcomes when comparing patients treated before 24 versus at 24–​48 hours. Criticism of Ahn’s review includes the fact that both acute and nonacute patients were included in the analysis. In a 2014 meta-​analysis by Chau et al., the authors concluded that there is no strong evidence to support 48 hours as a safe time point for surgical delay. They argued that both early and delayed surgery may result in improved neurologic outcomes; however, it is more likely that earlier surgical intervention is more beneficial, especially in the setting of acute neurologic compromise. Operating on CES patients at the earliest opportunity seems to be the most appropriate clinical practice. References and Further Reading

Ahn UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JP. Cauda equina syndrome secondary to lumbar disc herniation:  A meta-​analysis of surgical outcomes. Spine. 2000;25:1515–​1522. Chau AM, Xu LL, Pelzer NR, Gragnaniello C. Timing of surgical intervention in cauda equina syndrome: A systematic critical review. World Neurosurg. 2014 Mar–​Apr;81(3-​4): 640–​650. doi: 10.1016/​j.wneu.2013.11.007. Epub Nov 13, 2013. Review. PubMed PMID: 24240024.

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Fehlings MG, Zeidman SM, Rampersaud YR. Cauda equina syndrome. In:  Benzel EC, ed. Spine Surgery. Techniques, Complications, Avoidance and Management. Philadelphia, PA: Elsevier Churchill Livingstone; 2005. Qureshi A, Sell P. Cauda equina syndrome treated by surgical decompression: The influence of timing on surgical outcome. Eur Spine J. 2007;16(12):2143–​2151.

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Lumbar Stenosis Miner N. Ross and Khoi D. Than

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Case Presentation

A 68-​year-​old man is referred to a neurosurgeon for a chief complaint of heaviness in his legs. He noted the onset of this symptom, accompanied by a feeling of “tightness” in his lower back, roughly 1 month ago. There was no inciting event or trauma. He feels a constant, dull, aching heaviness that radiates from his lower back into both of his lateral thighs, although the left leg is somewhat worse than the right. None of his symptoms extends below his knees. This is exacerbated particularly by climbing stairs, as well as by standing or walking for prolonged periods, and is alleviated by sitting or lying down. He feels that his gait is stiff due to these symptoms and has also noted decreased endurance while exercising on his stationary bicycle. These symptoms have been progressively worsening and detracting from his quality of life. He denies any changes in his bowel or bladder habits. This patient’s past medical history includes hypertension, hyperlipidemia, gout, and obstructive sleep apnea, which are all under adequate control. He has osteoarthritis of both knees, for which he has undergone bilateral arthroscopy; he has no other surgical history relating to his back or legs. By the time of his presentation, he had already attempted physical therapy, which provided minimal improvement, as well as acupuncture, which relieved his back pain but not his lower extremity symptoms. On neurological examination, he has full strength of all major muscle groups as well as intact sensation throughout. The patellar and Achilles reflexes are diminished bilaterally; there is no Babinski sign or clonus present. Coordination is normal, as is regular gait; however, he is observed to have difficulty with tandem gait. Questions

1. What is the most likely diagnosis? 2. What imaging modality will be most helpful in making the diagnosis? 3. What anatomical areas must be imaged? 4. What is the appropriate timing of the diagnostic workup?

Assessment and Planning

This patient’s history is strongly suggestive of neurogenic claudication, a common presentation of symptomatic lumbar canal stenosis. As the lumbar and sacral nerve roots descend through the stenotic canal, their blood supply is compromised, and this ischemia is thought to give rise to pain, weakness, and sensory changes of the lower extremities.

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Classically, the symptoms of claudication are worsened by activity and relieved at rest, but they are also sensitive to positional changes of the spine. In extension, as in walking downhill or lying flat, the lumbar canal is narrowed further, whereas in flexion the canal is opened and symptoms are relieved. For instance, many patients will report that they need to lean on a shopping cart to complete a trip through the grocery store. Subacute to chronic onset of symptoms is more typical of claudication than of cauda equina or conus medullaris syndromes, which are surgical emergencies and invariably accompanied by acute bowel and bladder incontinence and saddle anesthesia due to compression of sacral nerve roots. Neurogenic claudication can be confused with vascular claudication due to arterial insufficiency, but this is generally excluded prior to referral to a neurosurgeon. A significant history of cardiovascular disease, diminished or absent peripheral pulses, or an abnormal ankle-​brachial index (ABI) of blood pressures should prompt reconsideration of a vascular diagnosis. Claudication due to lumbar stenosis may occur in isolation, as in the case example, or it may be accompanied by radicular symptoms. The pathologic processes (degeneration, trauma, infection) that can cause stenosis of the lumbar canal can similarly affect the lateral recesses or neural foramina. Magnetic resonance imaging (MRI) is the mainstay imaging technique for evaluation of the spine. It is excellent at visualizing the neural elements of the spinal cord and nerve roots, as well as the intervertebral discs and soft tissues. Canal stenosis is often identified due to a disc bulge or extrusion, chronic degenerative spondylosis, ligamentum flavum hypertrophy, or spondylolisthesis. In patients who are unable to undergo MRI, computed tomography (CT) myelography can be considered. Failure of the myelography dye to migrate cranially (i.e., a myelographic block) indicates a level of severe stenosis. For patients with identified spondylolisthesis, flexion-​extension plain films should be obtained to assess for pathologic motion, the presence or absence of which will guide surgical planning. In this patient, MRI of the lumbar spine demonstrated severe central as well as bilateral foraminal stenoses at L2–​L3 and L3–​L4; at L4–​L5 and L5–​S1 he had bilateral foraminal stenoses as well as grade I spondylolistheses of L4 on L5 and L5 on S1. See Figure 19.1A, B for sagittal and axial MRI slices. Flexion-​extension films in this case did not show any dynamic instability.

Oral Boards Review: Diagnostic Pearls

1. Lumbar stenosis does not usually cause focal neurological exam findings. In the presence of focal pain, sensory changes, or weakness of the lower extremities, attention should be given to the nerve roots or the peripheral nerves as a source for the findings. 2. The symptoms of lumbar stenosis are subacute to chronic in onset. In patients with sudden onset of weakness, numbness, or in those with bowel or bladder dysfunction, more urgent diagnoses such as cauda equina syndrome or conus medullaris syndrome should be ruled in or out expediently. 3. MRI is the first-​line imaging modality for evaluating neurological disorders of the lumbar spine. CT and plain films can aid in evaluation and surgical planning in select cases.

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A

B

Figure 19.1  (A) T2-​weighted sagittal magnetic resonance image (MRI) demonstrating this patient’s canal stenosis, most notable at L2–​L3. (B) T2–​weighted axial MRI through the L2-​L3 disc space. Note broad-​based stenosis extending into the lateral recesses as well as poor visualization of cerebrospinal fluid around the lumbosacral nerve roots. Questions

1. How do these radiologic findings direct surgical planning? 2. What is the appropriate timing of intervention in this patient?

Decision-​Making

Lumbar canal stenosis is diagnosed by imaging, with MRI being the gold standard. Neurogenic claudication is diagnosed by careful history-​taking, as described in the case presentation, typically in conjunction with a benign neurological examination.The corroboration of imaging findings with the patient’s described symptoms provides a surgical indication. It is entirely possible to have imaging findings of lumbar stenosis in an asymptomatic patient; likewise, patients may have many stenotic levels but only one that is the cause of their symptoms. A careful attempt should be made to determine where, and how much, to operate. Patients with degenerative spondylosis will frequently have more than one complaint. They may describe radicular symptoms in addition to those of neurogenic claudication. With appropriate imaging findings for foraminal stenosis, these patients can be offered a foraminotomy in addition to a laminectomy. A not-​infrequent finding of an extruded disc fragment may occur and cause or contribute to the symptoms of lumbar stenosis as well as lateral recess or foraminal stenosis. In these patients, a discectomy could be performed as well. Axial back pain is common but unlikely to respond to any surgical intervention; thus, in cases where this is the predominant complaint, surgery may be of very limited benefit to the patient. Lumbar stenosis is often managed conservatively, especially given that it tends to develop in an older population where patients may have comorbidities that make them poor surgical candidates. Conservative management may include nonsteroidal

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antiinflammatory medications, exercise, physical therapy/​rehabilitation, steroid injections, massage, yoga, or acupuncture. As these techniques are of minimal risk to the patient, it is reasonable to trial several of them before considering surgery. In most cases, primary care providers do not make the referral to a spine surgeon until conservative management has failed. Questions

1. What represents an appropriate trial of conservative management? 2. How should surgery be approached in a patient with multiple complaints related to the lumbar spine?

Surgical Procedure

Surgical decompression of the stenotic lumbar canal is best accomplished by laminectomy at the affected level or levels. This procedure can be performed in the traditional open fashion or with the use of more modern minimally invasive techniques. Prone positioning can be aided by the use of a Wilson frame, which can be opened to induce kyphosis that will open the interlaminar spaces. Fluoroscopy is obligatory for the proper localization of the level or levels to be operated on and can also be employed at the conclusion of the decompression to verify that no radiographic stenosis remains. The use of neuromonitoring is at the discretion of the surgeon, but in a case where no hardware is being placed and the decompression is extradural, it is unlikely to influence the outcome of the case. For an open procedure, once the correct levels are located fluoroscopically, a midline incision is made and a subperiosteal dissection is carried out using monopolar electrocautery to expose the spinous process and lamina bilaterally at each level to be decompressed. The interspinous ligaments above and below the level should be transected, and then a Leksell rongeur can be used to remove the spinous process. The remainder of the bony decompression can be accomplished with a high-​speed drill followed by the use of a Kerrison rongeur for more careful bone removal. It is helpful to leave the ligamentum flavum intact during this stage as it will protect the dura during the bone removal. Ultimately, the ligamentum flavum should also be removed, as it often contributes to canal stenosis even in the absence of bony compression. This can be accomplished with a combination of blunt dissection with a nerve hook as well as taking small pieces with a Kerrison rongeur. The adequacy of decompression can be verified by palpation with a nerve hook rostrally and caudally as well as out into the lateral recesses and foramina. Nerve hooks can be placed into the margins of the decompression and a fluoroscopic x-​ray taken to verify the radiographic extent of the decompression. Alternatives to nerve hooks include curettes and/​or Woodson elevators, depending on surgeon preference. If a durotomy is incurred, it can be repaired primarily by suturing, with or without a muscle graft, and a fibrin-​based sealant can be applied over the closure. Meticulous hemostasis should be achieved prior to wound closure to prevent formation of a spinal epidural hematoma. For wound protection and improved functional outcomes, the paraspinal muscles should be reapproximated.

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Many variations on the basic technique of laminectomy exist. In open laminectomy, some surgeons prefer to make partial laminectomies above and below the interlaminar space, with the idea of preserving the spinous processes and their ligamentous attachments (i.e., the posterior tension band). Hemilaminectomy (approaching from one side only) can provide adequate decompression if care is taken to drill under the contralateral lamina and remove all of the ligamentum flavum. Minimally invasive surgery through a tubular retractor relies on this concept and can provide excellent results in one-​or two-​ level decompressions. Minimally invasive surgery offers the advantages to the patient of smaller incisions and decreased muscle dissection, which reduces postoperative pain and allows faster return to activity.

Oral Boards Review: Management Pearls

1. There are multiple surgical approaches to lumbar decompression; selecting the correct approach for each patient depends on understanding the history, the imaging, and patient-​specific factors as they contribute to surgical risk. 2. The ligamentum flavum can be a major contributor to canal stenosis, and decompression is not complete unless it is removed.

Pivot Points

1. A patient presenting with bowel or bladder incontinence with saddle anesthesia has cauda equina syndrome until proven otherwise, and this surgical emergency should be ruled out before other evaluation is undertaken. 2. Patients with primarily axial back pain, without a significant history of neurogenic claudication, are unlikely to benefit from lumbar decompression even if they have radiographic stenosis on MRI. 3. Fusion may be considered in patients who have significant spondylolisthesis or pathologic motion where these are felt to be contributors to their clinical picture.

Aftercare

Most postoperative patients are able to mobilize within hours of surgery. Consultation with rehabilitation providers such as physical therapists may be helpful postoperatively, depending on each patient’s prior level of functioning. Antibiotics do not need to be continued beyond the intraoperative period. Pain can be managed with moderate-​ strength opioid medications in conjunction with acetaminophen, and muscle relaxers can be added as needed. A single overnight stay in the hospital following surgery provides a reasonable length of time over which to observe patients for any complications. One-​or two-​level open and minimally invasive cases can be discharged on the same day as surgery. Follow-​up imaging is typically not necessary in uncomplicated cases. Indeed, postsurgical changes make any spine MRI obtained within a short interval of surgery difficult to interpret.

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A follow-​up visit in the clinic setting for wound healing and pain management review is appropriate within 2–​3 weeks. Complications and Management

The most common intraoperative complication of lumbar decompression is an unintentional durotomy. However encountered or repaired in the operating room, most surgeons will opt to keep the patient on flat bed-​rest for 24 hours during recovery. The conventional wisdom holds that this decreases the pressure in the lumbar cistern until the durotomy closes, thereby decreasing the risk of cerebrospinal fluid (CSF) leak or pseudomeningocele formation. There is limited evidence for or against this practice, but the challenges of managing CSF leaks encourage caution when a durotomy is incurred. Some evidence does suggest that early mobilization in patients treated minimally invasively is well tolerated, as the amount of dead space into which CSF can leak is less. The most serious postoperative complications of lumbar decompression will manifest as a decline in the patient’s neurological exam. New or worsening weakness or sensation loss in the lower extremities is concerning for a compressive lesion affecting the lumbosacral nerve roots. Spinal epidural hematoma is the most feared of these; it can even present as a new-​onset cauda equina syndrome. Suspicion of an epidural hematoma necessitates emergent imaging and likely operative re-​exploration. A postsurgical abscess or a symptomatic pseudomeningocele can also present in this manner, but more often in a delayed fashion. Pain, paresthesias, or weakness in a dermatomal distribution may represent a nerve root that was injured in the course of surgery. These symptoms can be managed expectantly. A short course of steroids may be of benefit for patients in significant distress. Lumbar surgical incisions are at increased risk for wound complications due to being on a less visible part of the body, as well as being subject to the chafing of clothes and pressure when sitting or lying down. Surgical washout and revision may be necessary in cases of dehiscence or where a deep tissue infection is suspected. Superficial infections often respond well to a course of oral antibiotics directed at common skin flora.

Oral Boards Review: Complications Pearls

1. A durotomy should be repaired and is often managed with 24 hours of strict bed-​rest, but long-​term outcomes are equivalent in patients with and without a durotomy. 2. Any decline in a postsurgical patient’s neurological examination should be evaluated promptly as it will likely require operative management.

Evidence and Outcomes

Limited evidence is available comparing surgical intervention versus conservative management in lumbar stenosis. Amassing enough data for a systematic review is

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hindered by the lack of a well-​defined paradigm for conservative management as this may include a wide variety of medications and techniques that are themselves of varying effectiveness. Recent comparisons of minimally invasive surgical techniques with those of traditional open laminectomy are proving favorable. Minimally invasive surgery is frequently able to accomplish an equivalent decompression with less postoperative pain, a shorter hospital stay, and a lower risk for complications. Conventional open surgery as well as minimally invasive surgery should be complementary tools in the spine surgeon’s armamentarium. References and Further Reading

Machado GC, et  al. Surgical options for lumbar spinal stenosis. Cochrane Database Syst Rev. 2016;11:CD012421. Naraim AS, et al. Minimally invasive techniques for lumbar decompressions and fusions. Curr Rev Musculoskelet Med. 2017;10:559–​566. Overdevest G, et al. Effectiveness of posterior decompression techniques compared with conventional laminectomy for lumbar stenosis. Eur Spine J. 2015;24:2244–​2263. Zaina F, et al. Surgical versus non-​surgical treatment for lumbar spinal stenosis. Cochrane Database Syst Rev. 2016;1:CD010264.

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L4–​L5 Degenerative Spondylolisthesis Rani Nasser, Scott Zuckerberg, and Joseph Cheng

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Case Presentation

A 59-​year-​old woman with no significant past medical history presents with bilateral radicular leg pain (right worse than left), as well as axial back pain. She describes the radicular component of her pain as progressive over 9 months, and the axial back pain as constant over 4 years. The radicular pain crosses below the knee to the medial foot. Moreover, the shooting pain is greater than her axial back pain. She is only able to ambulate two blocks without her legs “giving out.” Leaning forward, such as leaning over a shopping cart, gives her transient relief. She has not had any success with conservative measures such as physical therapy or epidural steroid injections. On physical examination, she is full strength in all muscle groups, with good muscle bulk and intact reflexes. However, she had decreased light touch in her right medial foot. Questions

1. What is the most likely diagnosis? 2. What is the highest yield imaging modality? 3. What are the initial steps in management?

Assessment and Planning

Based on the clinical picture, the clinician may suspect foraminal narrowing.These findings are substantiated by the foraminal stenosis, as well as the L4–​L5 spondylolisthesis noted on computed tomography (CT) (Figure 20.1) and MRI (Figure 20.3). When assessing a spondylolisthesis, the clinician should suspect an underlying pars interarticularis defect (Figure 20.2). In addition, dynamic imaging may be beneficial to assess movement of the spondylolisthesis (Figure 20.4). This may guide management toward fusion as oppose to decompression alone. Decision-​Making

The initial management of patients presenting with axial back pain with radicular symptoms is largely conservative in the absence of neurological deficit.1 If the patient has persistent or progressive symptoms despite conservative measures, surgical decompression and/​or stabilization might be indicated.The Spine Patient Outcomes Research Trial (SPORT) was a 13-​center randomized cohort study comparing surgical with

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Figure 20.1  Sagittal computed tomography (CT) scan: L4–​L5 grade 1 spondylolisthesis.

Figure 20.2  Sagittal computed tomography (CT) scan: Right pars interarticularis visualized without defect (right). Left pars interarticularis visualized also without defect or fracture (left).

 

Figure 20.3  Sagittal magnetic resonance imaging (MRI) (left to right) demonstrating foraminal stenosis without significant central canal stenosis.

Figure 20.4  Flexion (left) and extension (right) lumbar x-​rays, not demonstrating any pathological movement.

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nonoperative management of degenerative spondylolisthesis.2 This study demonstrated that, after 4  years, patients treated surgically had substantially increased pain relief as compared to patients managed nonoperatively.2 Patients with a symptomatic L4–​L5 degenerative spondylolisthesis who are refractory to conservative management have been shown to have a beneficial treatment effect based on the SPORT trial (Treatment Effect = Change in Surgical Oswestry Disability Index − Nonoperative Change in Oswestry Disability Index).3 The decision to offer a laminectomy alone as oppose to a laminectomy and fusion must be carefully considered by the clinician. The degree of spondylisthesis may influence the surgeon’s decision-​ making toward offering a fusion.4 This, in concert with the degree of facet arthropathy, may also potentially destabilize a patient if he or she is treated with laminectomy alone.5 Ultimately, the decision to fuse/​decompress or decompress alone must be assessed on a case-​by-​case  basis. Surgical Procedure

If the surgeon opts to fuse and decompress a degenerative L4–​L5 spondylolisthesis, multiple options are available. Based on the surgeon’s preference, the patient may be stabilized using an open or minimally invasive transforaminal lumbar interbody fusion (TLIF), posterior lumbar interbody fusion (PLIF), or even posterolateral fusion with pedicle screw fixation. If the patient is positioned on an open Jackson table, they will fall into alignment, and often low-​grade spondylolisthesis maybe reduced by positioning alone.6 Special attention should be given to the padding on the anterior superior iliac spine (ASIS) and greater trochanter, so the patient is not rotated. Fusing a patient in a suboptimal position could lead to patient discomfort and construct failure. After positioning, a confirmatory x-​ray may help confirm proper alignment. During the standard subperiosteal dissection, care must be taken not to disturb the adjacent facets as this may accelerate their degeneration. Once the pars interarticularis–​transverse process junction is exposed, a match stick burr or awl maybe used to decorticate the pedicle screw starting point. Using a pedicle finder (straight sharp), the pedicle maybe cannulated with little force perpendicular to the plane of the superior articulating process. The surgeon may check the depth with a ball probe at 20  mm, to ensure no medical breaches. Afterward, the surgeon may medialize further and check again for breaches at 40 mm. Injecting a hemostatic matrix into the cannulated hole often controls bleeding. The surgeon at this point may decide to use pedicle markers with a confirmatory intraoperative CT spine or proceed to place the instrumentation. When deciding on a pedicle thread, it is beneficial to allow space for a rescue screw in the event of future revisions. Furthermore, depending on the degree of spondylolisthesis, the surgeon may opt to use reduction screws to help reduce the slip. Interbody fusion may augment the construct as well as help restore lordosis while reducing the slip (Figure 20.5).7 The decision on whether to place interbody via a transforaminal technique may vary, but meticulous endplate preservation is a key factor throughout all these techniques.8 In addition to restoring the natural disc height, the interbody graft will also indirectly decompress the foramina. The choice in graft

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Figure 20.5  Postoperative sagittal computed tomography (CT) scan demonstrating L4–​L5 transforaminal lumbar interbody fusion (TLIF) with complete facetectomy and reduction of spondylolisthesis.

footprint and shape may vary; however, the more anterior the graft is placed, the more lordosis maybe achieved.9 The surgeon may decide to augment the interbody fusion with a posterolateral arthrodesis. Once the L4 and L5 transverse processes are exposed and decorticated, autograft from the decompression or allograft maybe packed into the gutter. The rods should be as short as possible to not disturb the adjacent levels. Often, for a one-​level fusion, these rods are precut. When attempting to reduce an L4–​L5 spondylolisthesis, the L5 set screw should be placed bilaterally, anchoring the rod that has been shaped into lordosis. Once that is preliminarily secured, the L4 screw may be reduced to the rod using a tower reducer and then finally tightened. If neurophysiological monitoring is used, the technician should be notified before and after reduction. Aftercare

On postoperative day 1, the hematocrit and hemoglobin should be monitored as well drain output (if used). If the patient is meeting her goals, the Foley maybe removed and the patient should be allowed to ambulate with physical therapy. On postoperative day 2, intravenous narcotics should be weaned to oral medications, and the diet should be advanced. If the patient is unable to ambulate because of persistent pain and discomfort, a chemical deep vein prophylaxis in addition to mechanical prophylaxis may be considered.10 Postoperative imaging maybe obtained before discharge if intraoperative imaging was not acquired.

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Complications and Management

Intraoperative complications such as a dural tear should be repaired primarily if possible. If cerebrospinal fluid leak persists, a lumbar drain maybe considered.11 Postoperatively, the patient should follow-​up for standard wound checks to ensure there is no dehiscence or infection. If there is suspected drainage, an MRI may be helpful to rule out a deeper collection. Moreover, the patient should follow up with plain film x-​rays at 4 weeks and 3 months to monitor the hardware (if instrumented). Evidence and Outcomes

SPORT was a combined prospective randomized controlled and observational cohort study which determined the treatment effect of surgical versus nonsurgical management in patients with degenerative spondylolisthesis.2 The treatment effect (TE) was described as the change in Oswestry Disability Index (surgery) minus Change in Oswestry Disability Index (nonoperative).2 Across 13 centers, 395 patients were treated surgically as opposed to 210 who were managed conservatively. After 4 years, all the patients with degenerative spondylolisthesis in the surgical group had overall improvement in TE as compared to the nonsurgical group.2 References and Further Reading

1. Matsudaira K, Hara N, Oka H, et al. Predictive factors for subjective improvement in lumbar spinal stenosis patients with nonsurgical treatment: A 3-​year prospective cohort study. PloS One. 2016;11:e0148584. 2. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical compared with nonoperative treatment for lumbar degenerative spondylolisthesis. Four-​year results in the Spine Patient Outcomes Research Trial (SPORT) randomized and observational cohorts. J Bone Joint Surg (Am Vol). 2009;91:1295–​1304. 3. Pearson AM, Lurie JD, Tosteson TD, Zhao W, Abdu WA, Weinstein JN. Who should undergo surgery for degenerative spondylolisthesis? Treatment effect predictors in SPORT. Spine. 2013;38:1799–​1811. 4. Gandhoke GS, Kasliwal MK, Smith JS, et al. A multi-​center evaluation of clinical and radiographic outcomes following high-​g rade spondylolisthesis reduction and fusion. J Spinal Dis Techn. 2014. 5. Blumenthal C, Curran J, Benzel EC, et al. Radiographic predictors of delayed instability following decompression without fusion for degenerative grade I  lumbar spondylolisthesis. J Neurosurg. Spine. 2013;18:340–​346. 6. Asiedu GB, Lowndes BR, Huddleston PM, Hallbeck S. “The Jackson Table is a pain in the . . . ”: A qualitative study of providers’ perception toward a spinal surgery table. J Patient Safety. 2016. 7. Glassman SD, Carreon LY, Ghogawala Z, McGirt MJ, Asher AL. Benefit of transforaminal lumbar interbody fusion vs posterolateral spinal fusion in lumbar spine disorders: A propensity-​ matched analysis from the National Neurosurgical Quality and Outcomes Database Registry. Neurosurgery. 2015.

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8. Kuraishi S,Takahashi J, Mukaiyama K, et al. Comparison of clinical and radiological results of posterolateral fusion and posterior lumbar interbody fusion in the treatment of L4 degenerative lumbar spondylolisthesis. Asian Spine J. 2016;10:143–​152. 9. Shau DN, Parker SL, Mendenhall SK, et al.Transforaminal lumbar interbody graft placement using an articulating delivery arm facilitates increased segmental lordosis with superior anterior and midline graft placement. J Spinal Dis Techn. 2015;28:140–​146. 10. Wang TY, Sakamoto JT, Nayar G, et  al. Independent predictors of 30-​day perioperative deep vein thrombosis in 1346 consecutive patients after spine surgery. World Neurosurg. 2015;84:1605–​1612. 11. Kamenova M, Leu S, Mariani L, Schaeren S, Soleman J. Management of incidental dural tear during lumbar spine surgery. To suture or not to suture? World Neurosurg. 2016;87:455–​462.

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Isthmic Spondylolisthesis Evan Lewis and Charles A. Sansur

21

Case Presentation

The patient is a 57-​year-​old woman with a 3-​year history of low back pain and bilateral leg pain. Over the past 5 months she has developed progressive weakness in her feet and has an occasional trip due to her right foot being sporadically weak. Her past medical history is negative other than hypothyroidism. She has normal body mass index (BMI) and does not perform regular exercise. She works as a salesperson at a local large retailer. She smokes a half-​pack of cigarettes per day. On examination she has 4+/​5 ankle dorsiflexion weakness and extensor hallucis longus weakness bilaterally. She has a 1+ Achilles tendon reflexes bilaterally, and she has decreased sensation to light touch in the dermatomes of L4 and L5. Questions

1. What is the appropriate clinical workup, and what imaging modalities are required? 2. What is the differential diagnosis for a person with this presentation? It is appropriate to ask this patient if there are certain positions and/​or activities that improve or worsen her symptoms. It is important to assess what therapy she has had thus far. If the patient has not been prescribed physical therapy (PT) at this point, she should get a referral for PT. If she has not already tried nonsteroidal antiinflammatory drugs (NSAIDs), these should be recommended. She should be advised to stop smoking. She should be advised to engage in daily walks and core strengthening exercises to improve her overall spine support. Imaging at this point should start with plain x-​rays of the lumbar spine in the standing position with anteroposterior (AP) and lateral views, as well as dynamic studies with flexion and extension views. Because the patient has a neurological deficit, one can make the argument to request a non-​contrasted magnetic resonance imaging (MRI) study in addition to assessing for nerve compression after x-​rays have been completed. This patient had MRI (Figure 21.1) demonstrating severe bilateral facet arthropathy at L4–​L5 with resultant lateral recess stenosis. The primary differential diagnosis for a patient with this presentation should include lumbar stenosis, lumbar spondylosis, lumbar spondylolisthesis, and lumbar disc herniation. Lower on the list of the differential diagnosis is a neoplastic process, infection, and a vascular lesion such as arteriovenous fistula.

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Figure 21.1  Preoperative unenhanced T2-​weighted magnetic resonance image (MRI). (A) Axial section thorough L4–​L5 disc space. (B) Midline sagittal image.

Assessment and Planning

It was determined that the patient has resolution of her leg pain when she lies on her side and flexes forward. X-​rays demonstrate a grade 1 L4–​L5 spondylolisthesis with bilateral L4 pars defects. The flexion and extension films reveal 7  mm of movement between flexion and extension. The patient has near total resolution of sagittal malalignment with extension. Appropriately exercise, smoking cessation, PT, and NSAIDs were recommended. A follow-​up outpatient visit in 2–​3 months to was established to reassess the patient’s neurological status and degree of benefit from the recommended treatment strategy. Questions

1. What type of isthmic spondylolisthesis does this patient have? 2. What additional nonsurgical treatment options does this patient have? 3. At what point should you recommend surgical treatment?

Oral Board Reviews: Diagnostic Pearls

Wiltse et  al. have created a classification system for isthmic spondylolisthesis etiologies. This patient has a type A, or lytic, isthmic spondylolisthesis. Type B isthmic spondylolisthesis is characterized by an elongated pars, and type C consists of an acute pars fracture. In the absence of severe neurologic findings, surgery should never be the initial recommendation for intervention. Patients need to undergo conservative treatment for at least 3  months prior to consideration of surgery. This patient was instructed to quit smoking and to engage in activities to develop her core musculature, including physical therapy. If, after the patient completes this course of

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conservative treatment, she still continues to be debilitated by her symptoms, one can start to offer more invasive treatment strategies. These options may consist of epidural injections or facet rhizotomies. In the event that these treatments are not desired by the patient, or in the event that they do not successfully control the patient’s symptoms, surgical intervention is a reasonable treatment. At this point, because surgery is being offered, most spine experts would advocate for the patient to obtain additional x-​rays of the whole spine to assess global sagittal and coronal alignment. Decision-​Making

A variety of acceptable surgical options exist for this patient. These options include decompression without fusion, decompression with instrumented fusion from a posterior approach (with or without interbody grafting), decompression and fusion through combined lateral interbody approach and posterior approach, decompression and fusion using a combined anterior and posterior approach, and, finally, anterior or lateral stand-​ alone interbody fusion. The benefits of decompression without fusion include maintenance of motion and decreased risk of adjacent segment degeneration, while risks include inadequate relief of back pain and worsening deformity. The advantages of decompression with instrumented fusion from a posterior approach (with or without interbody grafting) would be the opportunity to address the patient’s back pain and radicular pain through a single approach. This approach also allows the surgeon to correct the spondylolisthesis, perform a wide decompression, and utilize the transverse processes for a posterolateral fusion. The disadvantages of this approach are higher blood loss (for an open case), limited ability to improve lumbar lordosis, and a decreased surface area for interbody bone fusion when compared to anterior interbody surface area. The advantages of fusion through a combined lateral interbody and posterior instrumented fusion would be the ability to correct the deformity, obtain an indirect decompression, and obviate the need for a posterior decompression. There would be a greater surface area for interbody fusion and likely decreased blood loss. There still is an opportunity to perform a posterior fusion. The disadvantages of this approach would be potential injury to the lumbosacral plexus and risk of injury to the great vessels. The advantages of fusion through an anterior approach with or without posterior instrumentation include the ability to correct the spondylolisthesis and obtain an indirect decompression, as above. Also, as in the lateral approach, there would be a greater surface area for interbody fusion and decreased blood loss. There still is an opportunity to perform a posterior fusion.The risks include potential injury to the lumbosacral plexus and risk of injury to the great vessels. There also is a risk of hernia formation if inadequate closure of the abdominal wall is performed. Surgical Procedure

Several of the already mentioned approaches utilize similar posterior access to the spine: decompression without fusion, decompression with fusion, or augmentation of fusion with interbody. These procedures all begin in a similar fashion. First the

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patient is positioned in the prone position on a Jackson table with chest, hip, and thigh pads. A fluoroscope is utilized to mark the appropriate levels. The surgical site is then prepped and draped in the usual sterile fashion. Incision is made sharply using a scalpel. Dissection is carried out with Bovie electrocautery. The fascia is divided over the spinous processes, and subperiosteal dissection is continued down the lamina. The dissection is stopped at the medial edge of the facet capsule and a L4 laminectomy is completed for patients undergoing decompression alone. Dissection is carried out over the joint capsule if the decision for fusion has been made. Care is taken to preserve the facet capsule of the L3–​L4 joint, and the L4–​L5 joint capsule is removed. Dissection is carried out over the transverse processes of L4 and L5. Attention is turned to pedicle instrumentation at this point. Pedicle screws can be placed either anatomically or radiographically. The entry point for the pedicle screw is at the convergence of the mid-​point of the transverse process and the pars interarticularis. Quite often, a mammillary process can be identified at this junction. A pilot hole is created at this point, and, using a blunt Lenke pedicle finder, the pedicle is cannulated. The tract is then palpated using a ball-​tip probe to assess for any breaches. Next, the tract is tapped and the process of assessing for breaches is repeated. Finally, the appropriate length and width pedicle screw is inserted. Once the instrumentation is in place, decompression can be carried out. Due to the addition of instrumentation, a more complete decompression can be carried out that may include a total facetectomy. Once the decompression has been completed, the rods can be secured. Attention is turned to arthrodesis, which is completed by decorticating the transverse processes bilaterally, and morselized autograft can be packed into the posterior lateral gutters. If an interbody is desired, this can be placed by one of two methods prior to placing the rods. Posterior lumbar interbody fusion (PLIF) does not require access to the foramina. The thecal sac is retracted medially, exposing the disc space. A box annulotomy is made in the disc space using a scalpel. Sequential paddle shavers are used to perform a discectomy in a piecemeal fashion. Upon removal of the disc, the endplates are thoroughly prepared. The PLIF cage is then malleted into position. Often bilateral PLIF cages are inserted. The transforaminal lumbar interbody fusion (TLIF) is carried out in a similar manner except some or all of the facet is removed, giving access to the disc space through the foramina, and a single cage is placed in a more oblique orientation (Figure 21.2). The operative incision is then closed. Care is taken to reapproximate the muscle and fascia with interrupted absorbable sutures. Next the dermis is closed using interrupted buried absorbable sutures and the skin is then closed. For an anterior approach, the patient is placed in the supine position on a Jackson flat-​top table.The anterior approach often utilizes the assistance of a vascular surgeon for the exposure. Commonly, a paramedian incision, lateral to the umbilicus, is made. When the layers of the abdominal wall have been penetrated, the peritoneum is retracted medially exposing the aorta and iliac vessels at the bifurcation.The great vessels are mobilized to grant exposure to the L4–​L5 disc space. A box annulotomy is created in the disc and the disc is removed in piecemeal fashion using curettes and pituitary rongeurs. An appropriately sized interbody graft is placed to provide distraction and indirect decompression.

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Figure 21.2  Postoperative x-​rays demonstrating pedicle screw fixation with Polyether ether ketone (PEEK) interbody. (A) Anteroposterior (AP) view. (B) Lateral view.

An integrated interbody with screws or a plating system can be utilized to secure the construct.

Oral Boards Review: Management Pearls

1. Preservation of the cephalad facet capsule reduces that likelihood of adjacent segment disease. 2. During the approach, exposure of the cephalad transverse process (TP) is often more difficult due to the anterior translation of the vertebral body. As such, careful attention must be paid to avoid nerve injury of exiting nerve during TP exposure. 3. It is important to perform a wide decompression of the exiting nerve roots before attempting to reduce the spondylolisthesis.Very often, reduction pedicle screws many facilitate reduction of the spondylolisthesis for higher grade cases.

Pivot Points

1. If, upon total facetectomy, there is no ability to correct spondylolisthesis, then discectomy and use of interbody grafting may facilitate correction. 2. If there is no motion or correction of slip with interbody grafting, then fusion in situ is appropriate. 3. If during a planned decompression without fusion the patient is found to have intraoperative instability, one should consider instrumented fusion.

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Aftercare

Postoperatively, the patient is recovered in the postanesthesia recovery room. Postoperative antibiotics should be continued for no longer than 24 hours. Plain x-​rays either during or after surgery are standard to assess hardware position. No further imaging studies are required unless a change in neurological exam is detected. Patients should be encouraged to ambulate as soon as possible. Efforts should be made to minimize bending, lifting, and twisting activities for fusion patients. Pain management can be obtained with opioids for the immediate postoperative period. NSAIDs should be avoided in fusion patients. Patients should be followed-​up in clinic for a wound check in 14 days and then again in several weeks. AP and lateral radiographs should be obtained for fusion patient to assess the hardware construct. Patients with decompression only with lack of resolution of pain or recurrent pain should undergo standing flexion/​extension radiographs to assess for instability or progression of spondylolisthesis. Physical therapy is often important in the aftercare to improve the patient’s core strength and ability to tolerate daily activities. Complications and Management

Cerebrospinal fluid (CSF) leak is a potential complication of spinal surgery with estimated incidence that varies widely throughout the literature. Durotomies are more frequent in revision cases. Many different techniques and algorithms have been described for management of CSF leaks. Primary closure of the durotomy with suture is recommended when possible. If not feasible, tight muscle and facial closure is recommended. Postoperative positioning for CSF leaks should be supine to reduce pressure in the lumbar cistern. CSF diversion may be considered for complex dural tears. Adjacent segment disease (ASD) is a problem associated with both instrumented and noninstrumented fusion. It results in accelerated degeneration of the adjacent motion segment. Different techniques, including dynamic fusion methods, have yet to demonstrate any reduction in ASD. Attention to preserve the cephalad facet capsule is important to reduce the chance of developing ASD.Treatment of ASD starts with nonoperative management, such as injections, NSAIDs, and physical therapy. If conservative therapy fails, extension of fusion to include the adjacent segment is considered.

Oral Boards Review: Complications Pearls

1. To properly close a durotomy, it is often necessary to allow more spinal fluid to drain to further empty the thecal sac because this will help prevent the nerves from drifting toward the durotomy. 2. Infection can often be addressed in the acute setting with a wound washout, with preservation of the hardware.

Evidence and Outcomes

There is controversy regarding fusion techniques in the treatment of spondylolisthesis. A 2016 study in The New England Journal of Medicine by Forsth et al. suggested that there was no difference in patients who underwent decompression alone versus decompression

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and fusion in the subset of patients with lumbar spondylolisthesis and claudication. Another study presented in the same journal by Ghogawala et al. was a randomized trial focusing on patients specifically with spondylolisthesis, and this study demonstrated significantly better outcomes in the fusion group at 2 years. There is some evidence to suggest that spondylolisthesis when treated with instrumentation and interbody arthrodesis has more favorable outcomes when compared to patients who underwent posterolateral fusion alone. References and Further Reading

Alentado V, et al. Independent predictors of clinically significant improvement after lumbar fusion surgery. Spine J. 2016 Sept 21. Forsth P, et al. A randomized, controlled trial of fusion surgery for lumbar spinal stenosis. N Engl J Med. 2016 Apr 14:374(15): 1413–​1423. Ghogawala Z, et al. Laminectomy plus fusion versus laminectomy alone for lumbar spondylolisthesis. N Engl J Med. 2016 Apr 14:374(15): 1424–​1434. Glassman SD, et  al. Benefit of transforaminal lumbar interbody fusion vs posterolateral spinal fusion in lumbar spine disorders:  A propensity-​ matched analysis from the National Neurosurgical Quality and Outcomes Database Registry. Neurosurgery. 2016 Sep:79(3):397–​405.

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Lumbar Degenerative Scoliosis Michael LaBagnara, Durga R. Sure, Christopher I. Shaffrey, and Justin S. Smith

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Case Presentation

A 79-​year-​old man presents with low back and right buttock pain, which extends to his right posterior thigh. The leg pain usually stops at the knee, but occasionally extends to his posterior calf and the plantar surface of his foot. Symptoms started approximately 2 years ago without an inciting event and have been progressively worsening. He reports that 40% of his overall pain is in his lower back, and 60% is in his right leg. Symptoms are worse with prolonged standing and walking and are relieved by bending forward or laying supine. Two years ago, he was able to walk several miles before having to stop and rest. Now he states he can barely walk a quarter-​mile before the heaviness in his legs and his back pain force him to rest. He is able to walk longer distances when using a shopping cart at the store. Up until 2 years ago, he was an avid cyclist and would ride 18–​30 miles per week. His symptoms have made cycling impossible. He denies any history of bowel or bladder incontinence and denies any altered sensation in his extremities. He states that his right foot has felt weak for more than a year. He underwent 6 weeks of ground-​based and aquatics-​based physical therapy 1 year ago without improvement and has had two lumbar epidural steroid injections without relief. His past medical history is significant for hypertension, gout, rheumatoid arthritis, osteopenia, bicuspid aortic valve, atrial fibrillation, aortic aneurysm, coronary artery disease, and hypothyroidism. His past surgical history includes coronary artery bypass graft, aortic repair, aortic valve replacement, left hip replacement, tonsillectomy, adenoidectomy, cholecystectomy, right knee arthroscopy, and SA node ablation. Detailed neurological examination reveals full strength in all extremities with the exception of 4/​5 right ankle dorsiflexion, 4+/​5 plantar flexion, and 4/​5 right extensor hallucis longus (EHL). Sensation to light touch and pin prick is preserved throughout. Deep tendon reflexes are 2+ in his upper extremities and 1+ in bilateral lower extremities. Toes are down-​going bilaterally. He has moderate difficulty moving from a seated position to standing, and his standing posture is preferentially bent forward. He is able to stand more erect, but states this worsens his back pain. Tandem gait is steady, with mild slapping of the right foot. He is able to elevate onto the toes and heel of his left foot, but unable to do either on the right.There is no tenderness to palpation over his bony spine; however, the lumbar spine is palpable eccentric to the right of midline.

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Questions

1. What is the most likely diagnosis? 2. What is the most appropriate imaging modality or modalities?

Assessment and Planning

This 79-​year-​old man has symptomatic lumbar spondylosis, lumbar spinal stenosis, and degenerative lumbar scoliosis. His claudication symptoms are relieved by sitting or bending forward, which is consistent with neurogenic claudication.This is in contrast to vascular claudication, the symptoms of which would typically be relieved by rest alone. His partial right foot drop suggests stenosis affecting the L5 nerve root, and his plantar flexion weakness suggests stenosis affecting the S1 root. The palpable bony spine eccentric to the midline suggests scoliosis of the lumbar spine.

Oral Boards Review: Diagnostic Pearls

1. Detailed history and physical exam are essential for reaching the correct diagnoses: a. Lumbar spinal stenosis: The patient’s history of a progressive decline in his ability to stand or walk, secondary to “heaviness” of his legs, suggests narrowing of the central canal in the lumbar spine. b. Spondylosis: Radiographic spondylosis is an expected finding in this patient’s age group. The presence of radicular symptoms and their laterality suggest asymmetric pathology. c. Scoliosis: Palpation of the bony spine should be a routine part of every neurologic examination. Deviation of the spine away from midline suggests underlying scoliosis. Palpation of the spine may be difficult in patients with larger body habitus. 2. Advanced imaging with either non-​contrast magnetic resonance imaging (MRI) or computed tomography (CT) myelogram should be obtained to evaluate the extent of disease and to formulate an interventional plan. 3. Standing long-​cassette radiographs (posteroanterior [PA] and lateral) should be obtained to assess global spinal alignment. Limited imaging of the spine, with either radiographs or advanced imaging modalities, may result in treatment plans based on insufficient information and potentially result in less than ideal outcomes.1 Even without the palpable deformity on this patient’s physical exam, surgeons should maintain a low threshold for obtaining standing long-​cassette radiographs.1 4. Dual-​energy x-​ray absorptiometry (DEXA) bone densitometry should be obtained in adult patients undergoing spinal deformity surgery, especially in older patients and those previously diagnosed with osteopenia or osteoporosis. The results may influence decision-​making with respect to implant selection, timing of surgery, or both. In the setting of nonemergent surgery for deformity correction, preoperative treatment with anabolic bone medications, such as teriparatide, may be considered.

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Decision-​Making

Advanced imaging, including CT myelogram and/​or MRI, should be obtained in patients with neurologic symptoms/​deficits and in cases in which treatment may include spinal implants. Comparing supine and standing imaging is also important when assessing the spine for alignment and flexibility. The CT scout image may be sufficient for the supine assessment in some cases. In this patient, MRI of the lumbar spine showed multilevel central canal and foraminal stenosis most severe at L3–​L4, L4–​L5, and L5–​S1 (Figure 22.1A–​C). A  CT myelogram was also obtained and demonstrated severe stenosis and provided detailed bony anatomy that can be helpful for surgical planning. For patients with prior spinal instrumentation, CT myelogram is the preferred imaging modality since CT imaging is generally less susceptible to metallic artifact compared with MRI. Standing full-​length PA and lateral radiographs are shown in Figure 22.2. These demonstrate dextroscoliosis (curve to the right; in contrast to levoscoliosis, which is to the left) of the lumbar spine with the apex at L2. Standard viewing orientation of the A

B

C

Figure 22.1 T2-​weighted magnetic resonance images. Left (A) and right (B) paracentral sagittal sections demonstrate multilevel foraminal stenosis. Axial (C) image at the level of L4–​L5 demonstrates severe canal stenosis.

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A

B

C

Figure 22.2  Posteroanterior (PA, A) and lateral (B and C) full-​length standing radiographs at the time of presentation. PA imaging (A) illustrates measurement of the global coronal alignment (−3.0 cm) and the coronal Cobb angle (47 degrees). Lateral imaging (B and C) demonstrates measurement of the sagittal vertical axis (+8.4 cm), T2–​T12 thoracic kyphosis (22 degrees), lumbar lordosis (37 degrees), pelvic incidence (52 degrees), pelvic tilt (23 degrees), and sacral slope (29 degrees).

PA radiograph is to have the patient’s left side on the viewer’s left side (i.e., true left, true right), and standard viewing orientation for the lateral long-​cassette radiograph is to have the patient facing to the right. Several spino-​pelvic parameters should be routinely assessed. Based on the PA radiograph (Figure 22.2A), the global coronal alignment is −3.0 cm (offset of a vertical plumbline dropped from the center of C7 relative to the central sacral vertical line, with shifts to the left and right represented as negative and positive values, respectively) and the coronal Cobb angle is 47 degrees (angle between the most horizontally angled endplates at the cephalad and caudal aspects of the curve). Based on the lateral radiograph (Figure 22.2B), the sagittal vertical axis (SVA) is +8.4 cm (offset of a vertical plumbline dropped from the center of C7 relative to the posterior-​superior corner of the sacrum, with shifts to the left and right represented as negative and positive values, respectively), the thoracic kyphosis (TK) is 22 degrees (often measured from T2–​T12 or T4–​T12), and the lumbar lordosis (LL) is 37 degrees (measured from the superior endplate of L1 to the superior endplate of S1). In addition, pelvic parameters should be measured (Figure 22.2C), including the pelvic incidence (PI), which is 52 degrees (angle subtended by a perpendicular line from the center of the sacral endplate and a line from the center of the sacral endplate to the center of the femoral head); the pelvic tilt (PT), which is 23 degrees (angle subtended by a line from the center of the sacral endplate to the center of the femoral head and a vertical reference line at the center of the femoral head); and the sacral slope (SS), which is 29 degrees (slope of the sacral endplate). PI is a morphologic parameter that helps to determine

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the amount of LL an individual should have, while the PT is a measure of pelvic retroversion, which is a compensatory measure for positive sagittal malalignment that, when abnormally elevated, can be a source of pain and disability. The PI is the sum of the PT and SS. The threshold radiographic spinopelvic parameters for an Oswestry Disability Index (ODI) score of more than 40 (severe disability) have been reported: PT of 22 degrees or greater, SVA of 4.7 cm or greater, and PI–​LL mismatch of 11 degrees or more.2 It is important to remember that these measures and thresholds do not, in and of themselves, constitute an indication for surgery but are meant instead to aid in understanding the complexities of spinal deformity in the context of patient symptoms. Notably, Lafage and colleagues recently defined spinopelvic alignment thresholds based on patient age and concluded that operative realignment targets should account for age and that younger patients require more rigorous alignment objectives.3 DEXA scan of the right hip and left wrist demonstrated T scores of −1.7 and −1.5, respectively, which reflect osteopenia. In scoliotic patients, DEXA scans of the spine have been shown to be less accurate predictors of osteoporosis, while scans of the hip and wrist have maintained reliability and are good alternatives in this patient population.4 This patient has progressively symptomatic lumbar spondylosis and stenosis, most notably in the fractional portion of his scoliosis curvature (L4–​S1). Although the patient demonstrates modest global coronal and sagittal malalignment, limited PI–​LL mismatch, and slightly elevated pelvic retroversion (PT), these are not likely the primary sources of this patient’s symptoms, especially if the patient’s advanced age is considered.3 After unsuccessful nonoperative management, he is seeking operative treatment.The presence of a moderate scoliosis, combined with a large component of mechanical lower back pain, make a limited decompression a less attractive option. A short-​segment decompression with segmental instrumentation and fusion from L3–​S1 may significantly improve his claudication symptoms by addressing his stenosis. However, this would place the upper instrumented vertebra near the apex of the coronal curvature. The risk of symptomatic curve progression as a result of this intervention would be relatively high and, as a general rule, is not recommended.This leaves the option of addressing both the stenosis and scoliosis at the same time.While this is a decidedly larger operation with increased operative and medical risks, it offers the best chance for improving the patient’s symptomatology. Questions

1. What additional testing should be performed prior to surgical intervention? 2. What expectations should be established prior to surgical intervention?

Surgical Procedure

After medical and cardiac clearance and an extensive discussion regarding the potential benefits, risks, and alternatives,5–​8 the patient underwent a T10–​iliac posterior segmental instrumented fusion with Ponte osteotomies from L1–​S1 and transforaminal interbody fusion at L4–​L5 and L5–​S1. There were no complications during the procedure. Intraoperative neuromonitoring, including motor evoked and somatosensory

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evoked potentials and free-​running electromyography (EMG), was used and did not demonstrate any abnormalities. He was mobilized on postoperative day 1 with physical therapy, and was discharged to inpatient rehabilitation on postoperative day 6. His leg pain had resolved by the time of his discharge. At the 6-​week postoperative visit, he was able to walk with less back pain than preoperatively. Motor strength in dorsiflexion, EHL, and plantar flexion was improved to 4+. Full-​length standing PA and lateral radiographs 36 months after surgery demonstrating improved alignment and spinal balance are displayed in Figure 22.3. At last follow-​up, his leg pain and neurogenic claudication remained resolved, his motor strength had returned to normal, and he only noted occasional mild low back discomfort.

Oral Boards Review: Management Pearls

1. In the absence of significant or progressive neurological deficits, nonoperative therapies should be attempted prior to surgical treatment for adult spinal deformity. 2. Spinopelvic parameters should be assessed preoperatively and help guide management decisions. 3. Full-​length standing films are essential for a proper assessment of alignment.

A

B

C

Figure 22.3  Posteroanterior (PA, A) and lateral (B and C) full-​length standing radiographs at 36-​month postoperative follow-​up. Posterior segmental instrumentation has been placed from T10 to the ilium, and interbody spacers have been placed at the L4–​L5 and L5–​S1 levels. PA imaging (A) illustrates measurement of the global coronal alignment (+1.1 cm) and the coronal Cobb angle (8 degrees). Lateral imaging (B and C) demonstrates measurement of the sagittal vertical axis (+4.8 cm), T2–​T12 thoracic kyphosis (29 degrees), lumbar lordosis (42 degrees), pelvic incidence (52 degrees), pelvic tilt (21 degrees), and sacral slope (31 degrees).

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Pivot Points

1. In a patient with neurologic deficit, MRI and/​or CT with myelogram is needed. 2. Age should be considered when determining goals for realignment. 3. Intraoperative neuromonitoring should be considered for surgical procedures to treat spinal deformity.

Aftercare

After surgery, an immediate neurologic evaluation is made and plain radiographs are obtained. If there is any decline in neurologic function, CT with or without myelogram should be considered for assessment. Deep venous thrombosis (DVT) prophylaxis with thromboembolic stockings and sequential compression devices are continued throughout the postoperative period, and early aggressive respiratory management is administered. Pharmacologic DVT prophylaxis (e.g., with heparin) should also be considered and is typically employed by the authors as early as postoperative day 1. Pain control can be challenging in the immediate postoperative period and use of patient-​controlled anesthesia and a pain team consult can both be beneficial. Physical therapy is begun early in the recovery phase. When able, standing full-​length PA and lateral radiographs are obtained to assess sagittal and coronal alignment. The authors use postoperative intravenous antibiotics until all wound drains have been removed. Enteral nutrition is begun as soon as possible postoperatively. If patients are unable to receive enteral nutrition, hyperalimentation should be considered. Routine clinical and radiographic follow-​up, including full-​length standing PA and lateral radiographs, are obtained at follow-​up intervals (e.g., 6 weeks, 3 and 6 months, and 1 and 2 years). Complications and Management

Complications can be divided into those that occur early and delayed.6,8,9 Early complications include the development of neurologic deterioration and postoperative wound infections. Deep wound infection rates vary between 1% and 8% and typically require surgical washout and appropriate antibiotic treatment.6 Perioperative mortality is fortunately rare and has been reported to be approximately 0.6%.6 Other complications including cerebrospinal fluid leak, DVT, pulmonary embolism, pneumonia, urinary tract infection, and cardiovascular sequelae can occur.6 Delayed complications, including pseudarthrosis, instrumentation failure, and proximal junctional kyphosis/​failure, can occur and may necessitate revision surgery.6,9 Evidence and Outcomes

Specific goals for adult spine deformity correction include global alignment restoration, decompression of neural elements, pain relief, and functional improvement. To assess these outcomes, it is important to use patient-​centered instruments that evaluate health-​related quality of life (HRQOL), such as the SF-​36, SRS-​22R, and ODI.7,8,10,11 These outcome measures allow practitioners to properly evaluate a

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patient’s clinical progress. There is strong evidence linking worsening functional and health status with increased positive SVA, increased PT, and decreased lumbar lordosis (increased PI–​LL mismatch).2,12 Restoration of alignment has likewise been shown to correlate with improved patient outcomes and decreased disability scores. Multiple studies have demonstrated the potential for surgical treatment to improve HRQOL in adults with lumbar scoliosis, and advances continue to be made in the management of these patients.7,8,10,11 References and Further Reading

1. Maggio D,Ailon TT, Smith JS, et al.Assessment of impact of standing long-​cassette radiographs on surgical planning for lumbar pathology:  An international survey of spine surgeons. J Neurosurg Spine. Jul 31 2015:1–​8. 2. Schwab FJ, Blondel B, Bess S, et  al. Radiographical spinopelvic parameters and disability in the setting of adult spinal deformity:  A prospective multicenter analysis. Spine. Jun 1 2013;38(13):E803–​E812. 3. Lafage R, Schwab F, Challier V, et al. Defining spino-​pelvic alignment thresholds: Should operative goals in adult spinal deformity surgery account for age? Spine. Jan 2016;41(1):62–​68. 4. Pappou IP, Girardi FP, Sandhu HS, et al. Discordantly high spinal bone mineral density values in patients with adult lumbar scoliosis. Spine. Jun 15 2006;31(14):1614–​1620. 5. Bess S, Line B, Fu KM, et  al. The health impact of symptomatic adult spinal deformity: Comparison of deformity types to United States population norms and chronic diseases. Spine. Feb 2016;41(3):224–​233. 6. Smith JS, Klineberg E, Lafage V, et  al. Prospective multicenter assessment of perioperative and minimum 2-​year postoperative complication rates associated with adult spinal deformity surgery. J Neurosurg Spine. Jul 2016;25(1):1–​14. 7. Smith JS, Lafage V, Shaffrey CI, et al. Outcomes of operative and nonoperative treatment for adult spinal deformity:  A prospective, multicenter, propensity-​matched cohort assessment with minimum 2-​year follow-​up. Neurosurgery. Jun 2016;78(6):851–​861. 8. Smith JS, Shaffrey CI, Glassman SD, et al. Risk-​benefit assessment of surgery for adult scoliosis: An analysis based on patient age. Spine. May 1 2011;36(10):817–​824. 9. Lapp MA, Bridwell KH, Lenke LG, et al. Long-​term complications in adult spinal deformity patients having combined surgery a comparison of primary to revision patients. Spine. Apr 15 2001;26(8):973–​983. 10. Bridwell KH, Glassman S, Horton W, et  al. Does treatment (nonoperative and operative) improve the two-​year quality of life in patients with adult symptomatic lumbar scoliosis:  A prospective multicenter evidence-​ based medicine study. Spine. Sep 15 2009;34(20):2171–​2178. 11. Smith JS, Shaffrey CI, Bess S, et  al. Recent and emerging advances in spinal deformity. Neurosurgery. 2016 (invited submission). 12. Glassman SD, Bridwell K, Dimar JR, Horton W, Berven S, Schwab F. The impact of positive sagittal balance in adult spinal deformity. Spine. Sep 15 2005;30(18):2024–​2029.

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Flat Back Deformity Yusef I. Mosley and James S. Harrop

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Case Presentation

A 68-​year-​old woman presents with a past medical history significant for rheumatoid arthritis, osteoporosis, and lower back pain that radiates into her lower extremities for more than 7 years. She underwent a lumbar decompression and fusion approximately 4 years prior to presentation. Approximately 2 weeks after her operative intervention, she developed severe back, hip, and leg pain. Her back and leg pain are equal in severity and both contribute to her diminished quality of life. She states that standing or walking for long periods of time exacerbates her symptoms. She tried physical therapy after her lumbar surgery; she had only mild improvement in her symptoms. She tried epidural steroid injections (EDSI), which brought some relief. Unfortunately, the EDSI are no longer effective in managing her symptoms. Currently, she states that she has weakness in both lower extremities, with her right leg being weaker than her left. She has an unsteady gait but requires no assistance with ambulation. She states that the pain has affected the ability to perform activities of daily living, sleep, travel, exercise, and enjoy her hobbies. Additionally, she complains of right arm numbness in the C6 distribution. However, she does not endorse any clumsiness with fine motor movements in her hand or bowel or bladder issues. She does not use any tobacco products. Questions

1. What is the most likely diagnosis? 2. What imaging is necessary to complete the workup? 3. What are the important anatomical areas to obtain imaging? Why? 4. What are other nonoperative therapies that would improve the outcome of an operation if it were needed? Detailed neurological assessment was performed and positive for abnormal gait, pitched forward posture while standing, and decreased range of motion in the cervical and lumbar spines. She does not have any pathologic reflexes, Hoffman sign, Babinski sign, or clonus in her lower extremities. Assessment and Planning

The neurosurgeon suspects that the patient has a sagittal balance issue from her appearance on physical exam and her clinical history. She also has complaints that could be

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indicative of a myelopathy caused by compression of the spinal cord below the cervical spine. Cervical myelopathy is unlikely secondary to the absence of any upper extremity signs or symptoms in the history and physical exam. The patient should have magnetic resonance imaging (MRI) of the thoracic and lumbar spine to rule out any severe stenosis that could be contributing to her symptoms. Severe stenosis in the thoracic region could potentially explain the unsteady gait, and severe stenosis in the lumbar spine could explain her posture. A patient will often obtain some relief of neural compression in the lumbar spine by leaning forward to increase foraminal size. Additionally, this patient should have a computed tomography (CT) scan of the lumbar and thoracic spine to better understand the bony anatomy, rule out any potential hardware failure from the prior operative intervention, rule out any pseudoarthrosis, and rule out any occult fractures that may have occurred. Additionally, CT scans have been used to assess the bone health by documenting Hounsfield units in patients with osteoporosis. Last, the patient should have both lumbar x-​ray (anteroposterior [AP]/​lateral/​flexion/​extension) and complete standing scoliosis x-​rays. The lumbar x-​rays will allow the surgeon to assess the previous hardware, and the dynamic films (flexion/​extension) will rule out any potential pseudoarthrosis or instability. The complete standing scoliosis x-​rays are taken to assess the global alignment of the patient and to document any pelvic incidence (PI) to lumbar lordosis (LL) mismatch and to evaluate her sagittal vertical axis (SVA). Another issue to assess in this patient are her history of rheumatoid arthritis and any potential antiinflammatory medications that are being taken that would inhibit a bony fusion. Also, the patient’s history of osteoporosis must be evaluated to see if she has been taking any medications to help improve her overall bone quality. A recent dual-​energy x-​ray absorptiometry (DEXA) scan would be useful to quantify the severity of her bone disease.

Oral Boards Review: Diagnostic Pearls

1. Physical examination: a. Complete neurological examination should be completed with attention paid to any myelopathic signs (Hoffman sign, clonus, hyperreflexia, etc.). These are important to assess because if a patient has both cervical and thoracolumbar pathology, the cervical may need to be addressed first. b. Careful assessment of the patient’s posture is needed. Patients with sagittal balance issues will often stand with knees bent and hips slight flexed. This posture is taken to compensate for the forward posture that the patient has developed over time. 2. Imaging studies: a. MRI can assess for any central or foraminal stenosis that would be contributing to the patient’s signs and symptoms.

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b. CT scan assess for any hardware failure, pseudoarthrosis, or occult fractures. Additionally, the Hounsfield units can be evaluated at a given vertebral body to assess the bone quality. c. Standing scoliosis x-​rays allow PI, LL, pelvic tilt (PT), and SVA to be measured. It is imperative to assess for any mismatch in the PI–​LL, which should be within 10 degrees +/​−. Normal PT should be approximately less than15 degrees; if higher, the patient is likely retroverting his or her pelvis to compensate for the positive sagittal balance. The SVA should be less than 5 cm in front of the posterosuperior corner of the S1 vertebral body. d. When evaluating a DEXA scan, it is important to assess the number and which portion of the bone was used to assess the bone quality. When the study concentrates on the spine, it can underestimate the severity of osteoporosis because of the osteophyte presence that increases the T-​score.Values should be obtained from the hip. (See notes under CT scan for evaluation of osteoporosis.)

The patient did not have any central stenosis in the thoracic and lumbar spine (Figure 23.1A,B). Her CT scan did not show any hardware failure, evidence of pseudoarthrosis, or occult fractures (Figure 23.2). Her lumbar x-​rays showed previous instrumentation from L3 to L5 without any evidence of pseudoarthrosis, hardware failure, or instability (Figure 23.3A,B). The standing scoliosis x-​rays showed an SVA of +15.5 cm, PI of 60 degrees, LL of 20 degrees, and a PT of 28 degrees (Figure 23.4A,B).

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Figure 23.1  (A) T2 sagittal magnetic resonance image (MRI) of the thoracic spine showing no central stenosis. (B) T2 sagittal MRI of the lumbar spine showing no central stenosis.

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Figure 23.2  (A) Sagittal computed tomography (CT) scan of the thoracic spine without any occult fractures or bony abnormalities. (B) Sagittal CT scan of the lumbar spine showing previous hardware without any instrumentation failures or pseudoarthrosis.

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Figure 23.3  (A) Lateral lumbar spine standing x-​ray showing previous hardware. (B) Anteroposterior (AP) lumbar spine standing x-​ray showing previous hardware.

 

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Figure 23.4  (A) Lateral standing scoliosis x-​ray. (B) Anteroposterior (AP) standing scoliosis  x-​ray.

Questions

1. How do the clinical and radiographic findings influence the surgical planning? 2. What is the appropriate timing of surgery? 3. What are the goals of the surgery, and how can they be accomplished?

Decision-​Making

This patient’s radiographic findings and clinical presentation suggest that she would benefit from a procedure that corrects her global alignment and PI–​LL mismatch. However, before discussing the appropriate operative approach, it is key to maximize this patient’s overall bone health.There are studies showing that older patients undergoing spinal surgery have a higher chance of having osteoporosis/​osteopenia compared to the rate of occurrence in the population of the same age group.The first step in the treatment algorithm should be a referral to an endocrinologist for medical management of the patient’s osteoporosis. A few examples of preventative therapies include vitamin D and calcium supplementation, parathyroid hormone, calcitonin, and estrogen replacement. There is no consensus on the length of time during which a patient should be on osteoporosis therapy prior to operative interventions. In fact, there have been publications that suggest that delaying surgery for lumbar herniated disc in osteoporotic patient could lead to less favorable outcomes 6 months after surgery.1 The patient in this presentation was evaluated by an endocrinologist and treated with teriparatide (Forteo) prior to her operative intervention.

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As stated, she has a significant PI–​LL mismatch, positive SVA, and increased PT. The goals of surgery are to correct her deformity with an approach that minimizes complications. She has about 40 degree mismatch between her PI and LL; additionally, one has to consider her elevated PT. The increase in her PT is her body attempting to correct the global alignment by retroverting her pelvis to bring her back into alignment. Schwab et al. published an anatomical spinal osteotomy classification system that reviews types of osteotomies and the amount of correction to be expected.2 This patient has a prior fusion from L3 to L5 and a mismatch of greater than 40 degrees; thus, she will need at least a Schwab grade 3 osteotomy (pedicle subtraction osteotomy [PSO]) to give her the majority of the correction necessary.This grade 3 osteotomy gives at least 30 degrees of correction. A  Schwab grade 4 osteotomy is an extended PSO with disc resection and can give a correction up to 45 degrees. While the PSO is a powerful technique for correction, it does come with an increase risk of hardware failure and pseudoarthrosis. The usage of bone morphogenic protein (BMP) would be recommended to assist in obtaining a solid fusion mass. Deformity correction can be achieved via a multitude of approaches including anterior/​posterior, lateral/​posterior, or posterior alone. An anterior approach via anterior lumbar interbody fusion (ALIF) combined with a posterior approach would allow for a large interbody graft at L5–​S1, which typically gives more lordosis at that level compared to a standard transforaminal lumbar interbody fusion (TLIF) at that same level. However, Dorward et al. showed that a TLIF had a shorter overall operative time in long constructs and had a better ability to correct any scoliosis or fractional curves.3 Once the determination is made of how the lumbar deformity is to be corrected, one must consider what will be the upper instrumented vertebrae (UIV) and distal anchor point for screws. This patient will likely need to have a distal instrumentation to the pelvis. This technique is useful in longer constructs given its ability to protect the sacral screw from failure and increase the chances of obtaining successful arthrodesis at the lumbosacral junction. Regarding the UIV, one should take into account that this patient has osteoporosis and this will increase the risk screw pullout and of proximal junction kyphosis (PJK) or failure (PJF). Several techniques are used to reduce the risk of PJK and PJF: • Longer fusion constructs and avoiding constructs that start or end at the cervicothoracic or thoracolumbar junction • At least three fixation points above and below the apex of the deformity • Hybrid constructs (pedicle screws, hooks, wires, percutaneous pedicle screws) to possibly improve fixation strength • Direction of the pedicle screw insertion affects pullout strength; purchase in subchondral bone is recommend to maximize fixation • Undertapping to increase the insertional torque and pullout strength of pedicle screws • “Hubbing” of pedicle screws adversely affects pullout strength and should be avoided • Use of cement augmentation at the UIV

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Questions

1. What are the perioperative complications associated with adult deformity surgery? 2. What are some preventative measures to reduce the risk of complications?

Surgical Procedure

Spine deformity surgery is performed under general anesthesia with Foley catheter placement, duplicate intravenous access, and arterial line placement. Neuromonitoring (somatosensory evoked potentials [SSEP], motor evoked potentials [MEPs], and electromyography [EMG]) is utilized to ensure that all neural elements are safe during placement of pedicle screws, osteotomies, and corrective maneuvers. Patient is positioned in the prone position with appropriate padding of bony prominences, such as the chest/​sternal region, hip/​anterior superior iliac spine (ASIS), thighs, and knees. Typically, a Jackson OSI table is used. Patient should be positioned in a manner that enhances lordosis in the lumbar spine. Preparing for potential complications in surgery is key to a good outcome. Exposure of spine from the posterior approach can lead to a significant amount of blood loss. The use of tranexamic acid (TXA) is common to decrease blood loss and the need for blood transfusion. Hui et al. showed in a meta-​analysis that TXA significantly reduces intraoperative and postoperative blood loss and reduced cell salvage transfusion amount. TXA is thrombogenic and can cause deep vein thrombosis or pulmonary embolism (DVT/​PE); however, this seems to be a rare occurrence. Other methods of reducing blood loss are usage of cell saver and high-​power coagulation devices. After the appropriate spinal levels have been exposed (with great care taken not to disrupt those facet joints that are not included in the construct), the removal of any prior instrumentation should be performed. Next, new instrumentation can be inserted. At the UIV, cement was injected into the vertebral body to reduce the risk of PJK/​PJF.5 Depending on the experience of the surgeon, pedicle screw placement can occur via free-​hand technique, which does not utilized any imaging for placement, navigation, or fluoroscopy. It is important to prevent any neurological injury with placement of pedicle screws; this can be accomplished by checking MEPs after the cannulation of a pedicle and/​or placement of a pedicle screw.Additionally, the pedicle screw can be directly stimulated after placement with EMG. Another way to check for appropriate placement is to utilize an intraoperative CT scan or fluoroscopy to assess for any screws that have not been placed adequately. Pedicle subtraction osteotomies are no small feat to accomplish. These require meticulous exposure of the pedicles located cranially and caudally to the pedicle that will be resected. For example, if the goal is for L3 PSO, then the L2 and L4 pedicles should be accessible and, at this point, should have a pedicle screw in place for the placement a temporary rod. After bony exposure, the lamina should be removed and adequate exposure should include the L2, L3, and L4 nerve roots. After the bone has been removed and the nerve roots have been visualized, then one temporary rod should be placed between the L2 and L4 pedicle screws. A wedge resection should then be performed bilaterally. After the appropriate amount has been removed, then the cap screws should be loosened to allow reduction of the osteotomy and appropriate closure of the osteotomy. 221

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There should be bone-​to-​bone contact to ensure appropriate fusion. A rod should be place connecting the UIV to the pelvic instrumentation. Appropriate decortication is performed, and a combination of autograft, allograft, and other products (e.g., BMP) should be placed on the bone to assist with fusion. It is important to place an additional rod at the level of the PSO to reduce the chance of rod fracture.

Oral Board Reviews: Management Pearls

1. Prevention of further complication is the key after appropriate placement of screws and placement of products both autograft and allograft for fusion. a. During exposure, take care to leave the supraspinal and intraspinal ligaments intact to prevent PJK/​PJF. b. Utilize of some of the techniques just discussed to prevent PJK/​PJF. 2. Time that the patient has been in the prone position and amount of fluid that has been given during surgery has been documented in contributing to a very rare complication of spine surgery—​postoperative blindness.Thus, it is sometimes safer to stage such large procedures to ensure adequate correction and patient safety. Many surgeons perform additional steps to prevent PJK/​PJF. Aftercare

Patients should be monitored in an intensive care or step-​down unit. There should be invasive monitoring of blood pressure in case the patient requires increased mean arterial

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Figure 23.5  (A) Lateral postoperative scoliosis x-​ray. (B) Anteroposterior (AP) postoperative scoliosis x-​ray.

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pressure (MAP) via pressors for appropriate spinal cord perfusion after the procedure. Additionally, patients typically have a history of narcotic use and may require a consultation with an inpatient pain management service for adequate pain control. There is no evidence that would suggest that patients have an improved outcome with a thoracolumbosacral (TLSO) brace after operative intervention; however, prescribing a TLSO brace postoperatively will allow the patient to maintain appropriate posture during the healing process. The patient will need physical therapy. Special attention should address hip contractures that can developed over time, to help with an appropriate recovery process. Appropriate follow-​up with imaging (Figure 23.5A,B) should be established to ensure that the patient does not develop any undiagnosed complications: PJK/​PJF, hardware failure, or infection. References and Further Reading

1. Lehman RA Jr, Kang DG, Wagner SC. Management of Osteoporosis in spine surgery. J Am Acad Orthop Surg. 2015 Apr; 23(4): 253–​263. doi: 10.5435/​JAAOS-​D-​14-​00042. 2. Schwab F, Blondel B, Chay E, et al.The comprehensive anatomical spinal osteotomy classification. Neurosurgery. 2014; 74(1): 112–​120. 3. Dorward IG, Lenke LG, Birdwell KH, et al. Transforaminal versus anterior lumbar interbody fusion in long deformity constructs: A matched cohort analysis. Spine (Phila PA 1976). 2013 May 20; 38(12): E755–​E762. doi: 10.1097/​BRS.0b013e31828d6ca3. 4. Hui S, Xu D, Ren Z, Chen X, Sheng L, Zhuagn Q, Li S. Can tranexamic acid conserve blood and save operative time in spinal surgery? A meta-​analysis. Spine J. 2017 Dec 122. Pii: S1529-​ 9430(17)31192-​0. doi: 10.1016/​j.spinee.2017.11.017. 5. Ghobrial GM, Eichberg DG, Kolcun JPG, Madhavan K, Lebwohl NH, Green BA, Gjolaj JP. Prophylactic vertebral cement augmentation at the uppermost instrumented vertebra and rostral adjacent vertebra for the prevention of proximal junctional kyphosis and failure following long-​segment fusion for adult spinal deformity. Spine J. 2017 Oct; 17(10): 1499–​1505. doi: 10.1016/​j.spinee.2017.05.015.

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Diskitis Jacob R. Joseph, Brandon W. Smith, and Mark E. Oppenlander

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Case Presentation

A 37-​year-​old woman with a history of intravenous heroin abuse presents to the emergency department complaining of acute on chronic back pain. She states that the pain began 3 months prior to presentation and was associated with nausea and chills. She describes the pain as being constant and feeling like muscular spasms, with radiation laterally across her back to both sides. She denies any pain radiating down her legs. She denies numbness or tingling. The pain has been progressively worsening since the onset and has only been responsive to heroin use. She denies any fevers but continues to have intermittent chills. In regards to her drug use, she states that she is usually an everyday user of heroin but has not had any for the past 3 days. She endorses symptoms of sweating, diarrhea, nausea, and shaking. She denies a history of trauma, bowel or bladder incontinence, urinary retention, or saddle anesthesia. On physical exam, she is nontoxic and afebrile. Her detailed neurologic examination was unremarkable, with full strength in all four extremities. Her sensation was intact without lateralization or sensory level. Her reflexes were symmetric throughout, and no pathologic reflexes were present. Palpation of her spine does not elicit significant pain, and no step-​offs are noted. Questions

1. What is the likely diagnosis? 2. What laboratory studies would be appropriate to obtain? 3. What imaging studies would be appropriate to obtain?

Assessment and Planning

The history of this patient makes the neurosurgeon suspect the presence of osteomyelitis and diskitis. The differential includes degenerative disc disease, traumatic spinal fracture, pathologic spinal fracture, bony tumor, leptomeningeal disease, sacroiliitis, pyelonephritis, and psoas abscess. However, the onset of back pain in a patient with a known history of intravenous drug abuse should immediately cause concern for osteomyelitis and diskitis. Risk factors for the development of osteomyelitis/​diskitis include not only intravenous drug abuse, but also acquired immunodeficiency syndrome (AIDS) and other immunocompromised states (such as transplant recipients or patients on chemotherapy). Other risk factors include diabetes mellitus, renal failure, cirrhosis, and distant infections.

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Gram-​positive organisms are most common, with Staphylococcus aureus being the most likely. Other common organisms include Staphylococcus epidermidis, Streptococcus viridans, Streptococcus pneumoniae, and enterococcus. Gram-​negative organisms are less common and are usually associated with gastrointestinal and genitourinary sources. Pseudomonas species are a consideration in intravenous drug abusers as well. Initial laboratory assessment should include a complete blood count (CBC) with differential to assess for increased white blood cell count or left shift. A  neutrophilic predominance suggests a typical bacterial infection, while a lymphocytic predominance raises suspicion for a mycobacterial or fungal infection. In addition to a CBC, an erythrocyte sedimentation rate (ESR) and c-​reactive protein (CRP) level should be obtained. ESR and CRP are nonspecific markers of acute inflammation but are reasonably sensitive for osteomyelitis/​diskitis. Even in cases where the diagnosis is obvious, measurement of ESR and CRP are useful to obtain at presentation so that response to treatment can be followed by serial measurements. Magnetic resonance imaging (MRI) is the most clinically useful test to establish a diagnosis of osteomyelitis/​diskitis. Imaging should be performed both with and without intravenous gadolinium. The entire spine should be imaged as infections are commonly multifocal. Typically, T1-​weighted precontrast images will reveal a hypointense signal in the affected vertebral bodies, while T2-​weighted images show hyperintensity in the affected vertebral bodies, disc space, and paravertebral soft tissues. The T2 hyperintensity suggests edema in these structures. Postcontrast T1-​weighted images reveal enhancement of the affected structures. If imaging reveals involvement of the bone, but not the disc, consideration should be made for alternative diagnoses, such as osteonecrosis. In certain patients such as those with incompatible implanted pacemakers or defibrillators, obtaining MRI in a safe and timely fashion is difficult. In these patients, alternative imaging modalities are necessary. Computed tomography (CT) can be helpful to assess the amount of vertebral body destruction present, which can help determine if instrumentation and fusion is indicated. In addition, the use of intravenous contrast with CT can be helpful to identify enhancing abscesses, including those in the epidural space and the psoas muscle. If there is concern for compression of the neural elements, a CT myelogram can be performed with intrathecal contrast. Other imaging studies such as radionuclide scans and positron emission tomography (PET) have been described to evaluate for osteomyelitis/​diskitis, though they are rarely necessary. Imaging of suspected osteomyelitis/​diskitis should also include evaluation for spinal deformity. While MRI or CT could show a focal kyphosis around the affected levels, they are performed in the lying position and could potentially miss a flexible deformity. Standing scoliosis radiographs can be helpful in this circumstance. In the present case, an MRI and CT were performed, demonstrating evidence of osteomyelitis/​diskitis at T10–​T11 (Figure 24.1).There was no evidence of epidural abscess (Figure 24.2). Her ESR was 34 and CRP was 2.7. Questions

1. What treatment is recommended for the patient at this time? 2. How would this patient’s pain be treated? 3. What would constitute treatment failure in this patient?

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C

D

Figure 24.1  Preoperative imaging in mid-​sagittal plane. (A) Sagittal computed tomography (CT) non-​contrast showing vertebral body destruction and focal kyphosis at T10–​T11. (B) Sagittal T2-​weighted magnetic resonance image (MRI) demonstrating T2 hyperintensity in the vertebral bodies and disc at T10–​T11. (C) Sagittal T1-​ weighted non-​contrast MRI demonstrating T1 hypointensity of the vertebral bodies. (D) Sagittal T1-​weighted gadolinium-​enhanced MRI showing diffuse contrast enhancement in the disc and vertebral bodies at T10–​T11.

Oral Boards Review: Diagnostic Pearls

1. Risk factors for the development of spontaneous osteomyelitis/​diskitis include intravenous drug abuse, AIDS, immunosuppression, diabetes mellitus, and renal failure. 2. Patients with risk factors who present with fever and back pain should be evaluated for diskitis. Initial evaluation includes CBC, ESR, and CRP, along with detailed neurologic examination. 3. MRI with and without contrast is the test of choice to evaluate for osteomyelitis/​diskitis.

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A

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C

Figure 24.2  Preoperative magnetic resonance image (MRI) in axial plane through T10–​T11. (A) Axial T2-​weighted MRI showing no evidence of cord compression. (B) Axial T1-​weighted non-​contrast MRI. (C) Axial T1-​weighted gadolinium-​ enhanced MRI showing no evidence of epidural abscess. Decision-​Making

When there is high suspicion of spinal osteomyelitis/​diskitis, urgent evaluation and imaging is warranted. Initial examination should be focused on identification of any associated neurologic deficit. If there is evidence of neurologic deficit, emergent spinal imaging should be performed. In the absence of neurologic deficit, surgical treatment is usually not needed emergently. However, the patient does require urgent medical treatment.The first step in treatment should be acquisition of blood and urine Gram stain and cultures, along with the previously mentioned lab testing. Direct cultures of the affected vertebral body or disc space may also be needed if other cultures are negative; this is accomplished via percutaneous needle biopsy under CT or fluoroscopic guidance. After cultures are drawn, immediate treatment with broad-​spectrum antibiotics is warranted. Initial treatment should be ensured to cover methicillin-​resistant Staphylococcus aureus (MRSA). Unless

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the patient is septic, or is likely to imminently become septic, then antibiotics can be deferred until cultures are done. Pain is a common presenting symptom and requires treatment. For acute pain, a combination of narcotics and muscle relaxers can be helpful. Steroids are not advisable due to the risk of worsening infection. Neuropathic pain medications such as gabapentin or pregabalin can help with radicular pain. If the patient complains of mechanical pain or pain with axial loading, consideration can be made for external bracing. If there is evidence of neurologic deficit, then emergent spinal imaging is necessary with MRI to identify a source of neural compression. If an epidural abscess is found, emergent decompression of the neural elements is necessary to preserve neurologic function. Even in the absence of neurologic deficit, if there is evidence of epidural abscess, a discussion should be had with the patient regarding risks and benefits of early operative decompression. The location of infection may also contribute to decision-​making in these cases. Infections near the spinal cord (cervical and thoracic spinal levels) are more likely to result in rapid neurologic decline and thus may warrant earlier intervention. There are several other considerations for operative intervention. If treatment with intravenous antibiotics does not result in symptomatic improvement or improvement of laboratory markers, then debridement of the disc space may be warranted. In addition, the presence of focal, progressive spinal deformity can warrant correction. Recalcitrant pain that does not respond to oral medications or bracing may also warrant fusion. Finally, if bacteriologic diagnosis is unable to be obtained through other measures, a biopsy may be needed. In the present patient, CT-​guided biopsy revealed MRSA, and she was treated with intravenous nafcillin. However, she continued to have severe mechanical and radicular pain despite large doses of pain medications and bracing. Due to this, she was offered surgical treatment. Questions

1. What are the goals of surgery in this patient? 2. What approach should be used?

Surgical Procedure

The specifics of surgery for osteomyelitis/​diskitis depend on the levels involved, location of infection, and degree of bone involvement. However, all procedures should be performed under general anesthesia with neuromonitoring. In cervical or thoracic cases, motor evoked potentials (MEPs) can be useful, while electromyography (EMG) and somatosensory evoked potentials (SSEPs) can be useful in all cases. Preoperative antibiotics should be avoided if a bacteriologic diagnosis from a biopsy is required. While the approaches are varied based on the level, the principles of surgery for osteomyelitis/​diskitis are similar. The first goal should be decompression of the neural elements. Also, a robust debridement of the disc space must be accomplished, with both aerobic and anaerobic cultures. If necessary, in cases with severe bony involvement, debridement of the vertebral bodies should also be completed. All cases with aggressive

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disc or bone debridement likely require fusion. Typically, anterior interbody fusion is combined with posterior supplementation. Interbody fusion with metallic implants or with bone autograft or structural allograft is likely safe. Titanium has bacteriostatic properties and is safe to use for posterior instrumentation. If there is evidence of a focal deformity, it should be corrected to restore anatomic alignment. Preoperative standing scoliosis films can be useful to calculate spino-​pelvic parameters. In all surgeries for infection, durotomy should be carefully avoided in these cases as there is a risk of inducing meningitis. Finally, a detailed and robust multilayered wound closure is necessary to prevent wound breakdown. In the cervical spine, most cases are best treated with an anterior approach. This approach allows for aggressive debridement of the disc space and evacuation of ventral abscesses. A corpectomy can be considered when necessary. Posterior instrumentation to supplement the anterior fusion can also be utilized when necessary. In patients with an isolated dorsal epidural abscess, a purely posterior approach with laminectomy with or without fusion can be considered. In the thoracic and lumbar spine, a posterior approach is sufficient if there is not significant deformity or bony destruction. If there is a focal deformity or extensive anterior compression, specialized ventral approaches are necessary. In the thoracic spine, these may include a transpedicular approach, costotransversectomy, lateral extracavitary approach, lateral retropleural approach, or thoracotomy. In the lumbar spine, this may involve an anterior transperitoneal or retroperitoneal approach, lateral transpsoas approach, or a transforaminal/​posterior approach to the disc. Again, extensive disc debridement should be carried out. Posterior stabilization should be performed after aggressive diskectomy. In the present patient, a T10–​T11 laminectomy with a left T11 transpedicular approach for debridement of the T10–​11 disc space was completed. A T9–​T12 posterolateral fusion was also completed (Figure 24.3). Bone allograft was used to perform an interbody fusion. A

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Figure 24.3  Postoperative x-​rays. Anteroposterior (AP) (A) and lateral (B) radiographs showing T9–​T12 fusion.

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Oral Boards Review: Management Pearls

1. In the absence of neurological deficit, medical management is appropriate. 2. Failures of medical management are defined by the development of neurologic deficit, progressive deformity, poor pain control, worsening laboratory markers, and persistent bacteremia. 3. Goals of surgery include bacteriological diagnosis, decompression of the neural elements, aggressive debridement of the disc space, and correction of deformity.

Pivot Points

1. If the patient presented with signs of sepsis, then aggressive fluid resuscitation and antibiotic treatment prior to confirmation of microbiological diagnosis is indicated. 2. If a large epidural abscess had been diagnosed preoperatively, then surgery should have been performed on presentation.

Aftercare

Postoperatively, the patient should be admitted to the general care ward. Some patients may warrant admission to the intensive care unit depending on blood loss during surgery or sepsis as a result of the infectious process. Regular neurologic checks should be performed to ensure stability of neurologic function. Postsurgical drains should be maintained in place for an extended period of time to minimize fluid buildup.The patient should be mobilized as soon as possible postoperatively with the assistance of physical and occupational therapy. A brace may be provided at the discretion of the surgeon. Pain control should be obtained with weaning of intravenous pain medications as soon as possible. Broad-​spectrum intravenous antibiotics should be continued in the perioperative period. A consultation with colleagues in infectious diseases should be obtained to help narrow coverage when speciation and sensitivities are obtained. A thorough evaluation to identify a source of the osteomyelitis/​diskitis is also critical. Specifically, an echocardiogram should be performed to rule out endocarditis. A dental evaluation should be considered if there is suspicion for an intraoral source of infection. An uncomplicated case of osteomyelitis/​diskitis usually requires at least 6 weeks of intravenous antibiotics. Cases that are more complicated may require a longer course. A peripherally inserted central catheter (PICC) should be placed for this purpose. Special consideration should be made for patients who have a history of intravenous drug use. In these patients, discharge to home with intravenous access may be unwise, and they may require an inpatient stay for the entire course of antibiotics. Standing scoliosis x-​rays (in a brace, if applicable) should be obtained postoperatively if a fusion was performed. In addition, a repeat MRI near the end of the course of antibiotics (6–​8 weeks after treatment initiation) can be helpful to follow disease progression. It should be noted that radiographic changes lag behind clinical changes. If the patient is improving clinically and in laboratory parameters, then subtle worsening 231

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Figure 24.4  An 8-​week follow-​up magnetic resonance image (MRI). Pre-​contrast (A) and post-​contrast (B) sagittal T1-​weighted MRI showing improvement in contrast enhancement. of the MRI should be taken in context. In the present patient, follow-​up MRI showed improvement of infection (Figure 24.4). Complications and Management

Complications of surgery for osteomyelitis/​diskitis are similar to surgery for other indications and are dependent on the spinal levels involved, approach, and extent of fusion. These complications will be discussed in detail elsewhere. A particular concern in surgery for primary spinal infections is wound infection and breakdown.To counteract this, the initial wound closure should be performed with care, ensuring an adequate fascial closure in the relevant areas. Wounds should be monitored closely postoperatively. If there is evidence of wound breakdown or infection, then antibiotic coverage should be expanded to include skin flora. If the situation necessitates it, a wound revision should be considered. Patients should be closely monitored for the development of meningitis postoperatively, particularly if the dura was violated. Early treatment with adequate dosing to ensure cerebrospinal fluid (CSF) penetration can be helpful. As with all spinal procedures, iatrogenic neurological injuries can occur, though they are rare. Careful neurologic examinations should be performed routinely. If there is suspicion for neurologic worsening, repeat MRI should be performed to ensure that there is no continued compression of the neural elements. If imaging is unremarkable, then rehabilitation should be begun as soon as feasible.

Oral Boards Review: Complications Pearls

1. Careful neurologic assessments are critical postoperatively to identify recurrence of compression. 2. Meningitis and sepsis are possible postoperatively and should be treated as early as possible when suspected.

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Evidence and Outcomes

While there are no randomized controlled trials of surgery for osteomyelitis/​diskitis, the literature is strongly in favor of surgery when there is associated neurologic compromise, progressive deformity, or recurrent bacteremia despite antimicrobial therapy without other sources. In cases with epidural abscess, the literature is less clear. Many have argued for early surgery and antibiotics, while others have argued for antibiotics alone. In cases of spinal cord involvement (cervical or thoracic spine), it appears that there may be a benefit to early surgery to preserve motor function, with a high rate of failure if medical therapy alone is attempted. There has been concern regarding the safety of instrumentation in the setting of active infection. However, several studies have suggested that there is not a significant added risk of perpetuating infection with decompression plus instrumentation when compared to decompression alone. Overall reported rates of reoperation are less than 10% after surgery for infection. While there have been numerous case reports and case series discussing various approaches for osteomyelitis/​diskitis, there are no proven techniques which are superior to others. In the cervical spine, most authors advocate for an anterior approach in cases of diskitis in order to achieve a robust diskectomy. In other situations, there are a variety of techniques that have been put forth with success, including open and minimally invasive techniques. References and Further Reading

Alton TB, Patel AR, Bransford RJ, Bellabarba C, Lee MJ, Chapman JR. Is there a difference in neurologic outcome in medical versus early operative management of cervical epidural abscesses? Spine J. 2015;15(1):10–​17. Berbari EF, Kanj SS, Kowalski TJ, et al. 2015 Infectious Diseases Society of America (IDSA) clinical practice guidelines for the diagnosis and treatment of native vertebral osteomyelitis in adults. Clin Infect Dis. 2015;61(6):e26–​e46. Bydon M, De la Garza-​Ramos R, Macki M, et al. Spinal instrumentation in patients with primary spinal infections does not lead to greater recurrent infection rates: An analysis of 118 cases. World Neurosurg. 2014;82(6):e807–​e814. Duarte RM,Vaccaro AR. Spinal infection: State of the art and management algorithm. Eur Spine J. 2013;22(12):2787–​2799. Hadjipavlou AG, Mader JT, Necessary JT, Muffoletto AJ. Hematogenous pyogenic spinal infections and their surgical management. Spine (Phila Pa 1976). 2000;25(13):1668–​1679. 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(2):326–​330. Urrutia J, Zamora T, Campos M. Cervical pyogenic spinal infections:  Are they more severe diseases than infections in other vertebral locations? Eur Spine J. 2013;22(12):2815–​2820.

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Case Presentation

A 61-​year-​old man was admitted to the hospital with a high-​grade fever of 103°F and worsening confusion. Eight days prior to presentation, the patient began to complain of leg pain in his right calf that radiated down to his foot. This was followed by pains in his neck, then shoulder, and eventually progressed to generalized muscle spasms in his back. He comes to the emergency department also with bilateral flank pain and was diagnosed with a urinary tract infection. On physical examination, the patient was assessed as having 4–/​5 generalized weakness in all four of his extremities. The patient, though awake, showed significant confusion and no focal neurologic deficits. Questions

1. What is the likely diagnosis? 2. What is the most appropriate imaging modality? 3. On what anatomical areas should the imaging studies be done?

Assessment and Planning

Despite low incidence rates, pyogenic infections of the spine are an important part of the differential diagnosis when evaluating patients who present with symptoms involving pain of the lower back, weakness of the extremities, radicular pain, and an accompanying fever. Because there are several conditions that have similar signs and symptoms as those seen in spine infections, it is important to apply effective use of imaging studies, labs, and patient history in the workup. Other conditions that invariably present with some of the nonspecific symptoms seen in spinal epidural abscesses (SEAs) can include pyelonephritis, discitis, spinal trauma vertebral osteomyelitis, and spinal subarachnoid hemorrhages. In the case of a true SEA there exists a tetrad of stages, as described by Heusner et al.These stages can be characterized with an initial stage of spinal ache or pain that proceeds into the second stage of nerve root pain; this is then followed by the third stage of weakness in the voluntary muscles that ultimately culminates rather rapidly (within approximately 6 days) in the fourth stage of paralysis. Despite these four stages being distinctly characterized in the literature, they most often exist on a continuum that lacks clearly defined borders between the possible symptoms. Very rarely will patients present with the described classical triad of fever, spine pain, and motor or sensory deficits. Patients will in fact present with varying and unique scenarios that can involve both systemic and

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localized manifestations. Correctly diagnosing the condition can be further complicated by the presence of nonspecific back or neck pains that are only sometimes accompanied by systemic signs, especially when considering the fact that an overwhelmingly large number of patients will present with symptoms of back pain at some point in their lives. Some key points to remember when considering a diagnosis of SEA is that a majority of patients with the condition will have focal tenderness (commonly in the lumbar spine due to the existence of a larger epidural space) and an elevated erythrocyte sedimentation rate (ESR), but less than half will have a fever or leukocytosis and only10%of patients will have severe deficits such as paraplegia or incontinence. Due to the sensitivity of the condition as well as the danger of rapid progression to an irreversible stage, most SEAs are considered a neurosurgical emergency. Infections of this nature can quickly lead to progressively worsening neurologic deficits brought about by direct compression of the spine by the abscess or through vascular compromise via venous thrombosis. Patients with cervical-​or thoracic-​level involvement have been reported to have poorer neurological outcomes than those with more common lumbar involvement. These types of outcomes and their uncertain variability make it paramount that a delay in diagnosis and treatment be avoided. Efficiency in the diagnosis of the condition can be improved by proper use of patient history, physical examination, and imaging studies, as well as the ability to recognize the predisposing risk factors on a patient-​to-​patient basis. Formation of the abscess will usually be due to direct inoculation secondary to some spinal trauma or surgical operation, through hematogenous spread (accounting for about half of SEAs and frequently secondary to a bacterial endocarditis) or from an extension of an adjacent infection. Patients at the highest risk of developing an abscess of this nature are those who are immunocompromised, but other predisposing factors can include malignancies, bacteremia, intravenous drug use, and the presence of foreign bodies. Imaging studies represent one of the most effective and useful tools for confirmation of a suspected diagnosis and for initiating evaluation and planning for surgical intervention. Radiography, while a less specific and sensitive test, can give indications of overall mechanical stability of the spine and any compromise in the alignment. Computed tomography (CT) will demonstrate the presence of spinal infections at an earlier timepoint than plain radiography. CTs will not reflect soft tissue involvement as readily as MRI but can help parse out any patterns of bony compromise. MRI, however, boasts both a high sensitivity and specificity for spinal infections and can provide a more accurate representation of the extent and involvement of the spinal abscess as well as help elucidate the true extent of the spinal cord compression that may be occurring. Therefore, the MRI remains the best tool for diagnosing SEAs through imaging. Both T1-​and T2-​weighted images should be obtained of the suspected area of the SEA, and diffusion-​weighted MRI should also be considered as scans showing a pattern of restricted diffusion can also be suggestive of an epidural abscess. T2-​weighted imaging also plays an important role in the determination of the composition of the abscess. An image that shows a hypointense lesion with homogenous enhancement on T2-​weighted imaging is indicative of a solid abscess, whereas a lesion appearing as a hyperintense collection with a peripherally enhancing rim but lacking central enhancement is characteristic of a fluid abscess. (On T1 this will be seen as a characteristically hypointense center with a hyperintense rim.) These are distinctions that can affect the surgical management of the abscess. It is also important to evaluate the entire spine when

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imaging to determine the full extent of the infection and to rule out secondary abscesses especially because thoracic or cervical level abscesses tend to produce rapid appearance of neurologic deficits. Laboratory tests to determine the ESR and c-​reactive protein (CRP) can also be used to partition those patients that are at higher risk. In the case of our patient T1-​weighted, T2-​weighted, and short T1 inversion recovery (STIR) sagittal and axial MRI images were obtained of the thoracic and lumbosacral spine. Additionally, contrast-​enhanced fat-​suppressed T1-​weighted sagittal and axial images were obtained. On evaluation, images showed a peripheral contrast-​ enhancing homogenous fluid signal dorsal to the entirety of the thoracic spinal cord which was compatible with an epidural abscess. Cervical imaging suggested that the fluid collection extended superiorly to the level of C2. Similar results were found in the lumbosacral images, which showed fluid collections at L1 and L3 as well as multilevel facet arthropathy resulting in central spinal canal stenosis. Figure 25.1A–​C are representative T1-​weighted post-​contrast images of the cervical, thoracic, and lumbar spines, respectively. Questions

1. What is the impact of these clinical and radiological findings in the surgical planning? 2. What is the most appropriate timing for intervention in this patient? 3. How should surgery be approached in a patient with a fluid SEA versus a fibrous one?

A

B

C

Figure 25.1  (A) T1-​weighted contrast-​enhanced sagittal cervical spine magnetic resonance image (MRI) demonstrating dorsal epidural abscess from the level of C2 through C7. (B) T1-​weighted contrast-​enhanced sagittal thoracic spine MRI demonstrating dorsal epidural abscess from the level of T1 through T12. (C) T1-​weighted contrast-​enhanced sagittal lumbar spine MRI demonstrating dorsal epidural abscess from the level of L3 through L4. There is a small ventral epidural abscess at L1.

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Decision-​Making

As mentioned previously, a series of stages spanning from spinal pain, to root pain, to voluntary muscle weakness, to finally paralysis is the traditional progression diagnostic of a SEA, but this is not often seen as distinctly in the hospital setting, and it requires that action be taken before full progression to neurologic deficits occurs. Patients will normally present to the doctor either in phase II (root pain) or phase III (voluntary muscle weakness) of the condition’s progression, and these are considered neurosurgical emergencies that must be immediately addressed. Though there has been some success in medical management of SEAs under the correct circumstances, surgical intervention remains the treatment of choice for management of many SEAs and should be immediately considered in patients presenting with spinal instability or neurologic deficits. Medical management coupled with surgical intervention has been often associated with better outcomes, especially when antibiotic treatment has been tailored for the specific organism obtained at the time of surgery. The initial antibiotic treatment should cover gram-​positive, gram-​negative, and anaerobic organisms until a specific organism has been isolated. It is important to assess and take into account the extent and spread of the abscess and to evaluate for any remote locations of secondary infection, as well as any spinal compression that has occurred, and tailor the surgical approach to target these areas. Surgical approaches can be targeted to the spinal level of the abscess and comprise the full extent of spinal cord involvement (if present), Liquid abscesses can be addressed with options for drainage and lavage (still dependent on spinal level and site of cord compression), whereas compressions caused by granulomatous abscesses may pose the challenge of more case-​specific approaches depending on size and location. The patient in this case presented with an MRI consistent with the formation of an epidural abscess along the entirety of the thoracic spine and extending superiorly to C2 and inferiorly to the level of L3. Due to the patient’s septic state as well as pain and muscle weakness of the extremities, emergency surgery was immediately indicated. Questions

1. How should levels of decompression be chosen? 2. Will laminectomies at the sites of maximal cord compression result in spinal deformity (i.e.,-​at cervicothoracic or thoracolumbar junction)?

Surgical Procedure

Though the approach most frequently used is that of a posterior laminectomy at the site of the abscess, abscesses that are causing ventral compression can be approached either laterally or anteriorly and may require stabilization. The necessity of stabilization and fusion in such cases poses an additional challenge because of the danger of secondary infection of the instrumentation that may be used, but studies have shown favorable results with the use of titanium mesh cages due to their reduced rates of postoperative infections and their resistance to biofilm formation. Because of the extent of the epidural abscess throughout the spinal cord in our presenting patient, a

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dorsal approach was decided upon with the patient positioned prone over a regular table. Chest rolls may be used to help support the patient, and the head should be placed in a Mayfield head adapter in a neutral position if posterior cervical access is necessary. This position will afford access to the entirety of the spine. With the aid of a C-​arm fluoroscope the desired levels must be localized. In a situation where the abscess spans nearly the entire length of the spinal cord it is desirable to target and mark a point of entry in each of the major anatomical regions of the spine, carefully considering those areas with the maximum collection of the epidural abscess or the major sites of spinal cord compression. The draping should allow for access down the entire length of the spine along the dorsal approach. The main goal for the procedure should be to address the issues of washing out the epidural abscess and relieving the points of cord compression. Because this epidural abscess extends throughout the spine, it is not advisable to perform a laminectomy of the entire spine; it is instead better to opt for making multiple skin incisions at the levels where there is the greatest cord compression from the epidural abscess and performing multiple skipped laminectomies.This will afford access to the epidural space of the spinal canal, which can then be washed out with the help of a catheter and an antibiotic irrigation. Other options to be considered to avoid the use of multilevel laminectomies included the creation of unilateral fenestrations at multiple levels or the use of suction and irrigation catheters that are snaked superiorly and inferiorly through the spinal canal from a mid-​level laminectomy access point. Following the incision, a subperiosteal dissection should be carried out to expose the lamina and the spinous processes of the targeted vertebrae. It is important to take care to preserve the spinous processes, the interspinous and supraspinous ligaments, and the facet joints at all levels in order to best preserve overall spine stability. After completion of a laminectomy, introduction of an irrigation catheter can be performed superiorly or inferiorly. Any purulent material should be thoroughly washed out with copious gentle irrigation until clear irrigation fluid can be visualized coming out of the open end and the epidural space has been cleared of purulent material. It is important to thoroughly wash out the spinal canal in order to both avoid the recurrence of the abscess and to make sure the spinal cord is properly decompressed. A similar procedure can be done at the other points selected for the multiple skipped laminectomies. Once the laminectomies and washout of the abscess have been performed, it is important to perform antibiotic irrigation of the wound sites with broad-​spectrum antibiotics with attention given to the paraspinous muscles at all incision sites. Surgical drains should be left to maximize removal of all infected material.

Oral Boards Review: Management Pearls

1. Instrumentation or external orthosis should be utilized if spinal instability is suspected either from the disease process or iatrogenic. 2. Routine repeat imaging is necessary to evaluate for recurrent disease or new disease. 3. Involve other specialities to treat infection in nearby structures (lung, pelvis, etc.).

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Pivot Points

1. Have a low threshold to reimage because recurrence of abscess is common. 2. There is no convincing evidence that instrumentation prevents resolution of infection because it is a foreign body. If there is concern about spinal stability, fusion should be pursued to prevent possible revision surgery.

Aftercare

Broad-​spectrum antibiotics should be administered, and the expertise of an infectious disease specialist can be sought. Surveillance of infection in other body fluids, such as blood and urine, should be monitored. A long-​term intravenous access catheter should be placed once blood cultures are negative in patients for whom intravenous antibiotics are indicated. The patient should be mobilized as soon as possible, and adequate pain control should be given. ESR and CRP values should be examined serially to ensure a downward trend indicating resolution of the infection. Follow-​up imaging may be obtained in 2–​3 weeks to assess for possible recurrence of disease as well as to assess for development of a spinal deformity. Complications and Management

Complications of surgery for epidural abscess are similar to surgery for other indications and depend on the spinal levels involved, approach, and number of levels treated. A particular concern in surgery for primary spinal infections is wound infection and breakdown.To counteract this, the initial wound closure should be performed with care, ensuring an adequate fascial closure in the relevant areas. Wounds should be monitored closely postoperatively. If there is evidence of wound breakdown or infection, then antibiotic coverage should be expanded to include skin flora. If the situation necessitates it, a wound revision should be considered. Patients should be closely monitored for the development of meningitis postoperatively, particularly if a durotomy was incurred. This information should be communicated to the infectious disease care team because this may alter the treatment regimen. Any change in neurologic exam should prompt the acquisition of updated imaging. Recurrences of abscess, new abscesses, or an epidural hematoma are all conditions that would require surgical intervention. References and Further Reading

Bond A, Manian FA. Spinal epidural abscess: A review with special emphasis on earlier diagnosis. Biomed Res Int. 2016;2016:1614328.ypo. Carragee EJ. The clinical use of magnetic resonance imaging in pyogenic vertebral osteomyelitis. Spine. 1997;22(7):780–​785. Colmenero JD, Jiménez-​mejías ME, Sánchez-​lora FJ, et al. Pyogenic, tuberculous, and brucellar vertebral osteomyelitis: A descriptive and comparative study of 219 cases. Ann Rheum Dis. 1997;56(12):709–​715.

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Cornett CA,Vincent SA, Crow J, Hewlett A. Bacterial spine infections in adults: Evaluation and management. J Am Acad Orthop Surg. 2016;24(1):11–​18. Dagirmanjian A, Schils J, Mchenry M, Modic MT. MR imaging of vertebral osteomyelitis revisited. AJR Am J Roentgenol. 1996;167(6):1539–​1543. Del curling O, Gower DJ, Mcwhorter JM. Changing concepts in spinal epidural abscess: a report of 29 cases. Neurosurgery. 1990;27(2):185–​192. Dietze DD, Fessler RG, Jacob RP. Primary reconstruction for spinal infections. J Neurosurg. 1997;86(6):981–​989. Eastwood JD,Vollmer RT, Provenzale JM. Diffusion-​weighted imaging in a patient with vertebral and epidural abscesses. AJNR. 2002;23:496–​498. Gala FB, Aswani Y. Imaging in spinal posterior epidural space lesions: A pictorial essay. Indian J Radiol Imaging. 2016;26(3):299–​315. Grieve JP, Ashwood N, O’Neill KS, Moore AJ. A retrospective study of surgical and conservative treatment for spinal extradural abscess. Eur Spine J. 2000;9(1):67–​71. Hadjipavlou AG, Mader JT, Necessary JT, Muffoletto AJ. Hematogenous pyogenic spinal infections and their surgical management. Spine. 2000;25(13):1668–​1679. Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med. 1948;239(23):845–​854. Khanna RK, Malik GM, Rock JP, Rosenblum ML. Spinal epidural abscess: evaluation of factors influencing outcome. Neurosurgery. 1996;39(5):958–​964. Kuklo TR, Potter BK, Bell RS, Moquin RR, Rosner MK: Single-​stage treatment of pyogenic spinal infection with titanium mesh cages. J Spinal Disord Tech. 2006;19(5):376–​382. Mittal S, Khalid M, Sabir AB, Khalid S. Comparison of magnetic resonance imaging findings between pathologically proven cases of atypical tubercular spine and tumour metastasis: A retrospective study in 40 patients. Asian Spine J. 2016;10(4):734–​743. Pfister HW,Von Rosen F,Yousry T. MRI detection of epidural spinal abscesses at noncontiguous sites. J Neurol. 1996;243(4):315–​317. Suppiah S, Meng Y, Fehlings MG, Massicotte EM, Yee A, Shamji MF. How best to manage the spinal epidural abscess? A current systematic review. World Neurosurg. 2016;93:20–​28. Tuchman A, Pham M, Hsieh PC. The indications and timing for operative management of spinal epidural abscess:  Literature review and treatment algorithm. Neurosurg Focus. 2014;37(2):E8. Youmans JR, Winn HR. Youmans Neurological Surgery. New York: Saunders; 2011. Zimmerer SM, Conen A, Müller AA, et al. Spinal epidural abscess: Aetiology, predisponent factors and clinical outcomes in a 4-​year prospective study. Eur Spine J. 2011;20(12):2228–​2234.

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Nonsurgical Spinal Diseases Lahiru Ranasinghe and Aimee M. Aysenne

It is just as important to recognize diseases and disorders that affect the spinal cord requiring surgical interventions as it to recognize medical etiologies of myelopathies and know preferred treatments. Neurosurgeons are expected to have a strong understanding of these disorders; they need to be able to recognize medical causes of myelopathies and know when surgical interventions are not indicated.These conditions vary from trauma and infections to autoimmune and degenerative conditions. This chapter will briefly describe the clinical and imaging features of these etiologies as well as discuss treatment options. Trauma

Trauma to the spinal cord can be directly or indirectly caused by mechanical forces and can be worsened with a subsequent inflammatory response leading to swelling and vascular occlusion, which ultimately perpetuates secondary spinal cord damage. With mechanisms varied from sport to falls to violence and motor vehicle accidents, trauma is the most common cause of myelopathy, with nearly everyone at risk of possible injury.1 Typically, the diagnosis of trauma is known by history or other injuries. American Spinal Injury Association (ASIA) and International Spinal Cord Society (ISCoS) scoring systems are effective and recommended tools for localizing and determining the severity of the lesion. They have also been validated for prognostication.2–​4 Initial interventions for patients with spinal cord trauma involve stabilization of the segment of spine likely to be involved in the trauma. In the cervical spine, this includes immobilization collars and in-​line mechanical stabilization with manual in-​line immobilization if intubation is required.2,5,6 In the thoracic and lumbar spine, log roll precautions are used. These techniques increase the likelihood of hospital-​acquired events that occur from immobilization including deep venous thrombosis, pulmonary embolism, and aspiration pneumonias and therefore should be discontinued as soon as the spine has safely been excluded from injury. If an asymptomatic patient with suspected cervical spine trauma is awake, neurologically intact, not intoxicated, and has no distracting injuries, the cervical spinal cord can be accurately evaluated on clinical exam of range of motion and point tenderness. If there is any question, a non-​contrasted computer tomography (CT) is recommended to evaluate the bony structures.7,8 Depending on the severity and mechanism of injury, protocolized vascular imaging of the cervical spine decreases the incidence of stroke.9 Magnetic resonance imaging (MRI) adds the evaluation of ligamentous injury.10

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Nonsurgical treatment options have had a controversial history. While many therapies have been shown to be effective in animal models, few have yielded success in human populations. Currently, the only medical management recommended is to maintain a mean arterial blood pressure greater than 85 mm Hg for 7 days post-​injury.11,12 Corticosteroids, while thought to be effective at treating other causes of myelopathy, have been shown to increase the likelihood of complications, including death, in the setting of spinal cord trauma and corticosteroids have been removed as a recommendation in the 2013 Guidelines for the management of acute cervical spine and spinal cord injuries.2,13 Therapeutic hypothermia has had mixed outcomes as an effective treatment option in spinal cord trauma, and more studies are needed to determine its role in spinal cord trauma.2,14 GM-​1 gangliosides have not been shown to be effective treatment options.2,15 In addition to the surgical management discussed in other chapters, rehabilitation is necessary for spinal cord recovery and for the patient to learn independence following a new neurological injury. Demyelinating Diseases: Transverse Myelitis, Multiple Sclerosis, and Neuromyelitis Optica Transverse Myelitis

Transverse myelitis is a broad catch-​all term for inflammation of the spinal cord. The etiologies of transverse myelitis include autoimmune, demyelinating, infectious, or postinfectious conditions. Infectious associations include bacteria such as Salmonella and Campylobacter jejuni and viral agents including Zika and enteroviruses. Autoimmune associations include lupus, sarcoidosis, systemic sclerosis, and Sjögren disease.16 Many more associated conditions have been described. When a known etiology is found, the diagnosis is more appropriately labeled with a more specific term. If transverse myelitis occurs without other clinical features or imaging findings, it may be considered a clinically isolated syndrome, previously thought to be a precursor to multiple sclerosis (MS), with as many as 88% of these patients progressing to meet criteria of MS.17 With more advanced immunologic evaluations and treatment options, this number has significantly decreased. Although numerous causes of transverse myelitis have been identified, many cases are still thought to be idiopathic. The Centers for Disease Control is currently actively tracking cases since 2014 for a better understanding (https://​www.cdc.gov/​ acute-​flaccid-​myelitis/​index.html).18 Because transverse myelitis has a rapid onset, it is common for patient to endorse an onset of symptoms over the course of a few hours to days. MRI findings demonstrate swelling and hyperintense T2 lesions in the spinal cord. Acute lesions may be contrast-​enhancing on T1-​weighted imaging and represent active inflammation. Lesions may be focal and well-​demarcated or diffuse.19 Cerebrospinal fluid (CSF) analysis often reveals an inflammatory process with leukocytosis but may not in as many as 43% of inflammatory transverse myelitis, and other conditions can also cause CSF leukocytosis.20 Treatment for transverse myelitis typically involves high-​ dose corticosteroids while some clinicians choose to add intravenous immunoglobulin (IVIg) or plasma exchange. Because the etiologies of TM are so varied, so are the outcome data.16,21

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Multiple Sclerosis

MS is a T-​cell–​mediated autoimmune condition causing demyelination of the central nervous system. Typical onset of MS is between 20 and 50 years, and MS is more common in women. The McDonald criteria, most recently updated in 2017, is the agreed upon standard for distinguishing MS from clinically isolated syndrome.The diagnosis hinges on the separation of two or more lesions in time or space. MRI is the most useful diagnostic tool, with CSF analysis helpful for demonstrating active inflammation from inside the central nervous system. In the case of MS, oligoclonal bands are present, and CSF is helpful to exclude other conditions that have specific antibody markers.22 There are four recognized patterns of progression for MS: relapsing-​remitting, primary progressive, secondary progressive, and relapsing-​progressive.These patterns display a general progression of the disorder, but relapsing-​remitting, secondary progressive, and relapsing-​progressive are marked by episodes of acute inflammatory attacks. This process of demyelination and subsequent plaque formation ultimately leads to the development of symptoms such as fatigue, difficulty walking, vision loss, urinary symptoms, and dementia. It is important to note that an “attack” for patients suffering from MS can be worsening old symptoms or the presentation of new symptoms.The severity and number of symptoms can vary from patient to patient.22 Acute MS attacks are often treated with high-​dose steroids as they have been for many years. The long-​term management of these patients has changed significantly in recent history with eight new medications approved for use in MS since 2010 and two more currently awaiting approval. The classes of these drugs include interferon, monoclonal antibodies, purine analogs, and sphingosine 1 phosphate receptor modulators.23,24 Due to the complexity and evolving therapies for MS, most patients should be treated in specialized centers. Neuromyelitis Optica and Neuromyelitis Optica Spectrum Disorder

Neuromyelitis optica (NMO) and neuromyelitis optica spectrum disorder (NMOSD) are other autoimmune demyelinating disorders presenting with spinal cord myelitis and optic neuritis. NMO is diagnosed with a longitudinal segment of the spinal cord extending three or more contiguous segments and seropositivity for anti-​AQP4 IgG.19,25 These two diagnostic criteria are effective for distinguishing NMO from MS and transverse myelitis Antibodies against aquaporin 4 (AQP4) water channels are found in the serum of between 50% and 90% of patients. Of those with negative NMO antibodies, antibodies to myelin oligodendrocyte glycoprotein (MOG-​IgG) have been found in more than half with suspected NMODS.25–​27 These antibodies are also found in the serum, and titers may help determine active state of disease. Over time, the spinal cord will atrophy.28 NMO is most common in non-​Caucasian women and will typically present with visual disturbances, spastic paresis, and loss of sensation. Bowel and bladder dysfunction as well as autonomic instability is also common with this condition. NMOSD are associated with a poor prognosis, with treatment options focused on decreasing inflammation. In the acute setting, steroids are again the mainstay, with some clinicians using IVIg or plasma exchange.29 Recently, clinicians are beginning to use rituximab for chronic treatment.30

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Vascular Myelopathies

Infarcts of the spinal cord are rare. They are described by location (cervical or thoracolumbar) and distribution of the spinal cord (anterior or posterior). Initially, patients experience severe pain, but progression with neurological deficits occurs rapidly thereafter. The anterior spinal artery supplies the anterior two-​thirds of the spinal cord, which include the spinothalamic and corticospinal tracts, and deficits include sensory disturbances relating to temperature and pain sensation and weakness. The posterior spinal artery supplies the posterior one-​third of the spinal cord, and this region includes the fasciculus gracilis and cuneatus. An infarct in this part of the spinal cord impacts the dorsal column–​medial lemniscus pathway resulting in a loss of proprioception and vibratory sense. Evaluation for etiology and secondary prevention of strokes is required for spontaneous infarcts. Additionally, spinal cord infarcts can occur with diseases of the descending aorta, including aortic dissection because the artery of Adamkiewicz supplies the thoracic cord via a direct branch from the aorta. This artery is also at risk during cross-​clamp for cardiopulmonary bypass. Some advise using a lumbar drain to allow for greater spinal cord perfusion pressure during and following surgery, but this is controversial.31–​34 Surfer’s myelopathy is a particularly rare vascular disorder with theoretical pathogenesis due to rapid hyperextension of the spine in a novice surfer; this leads to compression of the anterior spinal artery or embolization of fibrocartilaginous disc material from the thoracic region.35 Diffusion-​weighted imaging of the spinal cord is diagnostic but infrequently used for spinal cord infarcts.36 Spinal arteriovenous malformations are also rare causes of compressive myelopathies, which are covered in other chapters. Infectious Myelopathies Neurosyphilis

Syphilis is a sexually transmitted disease caused by the spirochete Treponema pallidum. Tertiary syphilis is characterized by gummas, aortitis, and neurologic disorders. Tabes dorsalis is a degeneration of the dorsal columns and dorsal roots below the lower thoracic region of the spinal cord resulting in positive Romberg sign, ataxia, paresthesias of the lower extremity, and sudden, sharp shooting pains known as lightning pains. A diagnosis of syphilis can be made using dark-​field microscopy to evaluate for spirochetes, a Venereal Disease Research Laboratory (VDRL) test, or fluorescent treponemal antibody absorption (FTA-​ABS) which is more specific for syphilis. The primary therapy for all stages of syphilis is penicillin G, with ceftriaxone being an alternative.37 HTLV-​1–​Associated Myelopathy/​Tropical Spastic Paraparesis

Human T-​lymphocyte virus 1 (HTLV-​1) is a retrovirus that preferentially infects CD4+ T cells and is more common in individuals infected with human immunodeficiency virus (HIV). The virus can be transmitted via breast milk, sexual intercourse, or blood. HTLV-​1 causes adult T-​cell leukemia and lymphoma, and can also cause tropical spastic paresis (TSP). HTLV-​1 is most commonly found in Japan, the Caribbean, Latin America, and Africa. Patients with TSP will classically present as 40-​to 50-​year-​olds who have defective lower extremity control marked by spasticity and weakness, back pain, sensory

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deficits, and urinary dysfunction. CSF analysis reveals HTLV-​1 antibodies, and MRI will show a hyperintense T2 lesion of the spinal cord.38,39 Unfortunately, treatment is mainly based on symptoms, which includes steroids.40 West Nile and Polio Virus

Both West Nile virus and polio can affect the anterior horn cells of the spinal cord, causing acute flaccid paralysis. Because the anterior horn is the synapse of the upper and motor neuron, findings associated with both can be found clinically in these conditions. Polio is caused by a human enterovirus of the Picornaviridae family and is transmitted via saliva or fecal contact with infected persons. Most infected people are asymptomatic.41 Prevention is via vaccine. Polio eradication became a global priority of the World Health Organization in 1988, and, by 2016, only three countries of the world still have the wild-​type virus based on surveillance screening:  Nigeria, Pakistan, and Afghanistan.42 West Nile is an RNA arbovirus from the Flaviviridae family. Because it is a mosquito-​ borne illness, predilection is in the summer months and prevention centers on mosquito control. Most human infections are asymptomatic but can affect nearly every part of the nervous system, especially in an immunocompromised host. Immunoglobulin M to West Nile virus may be found in the infected host and in the spinal fluid of those with central nervous system manifestations. Long-​term postinfectious sequelae including persistent denervation of affected muscle groups resulting in weakness.43,44 Metabolic Derangements: Combined Subacute Degeneration (Vitamin B12 Deficiency) and Copper Deficiency Myelopathy Combined Subacute Degeneration

Vitamin B12 deficiencies can present with neurological manifestations including abnormal sensation, spastic paresis, and gait and proprioception disturbances. Patients may also show signs of dementia. These symptoms are manifested by demyelination of the dorsal and lateral columns of the spinal cord resulting in a spongy appearance, gliosis, and white matter edema. On T2-​weighted MRI, these morphological changes will be presented as hyperintense T2 lesions within the affected region of the spinal cord. It is important to note that folate, vitamin E, and copper deficiencies can present with similar symptoms, and laboratory studies and assays are vital to diagnosis.45–​47 Additionally, patients may demonstrate elevated homocysteine levels and megaloblastic anemia on peripheral blood smear. Long-​ term treatment of subacute combined degeneration depends on the cause of vitamin B12 deficiency, but supplementation with intramuscular injections of vitamin B12 is a common early intervention. Nitrous oxide exposure inactivates vitamin B12, causing a functional deficiency and can result in a similar manifestation.48 Copper Deficiency Myelopathy

Copper deficiency myelopathy (CDM) is clinically indistinguishable from subacute combined degeneration. Patients most commonly affected by CDM are usually in their fifth or sixth decade of life who have had prior upper GI procedures, zinc overload, or a malabsorption disorder, all of which lead to decreased absorption of dietary

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copper. Copper deficiency myelopathy can be treated with oral or parenteral copper supplementation.49 Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease)

Amyotrophic lateral sclerosis (ALS) is a rapidly progressing neurodegenerative disorder affecting the anterior horn cells of the spinal cord. Patients present with both upper and lower neuron findings including muscle fasciculations, weakness, and spasticity. Bulbar symptoms, including difficulties swallowing and speaking, often present first. Ultimately, most patients die from respiratory dysfunction. Nerve conduction studies and electromyography (EMG) are gold standards for diagnosis. Treatment of ALS is primarily symptomatic management. Riluzole has been approved by the US Food and Drug Administration (FDA) for treatment of ALS but has marginal benefits.50,51 Friedrich Ataxia

Friedrich ataxia (FA) is an autosomal recessive disorder caused by a GAA trinucleotide expansion of the frataxin gene on chromosome 9q13 resulting in disruption of oxidative phosphorylation in the mitochondria. This disease typically presents by the age of 10 with gait ataxia, but over time, it progresses to loss of deep tendon reflexes, dysarthria, loss of proprioception, kyphoscoliosis, and cardiomyopathy. Loss of myelinated neurons in the dorsal root ganglion, dentate nucleus, dorsal columns, and sensory neurons are all present in FA.52,53 MRI scans will typically reveal degeneration of the cervical spinal cord and the superior cerebellar peduncles. Additionally, T2-​weighted scans will show hypointensity in the dentate nucleus.54,55 Cardiac abnormalities can include concentric hypertrophy, dilation, or mural thrombi, all of which can be demonstrated on echocardiography. Treatment is symptomatic management, addressing issues with coordination, scoliosis, and cardiomyopathy.56 References and Further Reading

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cervical spine in a cadaver model of intubation. Ann Emerg Med. 2000 Oct;36(4):293–​300. PubMed PMID: 11020675. 6. Lennarson PJ, Smith DW, Sawin PD, Todd MM, Sato Y, Traynelis VC. Cervical spinal motion during intubation: Efficacy of stabilization maneuvers in the setting of complete segmental instability. J Neurosurg. 2001 Apr;94(2 Suppl):265–​270. PubMed PMID: 11302629. 7. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-​Radiography Utilization Study Group. N Engl J Med. 2000 Jul 13;343(2): 94–​99. Erratum in: N Engl J Med 2001 Feb 8;344(6):464. PubMed PMID: 10891516. 8. Bush L, Brookshire R, Roche B, et al. Evaluation of cervical spine clearance by computed tomographic scan alone in intoxicated patients with blunt trauma. JAMA Surg. 2016 Sep 1;151(9):807–​813. doi: 10.1001/​jamasurg.2016.1248. PubMed PMID: 27305663. 9. Tso MK, Lee MM, Ball CG, Morrish WF, Mitha AP, Kirkpatrick AW, Wong JH. Clinical utility of a screening protocol for blunt cerebrovascular injury using computed tomography angiography. J Neurosurg. 2017 Apr;126(4):1033–​1041. doi:  10.3171/​2016.1.JNS151545. Epub Apr 22, 2016. PubMed PMID: 27104846. 10. Martínez-​Pérez R, Cepeda S, Paredes I, Alen JF, Lagares A. MRI prognostication factors in the setting of cervical spinal cord injury secondary to trauma. World Neurosurg. 2017 May;101:623–​ 632. doi:  10.1016/​ j.wneu.2017.02.034. Epub Feb 16, 2017. PubMed PMID: 28216400. 11. Catapano JS, John Hawryluk GW, Whetstone W, et al. Higher mean arterial pressure values correlate with neurologic improvement in patients with initially complete spinal cord injuries. World Neurosurg. 2016 Dec;96:72–​79. doi: 10.1016/​j.wneu.2016.08.053. Epub Aug 23, 2016. PubMed PMID: 27565460; PubMed Central PMCID: PMC5127746. 12. Yue JK, Winkler EA, Rick JW, et  al. Update on critical care for acute spinal cord injury in the setting of polytrauma. Neurosurg Focus. 2017 Nov;43(5):E19. doi:  10.3171/​ 2017.7.FOCUS17396. PubMed PMID: 29088951. 13. Kronvall E, Sayer FT, Nilsson OG. [Methylprednisolone in the treatment of acute spinal cord injury has become more and more questioned]. Lakartidningen. 2005 Jun 13-​26;102(24-​ 25):1887–​1888, 1890. Swedish. PubMed PMID: 16044768. 14. Alkabie S, Boileau AJ. The role of therapeutic hypothermia after traumatic spinal cord injury—​ A systematic review. World Neurosurg. 2016 Feb;86:432–​ 449. doi:  10.1016/​ j.wneu.2015.09.079. Epub Dec 22, 2015. PubMed PMID: 26433095. 15. Chinnock P, Roberts I. Gangliosides for acute spinal cord injury. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD004444. PubMed PMID: 15846715. 16. Gastaldi M, Marchioni E, Banfi P, et al. Predictors of outcome in a large retrospective cohort of patients with transverse myelitis. Mult Scler. 2017 Sep 1:1352458517731911. doi: 10.1177/​ 1352458517731911. [Epub ahead of print] PubMed PMID: 28967297. 17. Brex PA, Ciccarelli O, O’Riordan JI, Sailer M, Thompson AJ, Miller DH. A longitudinal study of abnormalities on MRI and disability from multiple sclerosis. N Engl J Med. 2002 Jan 17;346(3):158–​164. PubMed PMID: 11796849. 18. Centers for Disease Control. CDC website:  https://​www.cdc.gov/​acute-​flaccid-​myelitis/​ index.html 19. Balashov K. Imaging of central nervous system demyelinating disorders. Continuum (Minneap Minn). 2016 Oct;22(5, Neuroimaging):1613–​1635. PubMed PMID: 27740991.

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20. Barreras P, Fitzgerald KC, Mealy MA, et al. Clinical biomarkers differentiate myelitis from vascular and other causes of myelopathy. Neurology. 2018 Jan 2;90(1):e12–​e21. doi: 10.1212/​ WNL.0000000000004765. Epub Dec 1, 2017. PubMed PMID: 29196574; PubMed Central PMCID: PMC5754646. 21. de Seze J, Stojkovic T, Breteau G, et al. Acute myelopathies: Clinical, laboratory and outcome profiles in 79 cases. Brain. 2001 Aug;124(Pt 8):1509–​1521. PubMed PMID: 11459743. 22. Thompson AJ et al. 2018. 23. Vidal-​ Jordana A. New advances in disease-​ modifying therapies for relapsing and progressive forms of multiple sclerosis. Neurol Clin. 2018 Feb;36(1):173–​183. doi:  10.1016/​ j.ncl.2017.08.011. PubMed PMID: 29157398. 24. Mitsikostas DD, Goodin DS. Comparing the efficacy of disease-​modifying therapies in multiple sclerosis. Mult Scler Relat Disord. 2017 Nov;18:109–​116. doi: 10.1016/​j.msard.2017.08.003. Epub Aug 18, 2017. PubMed PMID: 29141791. 25. Wingerchuk DM, Lennon VA, Lucchinetti CF, Pittock SJ, Weinshenker BG. The spectrum of neuromyelitis optica. Lancet Neurol. 2007 Sep;6(9):805–​815. PubMed PMID: 17706564. 26. Pittock SJ, Lucchinetti CF. Neuromyelitis optica and the evolving spectrum of autoimmune aquaporin-​4 channelopathies:  A decade later. Ann N Y Acad Sci. 2016 Feb;1366(1):20–​39. doi: 10.1111/​nyas.12794. Epub Jun 10, 2015. PubMed PMID: 26096370; PubMed Central PMCID: PMC4675706. 27. Hinson SR, Lennon VA, Pittock SJ. Autoimmune AQP4 channelopathies and neuromyelitis optica spectrum disorders. Handb Clin Neurol. 2016;133:377–​403. doi:  10.1016/​B978-​0-​ 444-​63432-​0.00021-​9. PubMed PMID: 27112688. 28. Wang Y, Wang Y, Tan S, Lu Z. Spinal cord atrophy in neuromyelitis optica spectrum disorders. Mult Scler Relat Disord. 2016 Jul;8:9–​10. doi:  10.1016/​j.msard.2016.04.007. Epub Apr 9, 2016. PubMed PMID: 27456868. 29. Bonnan M, Valentino R, Debeugny S, Merle H, Fergé JL, Mehdaoui H, Cabre P. Short delay to initiate plasma exchange is the strongest predictor of outcome in severe attacks of NMO spectrum disorders. J Neurol Neurosurg Psychiatry. 2017 Oct 13. pii: jnnp-​2017-​316286. doi: 10.1136/​jnnp-​2017-​316286. [Epub ahead of print] PMID:29030418. 30. Evangelopoulos ME, Andreadou E, Koutsis G, et al. Treatment of neuromyelitis optica and neuromyelitis optica spectrum disorders with rituximab using a maintenance treatment regimen and close CD19 B cell monitoring. A  six-​year follow-​up. J Neurol Sci. 2017 Jan 15;372:92–​96. doi: 10.1016/​j.jns.2016.11.016. Epub Nov 10, 2016. PMID: 28017256. 31. Nasr DM, Rabinstein A. Spinal cord infarcts:  Risk factors, management, and prognosis. Curr Treat Options Neurol. 2017 Aug;19(8):28. doi:  10.1007/​s11940-​017-​0464-​3. PubMed PMID: 28688063. 32. Romi F, Naess H. Spinal cord infarction in clinical neurology: A review of characteristics and long-​term prognosis in comparison to cerebral infarction. Eur Neurol. 2016;76(3-​4):95–​98. Epub Aug 4, 2016. PubMed PMID: 27487411. 33. Rigney L, Cappelen-​ Smith C, Sebire D, Beran RG, Cordato D. Nontraumatic spinal cord ischaemic syndrome. J Clin Neurosci. 2015 Oct;22(10):1544–​ 1549. doi:  10.1016/​ j.jocn.2015.03.037. Epub Jul 4, 2015. PubMed PMID: 26154150. 34. Rabinstein AA. Vascular myelopathies. Continuum (Minneap Minn). 2015 Feb;21(1 Spinal Cord Disorders):67–​ 83. doi:  10.1212/​ 01.CON.0000461085.79241.e0. PubMed PMID: 25651218.

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35. Freedman BA, Malone DG, Rasmussen PA, Cage JM, Benzel EC. Surfer’s myelopathy:  A rare form of spinal cord infarction in novice surfers: A systematic review. Neurosurgery. 2016 May;78(5):602–​611. doi: 10.1227/​NEU.0000000000001089. PubMed PMID: 27082966. 36. Tanenbaum LN. Clinical applications of diffusion imaging in the spine. Magn Reson Imaging Clin N Am. 2013 May;21(2):299–​320. doi: 10.1016/​j.mric.2012.12.002. Epub Mar 7, 2013. PubMed PMID: 23642555. 37. Marra CM. Neurosyphilis. Continuum (Minneap Minn). 2015 Dec;21(6 Neuroinfectious Disease):1714–​1728. doi: 10.1212/​CON.0000000000000250. PubMed PMID: 26633785. 38. Gessain A, Mahieux R. Tropical spastic paraparesis and HTLV-​ 1 associated myelopathy: Clinical, epidemiological, virological and therapeutic aspects. Rev Neurol (Paris). 2012 Mar;168(3):257–​ 269. doi:  10.1016/​ j.neurol.2011.12.006. Epub Mar 7, 2012. PubMed PMID: 22405461. 39. Matsuura E, Nozuma S,Tashiro Y, Kubota R, Izumo S,Takashima H. HTLV-​1 associated myelopathy/​tropical spastic paraparesis (HAM/​TSP):  A comparative study to identify factors that influence disease progression. J Neurol Sci. 2016 Dec 15;371:112–​116. doi:  10.1016/​ j.jns.2016.10.030. Epub Oct 21, 2016. PubMed PMID: 27871430. 40. Oh U, Jacobson S. Treatment of HTLV-​ I-​ associated myelopathy/​ tropical spastic paraparesis:  Toward rational targeted therapy. Neurol Clin. 2008 Aug;26(3):781–​797, ix-​x. doi:  10.1016/​ j.ncl.2008.03.008. PubMed PMID:  18657726; PubMed Central PMCID: PMC2610848. 41. Kabir M, Afzal MS. Epidemiology of polio virus infection in Pakistan and possible risk factors for its transmission. Asian Pac J Trop Med. 2016 Nov;9(11):1044–​1047. doi: 10.1016/​ j.apjtm.2016.09.006. Epub Oct 24, 2016. PubMed PMID: 27890362. 42. Tangermann RH, Lamoureux C, Tallis G, Goel A. The critical role of acute flaccid paralysis surveillance in the Global Polio Eradication Initiative. Int Health. 2017 May 1;9(3):156–​163. doi: 10.1093/​inthealth/​ihx016. PubMed PMID: 28582560. 43. Athar P, Hasbun R, Nolan MS, Salazar L, Woods SP, Sheikh K, Murray KO. Long-​term neuromuscular outcomes of West Nile virus infection: A clinical and electromyographic evaluation of patients with a history of infection. Muscle Nerve. 2018 Jan;57(1):77–​82. doi: 10.1002/​ mus.25660. Epub Jun 17, 2017. PubMed PMID: 28380696. 44. Leis AA, Stokic DS. Neuromuscular manifestations of West Nile virus infection. Front Neurol. 2012 Mar 21;3:37. doi:  10.3389/​ fneur.2012.00037. eCollection 2012. PubMed PMID: 22461779; PubMed Central PMCID: PMC3309965. 45. Goodman BP. Metabolic and toxic causes of myelopathy. Continuum (Minneap Minn). 2015 Feb;21(1 Spinal Cord Disorders):84–​ 99. doi:  10.1212/​ 01.CON.0000461086.79241.3b. PubMed PMID: 25651219. 46. Hemmer B, Glocker FX, Schumacher M, Deuschl G, Lücking CH. Subacute combined degeneration: Clinical, electrophysiological, and magnetic resonance imaging findings. J Neurol Neurosurg Psychiatry. 1998 Dec;65(6):822–​827. PubMed PMID: 9854956; PubMed Central PMCID: PMC2170379. 47. Scalabrino G. Cobalamin (vitamin B(12)) in subacute combined degeneration and beyond: Traditional interpretations and novel theories. Exp Neurol. 2005 Apr;192(2):463–​479. Erratum in: Exp Neurol. 2005 Aug;194(2):561. PubMed PMID: 15755562. 48. Hathout L, El-​Saden S. Nitrous oxide-​induced B12 deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B12. J Neurol Sci. 2011 Feb 15;301(1–​2):1–​8. doi: 10.1016/​ j.jns.2010.10.033. Epub Nov 26, 2010. PubMed PMID: 21112598.

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49. Winston GP, Jaiser SR. Copper deficiency: An unusual case of myelopathy with neuropathy. Ann Clin Biochem. 2008 Nov;45(Pt 6):616–​617. doi: 10.1258/​acb.2008.008122. Epub Sep 9, 2008. PubMed PMID: 18782809. 50. Kiernan MC, Vucic S, Cheah BC, et  al. Amyotrophic lateral sclerosis. Lancet. 2011 Mar 12;377(9769):942–​955. doi: 10.1016/​S0140-​6736(10)61156-​7. Epub Feb 4, 2011. PubMed PMID: 21296405. 51. Rowland LP. Ameliorating amyotrophic lateral sclerosis. N Engl J Med. 2010 Mar 11;362(10):953–​954. doi: 10.1056/​NEJMcibr0912229. PubMed PMID: 20220193. 52. Harding AE. Friedreich’s ataxia:  A clinical and genetic study of 90 families with an analysis of early diagnostic criteria and intrafamilial clustering of clinical features. Brain. 1981 Sep;104(3):589–​620. PubMed PMID: 7272714. 53. Dürr A, Cossee M,AgidY, et al. Clinical and genetic abnormalities in patients with Friedreich’s ataxia. N Engl J Med. 1996 Oct 17;335(16):1169–​1175. PubMed PMID: 8815938. 54. Koeppen AH, Becker AB, Qian J, Feustel PJ. Friedreich ataxia: Hypoplasia of spinal cord and dorsal root ganglia. J Neuropathol Exp Neurol. 2017 Feb 1;76(2):101–​108. doi: 10.1093/​jnen/​ nlw111. PubMed PMID: 28082326. 55. Koeppen AH. Friedreich’s ataxia: Pathology, pathogenesis, and molecular genetics. J Neurol Sci. 2011 Apr 15;303(1-​2):1–​12. doi: 10.1016/​j.jns.2011.01.010. PubMed PMID: 21315377; PubMed Central PMCID: PMC3062632. 56. Dürr A. Friedreich’s ataxia: Treatment within reach. Lancet Neurol. 2002 Oct;1(6):370–​374. PubMed PMID: 12849398.

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Index

acute traumatic central cord syndrome (ATCCS) aftercare,  37–​38 anterior cervical discectomy and fusion, 35 ASIA motor score, 32 assessment and planning, 31–​32 case presentation, 31 complications and management, 38 decision-​making, 34, 38 diagnosis, 33 imaging studies showing ATCCS, 32 surgical procedure, anterior cervical discectomy and fusion, 34 surgical procedure, laminectomy, 36, 37 surgical procedure, laminoplasty, 34, 36 surgical procedure, planning, 34 surgical procedure, technique, 36 two-​level anterior cervical discectomy and fusion, 35 adjacent segment disease (ASD), 204 adult degenerative scoliosis. See flat back deformity; lumbar degenerative scoliosis air embolism, following cervical foraminotomy, 106 American Spinal Injury Association (ASIA), 12, 32, 243 amyotrophic lateral sclerosis (ALS), 248 Anderson and D’Alonzo classification for fractures, 1, 2 anterior cervical corpectomy with fusion (ACCF), 86–​87, 88 anterior cervical discectomy with fusion (ACDF) vs. CDR, 99 for cervical radiculopathy due to central disc, 93–​99 indications for, 34 for ossification of posterior longitudinal ligament, 86–​87, 88 surgical procedure, ventral approach, 95–​97 surgical technique, 36 three-​level,  35 two-​level,  35 anterior lumbar interbody fusion (ALIF), 220 anticholinergic medications, for symptomatic bradycardia,  17–​18

antiplatelet agents, ATCCS and, 38 AO (Arbeitsgemeinschaft für Osteosynthesefragen) classification, 125, 126 arachnoid cysts, 110 arteriovenous fistulas (AVFs), 111 arteriovenous malformations (AVMs), 111 astrocytomas assessment and planning, 141–​42 diagnosis, 143 management, 145 surgical procedure, 145 treatment, 144 atelectasis, preventing, 38 atlantoaxial instability aftercare,  46–​47 assessment and planning, 41–​43 case presentation, 41 complications and management, 47 CT scan showing rheumatoid pannus causing upper cervical stenosis, 42 decision-​making,  43–​44 diagnosis, 43 evidence and outcomes, 47 intraoperative x-​rays showing C1 lateral mass–​C2 pars screw-​rod placement, 45 management, 46 MRI showing severe canal stenosis and associated T2 signal abnormality at 1–​11, 42 postoperative lateral and anteroposterior cervical x-​rays, 46 surgical procedure, 44–​45 See also basilar invagination and cranial settling atlantodental interval (ADI), measuring, 43 atlanto-​occipital dislocation (AOD) aftercare, 28 assessment and planning, 21–​23 Bellbarba classification system, 25 case presentation, 21

253

254

Index

atlanto-​occipital dislocation (AOD) (Cont.) complications and management, 28–​29 decision-​making,  24–​25 diagnosis, 23 evidence and outcomes, 29–​30 Harris method, 24 management,  27–​28 occipital–​C4 fusion, 27 scans showing atlanto-​occipital dislocation, 22 surgical procedure, 25–​27 Traynelis Classification System, 25, 26 atropine, for symptomatic bradycardia, 17–​18 autonomic dysreflexia, in cervical fracture dislocation, 17–​18 axial back pain management,  191–​94 treatment, 185, 187 basilar impression, 49 basilar invagination and cranial settling aftercare,  58–​59 assessment and planning, 49–​51 case presentation, 49 complications and management, 59–​60 CT images showing adequate ventral decompression, 58 CT images showing basilar invagination with significant upward translation of the odontoid into the posterior fossa, 50 CT images showing basilar invagination with upward migration of the C1-​C2 complex into the cranial vault, 51 decision-​making,  52–​53 diagnosis, 52 evidence and outcomes, 60–​61 illustration of anterior cervical spine during surgery, 57 illustration showing relevant normal anatomy and operative angles, 59 intraoperative photographs showing C1 ring, resection, and transverse ligaments, 56 management,  57–​58 surgical procedure, endoscopic approaches, 56–​57 surgical procedure, extended transoral approaches, 55–​56 surgical procedure, transoral-​transpharyngeal approach, 54–​55 basion-​axial interval (BAI), 24 basion-​dental interval (BDI), 24 Bellbarba classification system, 25 bilateral hand pain and numbness, in atlantoaxial instability, 41 Brooks and Jenkins technique, 45, 47

254

burst fractures, L3 pathologic, 160, 163. See also thoracolumbar burst fractures C5 palsy following cervical foraminotomy, 107 following surgery for cervical myelopathy, 68 following surgery for ossification of posterior longitudinal ligament, 90 Campylobacter jejuni, 244 cauda equina syndrome (CES) aftercare, 180 assessment and planning, 175–​76 case presentation, 175 complications and management, 180–​81 compressive vs. noncompressive etiologies, 176 decision-​making,  177–​78 diagnosis, 176 differential diagnosis, 175 evidence and outcomes, 181 management,  179–​80 MRI at L4-​L5 level showing acute disc herniation, 177 surgical procedure, 178–​79 central cord injury/​central cord syndrome. See acute traumatic central cord syndrome cerebrospinal fluid (CSF) leak in cervical fracture dislocation, 18 decreasing risk of, 188 following cervical foraminotomy, 106–​7 following laminoplasty, 145, 146, 147 following surgery for basilar invagination, 59–​60 following surgery for intramedullary spinal cord tumors, 146, 147 following surgery for isthmic spondylolisthesis, 204 following surgery for ossification of posterior longitudinal ligament, 90 cervical arthroplasty complications and management, 98 contraindications for, 97 indications for, 97 reoperation rate following, 99 suitable candidates for, 95 surgical procedure, 96 See also cervical radiculopathy, central disc cervical collar, in atlanto-​occipital dislocation, 21, 22–​23, 25, 27, 28 cervical disc replacement (CDR) vs. ACDF, 99

 

Index

complications and management, 98 contraindications for, 95 surgical procedure, ventral approach, 95–​97 cervical foraminotomy. See cervical radiculopathy, central disc cervical fracture dislocation aftercare, 17 assessment and planning, 11–​13 case presentation, 11 complications and management, 18–​19 CT demonstrating C5-​C6 cervical fracture dislocation, 13 decision-​making,  15 diagnosis,  14–​15 evidence and outcomes, 19 jumped facets, 12–​13 management, 17 MRI depicting C5-​C6 spinal canal comprise, 14 surgical procedure, 16 See also odontoid fracture type II cervical myelopathy assessment and planning, 83–​84 in atlantoaxial instability, 41 diagnosis, 83 differential diagnosis, 81 scales for, 84–​86 treatment,  84–​86 cervical myelopathy, kyphosis aftercare, 77 assessment and planning, 71–​73 case presentation, 71 complications and management, 77–​79 decision-​making,  74 diagnosis,  72–​73 evidence and outcomes, 79 images confirming good correction of cervical kyphosis, 78 images showing multiple degenerative changes causing severe kyphosis, 72 management,  76–​77 strategies to achieve correction of, 76–​77 surgical procedure, 75 x-​rays of cervical spine ruling out fusion of facet joints, 73 x-​rays of cervical spine showing satisfactory sagittal and coronal alignment, 75 cervical myelopathy, lordosis aftercare, 68 assessment and planning, 63–​64 case presentation, 63

complications and management, 68–​69 decision-​making,  65–​66 diagnosis, 65 differential diagnosis, 63 evidence and outcomes, 69 management,  67–​68 MRI showing 21–​41 surgical procedure, 66–​67 cervical radiculopathy, central disc aftercare, 97 assessment and planning, 93–​95 case presentation, 93 complications and management, 98 decision-​making,  95 diagnosis, 95 evidence and outcomes, 98–​99 images showing lateral disc extrusion with extension to neural foramen, 94 postoperative image of disc replacement, 96 surgical procedure, 95–​97 cervical radiculopathy, lateral disc foraminotomy aftercare, 106 assessment and planning, 101–​2, 103 case presentation, 101 complications and management, 106–​7 contraindications to, 103 decision-​making,  103 diagnosis,  102–​3 evidence and outcomes, 107 illustration of anterior and posterior approaches for cervical foraminotomy, 105 images showing foraminal stenosis and disc herniation vs. normal cervical lordosis, 102 management,  105–​6 surgical procedure, anterior approach, 104 surgical procedure, posterior approach, 104–​5 cervical spine fracture. See cervical fracture dislocation Chiari type I malformations, in basilar invagination, 50–​51, 55 CNS (Congress of Neurological Surgeons), 12, 14 combined subacute degeneration (vitamin B12 deficiency), 247 compressive disc herniation pathologies arachnoid cysts, 110 degenerative, 109 disc herniation of thoracic spine, 110 infectious (epidural abscesses), 110–​11 neoplastic, 111

255

256

Index

traumatic, 110 vascular (AVMs and AVFs), 111 See also cauda equina syndrome condyle-​C1 interval (CCI), 24–​25 congenital arcuate foramen, in odontoid fracture type II, 8 Congress of Neurological Surgeons (CNS), 12, 14 copper deficiency myelopathy (CDM), 247–​48 costotransversectomy to thoracic spine, 114–​15 cranial settling, 49–​50, 52. See also basilar invagination and cranial settling cruciate paralysis, 23 CT myelogram is indications for, 209–​11 degeneration, differential diagnosis, 63 degenerative cervical myelopathy. See cervical myelopathy, kyphosis degenerative spondylolisthesis. See spondylolisthesis, L4–​L5 degenerative demyelinating disc herniation pathologies multiple sclerosis, 111–​12 transverse myelitis, 112 demyelinating spinal diseases multiple sclerosis, 245 neuromyelitis optica and neuromyelitis optica spectrum disorder, 245 transverse myelitis, 244 dens fracture. See odontoid fracture type II DEXA (dual-​energy x-​ray absorptiometry) bone densitometry evaluation of, 217 indications for, 208, 216 dextroscoliosis,  209–​11 disc herniation of thoracic spine, 110 diskitis aftercare, 231 assessment and planning, 225–​26 case presentation, 225 complications and management, 232 decision-​making,  228–​29 diagnosis, 227 differential diagnosis, 225 evidence and outcomes, 233 followup MRI at 8 weeks, 232 images showing vertebral body destruction and focal kyphosis, 227 management, 231 postoperative x-​rays, 230

256

preoperative MRI, 228 surgical procedure, 229–​30 dorsolateral/​lateral approaches to thoracic spine, 114–​15 dropped head syndrome, causes, 71 dysphagia in cervical fracture dislocation, 18 following cervical foraminotomy, 107 in odontoid fracture type II, 8 ECOG (Eastern Cooperative Oncology Group) scoring, 171–​72 elderly patients contraindications for rigid external immobilization, 4 posterior approach in odontoid fracture type II, 8–​9 superiority of surgery in odontoid fracture type II, 9 enterococcus,  225–​26 enteroviruses, 244, 247 ependymomas assessment and planning, 141–​42 diagnosis, 143 management, 145 risk factors for, 144 treatment, 144 epidural abscesses. See spinal epidural abscesses epidural spinal cord compression delineating degree of, 136 management, 140 ESCC (Epidural Spinal Cord Compression) grading scale,  163–​67 esophageal injuries, in cervical fracture dislocation, 18–​19 Ewing’s sarcoma, treatment, 133 extradural spinal tumors aftercare, 139 assessment and planning, 133 complications and management, 139 decision-​making,  135–​37 diagnosis,  134–​35 differential diagnosis, 133 epidural spinal cord compression scale, 136 evidence and outcomes, 140 images depicting T3 cage, 138 images showing spinal cord compression, 135 management, 138 surgical procedure, 137 flat back deformity aftercare,  222–​23

 

Index

assessment and planning, 215–​16 case presentation, 215 CT scans showing previous hardware without instrumentation failures, 218 decision-​making,  219–​20 diagnosis,  216–​17 management, 222 MRIs showing no central stenosis, 217 surgical procedure, 221 x-​rays showing postoperative scoliosis, 222 x-​rays showing previous hardware, 218 x-​rays showing standing scoliosis, 219 foraminotomy contraindications to, 103 See also cervical radiculopathy, lateral disc foraminotomy fracture dislocation. See cervical fracture dislocation fracture reduction, in cervical fracture dislocation, 15–​17 Friedrich ataxia (FA), 248 fusion anterior cervical corpectomy with fusion, 86–​87, 88 anterior cervical discectomy with fusion, 34, 35, 36, 86–​87, 88,  93–​99 anterior lumbar interbody fusion, 220 C1-​C2 fusion for odontoid fracture type II, C1.P18 CDR vs. anterior cervical discectomy and fusion, 99 images of cervical spine with posterior C1-​C2 fusion, 7 instrumented fusion for isthmic spondylolisthesis, 205 interbody fusion, 194–​95 occipital–​C4 fusion, 27 posterior lumbar interbody fusion, 194–​95, 201–​2 posterolateral fusion, 194–​95 transforaminal lumbar interbody fusion, 194–​95, 201–​2, 220 Gallie technique, 45 Goel and Laheri technique, 44–​45, 47 Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injury, 12, 14 halo orthosis, in cervical fracture dislocation, 18 halo vest, in atlanto-​occipital dislocation, 22–​23, 25, 27, 28 Harms and Melcher technique, 44–​45, 47 Harm’s technique, 44–​45, 47 Harris method, 24 hemangioblastomas, diagnosis, 143 hematomas, following cervical foraminotomy, 106 herniated discs

as cause of cauda equina syndrome, 176 emergent decompression for, 177 images showing foraminal stenosis and disc herniation vs. normal cervical lordosis, 102 MRI at L4-​L5 level showing acute disc herniation, 177 risk and benefit profile of surgery for, 178 surgical procedure, 179 thoracic disc herniation, 109–​19 herniated thoracic disc (HTD). See thoracic disc herniation Hoffmann reflex, in cervical spondylotic myelopathy, 65 Horner syndrome, following cervical foraminotomy, 106–​7 HTLV-​1–​associated myelopathy,  246–​47 hyperextension spinal cord injury, ATCCS due to, 32–​33 infectious myelopathies HTLV-​1–​associated myelopathy/​tropical spastic paraparesis,  246–​47 neurosyphilis, 246 West Nile virus and polio virus, 247 See also spinal epidural abscesses instrumented fusion for isthmic spondylolisthesis, 205 interbody fusion augmentations for, 195 benefits of, 194–​95 for spondylolisthesis, 194 International Spinal Cord Society (ISCoS), 243 intradural extramedullary spinal tumors. See spinal cord tumors, intradural extramedullary intramedullary spinal cord tumor (IMSCT). See spinal cord tumors, intramedullary isthmic spondylolisthesis (IS) aftercare, 204 assessment and planning, 200 case presentation, 199 classification system, 200 complications and management, 204 decision-​making,  201 diagnosis, 200 differential diagnosis, 199 evidence and outcomes, 204–​5 management, 203 MRI showing L4-​L5 disc space, 200 post-​operative x-​rays showing pedicle screw fixation with PEEK interbody, 203 surgical procedure, 201–​2

257

258

Index

Japanese Orthopedic Association scale, 81, 86 jumped facets, 12–​13 kyphosis aftercare, 77 assessment and planning, 71–​73 complications and management, 77–​79 decision-​making,  74 diagnosis,  72–​73 evidence and outcomes, 79 images confirming good correction of cervical kyphosis, 78 images showing multiple degenerative changes causing severe kyphosis, 72 management,  76–​77 post laminectomy, 65–​66, 67, 147, 153, 157 reducing risk of PJK, 220, 222 selection of surgical approach in, 68 strategies to achieve correction of, 76–​77 surgical procedure, 75 x-​rays of cervical spine ruling out fusion of facet joints, 73 x-​rays of cervical spine showing satisfactory sagittal and coronal alignment, 75 laminectomy kyphosis following, 147, 153, 157 vs. laminoplasty, 144–​45, 147 for lumbar stenosis, 186 surgical procedure, 187 traditional open vs. minimally invasive techniques, 186, 189 laminoplasty advantages of, 153 avoiding CSF leak following, 145, 146, 147 vs. laminectomy, 144–​45, 147 lateral disc foraminotomy. See cervical radiculopathy, lateral disc foraminotomy lateral extracavitary approach to thoracic spine, 115 lateral parascapular extrapleural approach to thoracic spine, 115 levoscoliosis,  209–​11 lightning pains, 246 lordosis. See cervical myelopathy, lordosis Lou Gehrig’s Disease, 248 lumbar degenerative scoliosis aftercare, 213 assessment and planning, 208 case presentation, 207 complications and management, 213

258

decision-​making,  209–​11 diagnosis, 208 evidence and outcomes, 213–​14 management,  212–​13 MRI showing foraminal and canal stenosis, 209 radiographs at 36-​month postoperative follow-​up, 212 radiographs at time of presentation, 210 surgical procedure, 211–​12 lumbar lordosis (LL), documentation with standing scoliosis x-​rays,  216 lumbar nerve compression. See cauda equina syndrome lumbar stenosis aftercare, 187 assessment and planning, 183–​84 case presentation, 183 complications and management, 188 decision-​making,  185 diagnosis, 184, 208 evidence and outcomes, 188–​89 management, 187 MRIs showing L2-​L3 stenosis, 185 surgical procedure, 186–​87 lupus, 244 Magerl’s C1–​C2 transarticular, 47 meningiomas assessment and planning, 150–​51 complications and management, 156 diagnosis, 151–​52, 155 surgical procedure, 153–​54, 155–​56 metabolic spinal derangements combined subacute degeneration (vitamin B12 deficiency), 247 copper deficiency myelopathy, 247–​48 metastatic tumors deep vein thrombosis with, 139 diagnosis, 134 management, 140 thoracic cord compression due to, 133 microdiscectomy, 103–​4, 107 microsurgery, for intramedullary spinal cord tumors, 145 minimally invasive approaches to thoracic spine, 117 minimally invasive surgery aftercare,  187–​88 benefits of, 187 vs. traditional open laminectomies, 186, 189

 

Index

multiple myeloma diagnosis, 163 indication for spinal surgery in, 171 multiple sclerosis (MS), 111–​12, 244, 245 neck hematoma, following cervical foraminotomy, 106 neck pain, in atlantoaxial instability, 43–​44 neoplastic disc herniation, 111 neurofibromas assessment and planning, 150 diagnosis, 151–​52, 155 neurogenic claudication assessment and planning, 183–​84 diagnosis, 185 management, 187 neurologic deficits preventing, 238 in spinal epidural abscesses, 236 neuromonitoring during surgery for intradural extramedullary spinal cord tumors, 154–​55, 156, 157 during surgery for intramedullary spinal cord tumors, 144–​46 neuromyelitis optica (NMO), 245 neuromyelitis optica spectrum disorder (NMOSD), 245 neurosyphilis, 246 NOMS (neurologic, oncologic, mechanical, and systemic) framework, 135–​36, 163, 164, 171, 172 noncompressive disc herniation pathologies demyelinating,  111–​12 metabolic (vitamin B12 deficiency), 112 vascular (spinal arterial thrombosis), 112 nonsurgical spinal diseases amyotrophic lateral sclerosis, 248 demyelinating diseases, 244–​45 Friedrich ataxia, 248 infectious myelopathies, 246–​47 metabolic derangements, 247 trauma,  243–​44 vascular myelopathies, 246 Nurick myelopathy scale, 84–​86 occipital neuralgia, in odontoid fracture type II, 8 occipitocervical dislocation. See atlanto-​occipital dislocation occipitocervical junction pathology. See basilar invagination and cranial settling odontoid fracture type II

aftercare, 7 Anderson and D’Alonzo classification for fractures, 1, 2 assessment and planning, 1–​2 case presentation, 1 complications and management, 8 complications and management, intraoperative, 7 complications and management, postoperative, 8 decision-​making,  3–​4 diagnosis, 1 evidence and outcomes, 8–​9 Hamm’s technique and retraction of C2 nerve root, 5 images of cervical spine with posterior C1-​C2 fusion, 7 management, 6 risk factors for nonunion, 3 sagittal view of cervical spine showing type II C odontoid fracture, 4 sub classifications proposed by Grauer, 2, 3 surgical procedure, 6 surgical procedure, approach, 5 surgical procedure, positioning, and preparation, 5 odontoid screw fixation, 2 ossification of posterior longitudinal ligament, cervical aftercare, 89 assessment and planning, 81–​83 case presentation, 81 complications and management, 90 CT image showing continuous type of ossification., 82 CT image showing double-​layer sign, 82 CT image showing single-​layer sign for dural penetration, 85 CT image with representative segmental variant ossification of the posterior longitudinal ligament, 84 decision-​making,  84–​86 diagnosis, 83 differential diagnosis, 81 evidence and outcomes, 90 management, 87 Modified Japanese Orthopedic Association Scale, 86 MRI image showing ossification of the posterior longitudinal ligament, 83 Nurick’s Classification System, 85 postoperative images of C4 to T10 laminectomy, 89 surgical procedure, anesthesia and neuromonitoring, 87 surgical procedure, anterior approach, 88 surgical procedure, pivot points, 89 surgical procedure, posterior approach, 88 osteogenesis imperfecta, basilar invagination and, 49–​50

259

260

Index

osteomyelitis antibiotic treatment, 231 complications and management, 232 diagnosis,  226–​27 evidence and outcomes, 233 risk factors for, 225–​26 surgery for, 229–​30 See also spinal epidural abscesses Oswestry Disability Index (ODI) score, 196, 211 pars interarticularis defect assessment and planning, 200 classification system for isthmic spondylolisthesis, 200 underlying spondylolisthesis, 191 pedicle screw fixation, surgical procedure, 194–​95 pedicle subtraction osteotomies, 221–​22 PEEK (polyether ether ketone), 203 pelvic incidence (PI) assessment of, 217 documentation with standing scoliosis x-​rays, 216, 217 PI–​LL (pelvic incidence and lumbar lordosis) mismatch assessment of, 217 treatment,  219–​20 platybasia,  49–​50 pneumonia preventing, 38 polio virus, 247 positive Babinski reflex, in cervical spondylotic myelopathy, 65 posterior atlantodental interval (PADI), measuring, 43 posterior longitudinal ligament, ossification of. See ossification of posterior longitudinal ligament, cervical posterior lumbar interbody fusion (PLIF), surgical procedure, 194–​95,  201–​2 posterolateral fusion, surgical procedure, 194–​95 postlaminectomy kyphosis following surgery for intradural extramedullary spinal cord tumors, 153, 157 following surgery for intramedullary spinal cord tumors, 147 Powers ratio, 24 prereduction MRIs, controversy over in cervical fracture dislocation, 15 proximal junction failure (PJF), reducing risk of, 220, 222 proximal junction kyphosis (PJK), reducing risk of, 220, 222 Pseudomonas species, 225–​26

260

radiation therapy determining response to, 163–​67 impairment of arthrodesis during, 170 role of surgery in, 167 radiation-​sensitive spine tumors aftercare, 169 assessment and planning, 159–​60 case presentation, 159 complications and management, 170 decision-​making,  163–​67 diagnosis,  161–​63 ECOG (Eastern Cooperative Oncology Group) scoring,  171–​72 ESCC (Epidural Spinal Cord Compression) grading scale,  163–​67 evidence and outcomes, 171–​72 images showing L3-​level fractures, 160 intraoperative fluoroscopy for guidance of Jamshidi needle placement,  167–​69 NOMS (Neurologic, Oncologic, Mechanical and Systemic) framework, 163, 164, 171, 172 post-​treatment images, 170 SINS (Spinal Instability Neoplastic Score), 161–​62, 163–​67 summary of expected radiation response by histology, 166 surgical procedure, 167–​69 radiculopathy in ossification of posterior longitudinal ligament, 83–​84 treatment,  84–​86 retropleural thoracotomy approach to thoracic spine, 117 rule of twelves, 24 Salmonella sp., 244 sarcoidosis, 244 schwannomas assessment and planning, 150 diagnosis, 151–​52, 155 scoliosis. See flat back deformity; lumbar degenerative scoliosis SINS (Spinal Instability Neoplastic Score), 136, 161–​62, 163–​67 Sjögren disease, 244 slipped vertebra. See isthmic spondylolisthesis spinal arterial thrombosis, 112 spinal cord tumors, extradural aftercare, 139 assessment and planning, 133 case presentation, 133 complications and management, 139

 

Index

decision-​making,  135–​37 diagnosis,  134–​35 differential diagnosis, 133 epidural spinal cord compression scale, 136 evidence and outcomes, 140 images depicting T3 cage, 138 images showing spinal cord compression, 135 management, 138 surgical procedure, 137 spinal cord tumors, intradural extramedullary aftercare, 156 assessment and planning, 149–​51 case presentation, 149 cervical spine presentation, 151 complications and management, 156–​57 CT showing intradural partially calcified tumor, 152 decision-​making,  153 diagnosis, 151, 155 differential diagnosis, 149–​50 evidence and outcomes, 157 lumbar spine presentation, 151 MRI showing gross total resection of T2-​T3 mass, 154 MRI showing T2-​T3 mass, 150 surgical procedure, 153–​54, 155–​56 thoracic spine presentation, 151 spinal cord tumors, intramedullary aftercare,  146–​47 assessment and planning, 141–​42 case presentation, 141 complications and management, 147 decision-​making,  144 diagnosis,  143–​44 differential diagnosis, 141–​42 evidence and outcomes, 147–​48 images showing cervicothoracic intramedullary spinal cord tumor, 142 images showing spinal astrocytoma, 143 management,  145–​46 risk factors for, 144 surgical procedure, 144–​45 spinal cord tumors, radiation-​sensitive aftercare, 169 assessment and planning, 159–​60 case presentation, 159 complications and management, 170 decision-​making,  163–​67

diagnosis,  161–​63 ECOG (Eastern Cooperative Oncology Group) scoring,  171–​72 ESCC (Epidural Spinal Cord Compression) grading scale,  163–​67 evidence and outcomes, 171–​72 images showing L3-​level fractures, 160 intraoperative fluoroscopy for guidance of Jamshidi needle placement,  167–​69 NOMS (Neurologic, Oncologic, Mechanical and Systemic) framework, 163, 164, 171, 172 post-​treatment images, 170 SINS (Spinal Instability Neoplastic Score), 161–​62, 163–​67 summary of expected radiation response by histology, 166 surgical procedure, 167–​69 spinal deformity causes of, 71 See also cervical myelopathy, kyphosis spinal epidural abscesses (SEA) aftercare, 240 assessment and planning, 235–​37 case presentation, 235 complications and management, 240 decision-​making,  238 differential diagnosis, 235–​36 evidence and outcomes, 233 images showing dorsal epidural abscesses, 237 infectious disc herniation, 110–​11 management,  239–​40 risk factors for, 225–​26 risks and benefits of operative decompression, 229 surgical procedure, 238–​39 surgical procedure and, 230, 231 tetrad of stages, 235–​36, 238 spinal infections. See spinal epidural abscesses spinal instability due to multiple myeloma, 171 SINS (Spinal Instability Neoplastic Score), 136, 161–​62,  163–​67 treatment outcomes, 171–​72 spinal metastasis incidence of, 133–​34 symptoms,  133–​34 Spine Patient Outcomes Research Trial (SPORT), 191–​94, 196 Spine Trauma Study Group, 125

261

26

Index

spondylolisthesis, isthmic aftercare, 204 assessment and planning, 200 case presentation, 199 classification system, 200 complications and management, 204 decision-​making,  201 diagnosis, 200 differential diagnosis, 199 evidence and outcomes, 204–​5 management, 203 MRI showing L4-​L5 disc space, 200 post-​operative x-​rays showing pedicle screw fixation with PEEK interbody, 203 surgical procedure, 201–​2 spondylolisthesis, L4–​L5 degenerative assessment and planning, 191 case presentation, 191 complications and management, 196 CT showing L5-​L5 grade 1 spondylolisthesis, 192 CT showing right and left pars interarticularis, 192 CT showing TLIF with complete facetectomy and reduction of spondylolisthesis, 195 decision-​making,  191–​95 evidence and outcomes, 196 MRI showing foraminal stenosis, 193 x-​rays (no pathological movement), 193 spondylosis, 109–​10, 208 Spurling test, 101–​2 Staphylococcus aureus,  225–​26 Staphylococcus epidermidis,  225–​26 stenosis C3–​C4, C4–​C5, and C5–​C6 stenosis, 64–​64 foraminal stenosis and C5 palsy, 68 intubation in severe cervical stenosis, 66 selection of surgical approach, 65 See also lumbar stenosis Streptococcus pneumoniae,  225–​26 Streptococcus viridans,  225–​26 Surfer’s myelopathy, 246 syphilis, 246 systemic sclerosis, 244 the transverse atlantal ligament (TAL), assessment of, 43 thoracic central disc, 114, 115

262

thoracic cord compression, extradural tumor aftercare, 139 assessment and planning, 133 case presentation, 133 complications and management, 139 decision-​making,  135–​37 diagnosis,  134–​35 differential diagnosis, 133 epidural spinal cord compression scale, 136 evidence and outcomes, 140 images depicting T3 cage, 138 images showing spinal cord compression, 135 management, 138 surgical procedure, 137 thoracic disc herniation aftercare, 119 case presentation, 109 complications and management, 114 compressive pathologies, 109–​11 decision-​making,  113–​17 differential diagnosis, 109–​12 dorsolateral/​lateral approaches,  114–​15 evidence and outcomes, 114 management, 119 minimally invasive approaches, 117 noncompressive pathologies, 111–​12 surgical procedure, 117–​19 ventral approaches, 117 ventrolateral approaches, 115–​17 thoracic giant disc, 112 thoracic lateral disc, 114–​15 thoracic myelopathy diagnosis, 112 differential diagnosis, 111–​12 thoracolumbar burst fractures aftercare, 129 assessment and planning, 123–​25 case presentation, 123 complications and management, 129–​30 decision-​making,  127–​28 diagnosis,  126–​27 evidence and outcomes, 130–​31 images showing burst fractue, compression, and disruption, 124 images showing burst fracture with mild bony retropulsion, 126

 

Index

indications for surgical intervention, 128 surgical procedure, 128–​29 TLICS (Thoracolumbar Injury Classification and Severity) score, 125, 126–​27, 130 tranexamic acid (TXA), benefits and drawbacks of, 221 transarticular screw in atlantoaxial instability, 44, 45–​46, 47 complications and management, 47 intraoperative x-​rays showing C1 lateral mass–​C2 pairs screw-​rod placement, 45 transforaminal lumbar interbody fusion (TFIL) for spondylolisthesis, 194 surgical procedure, 194–​95 transforaminal lumbar interbody fusion (TLIF) for flat back deformity, 220 surgical procedure, 201–​2 transoral-​transpharyngeal approach, in basilar invagination and cranial settling, 54–​55, 57 transpedicular approach to thoracic spine, 114 transthoracic thoracoscopy to thoracic spine, 117 transthoracic thoracotomy to thoracic spine, 115–​16 transverse myelitis, 112, 244 traumatic disc herniation, 110

traumatic spinal conditions, 243. See also acute traumatic central cord syndrome–​44 Traynelis Classification System, 25, 26 Treponema pallidum, 246 tropical spastic paraparesis, 246–​47 type II odontoid fracture. See odontoid fracture type II vascular compromise, in spinal epidural abscesses, 236 vascular myelopathies, 246 venous thromboemboli (VTE), preventing, 139 ventral approaches to thoracic spine, 117 ventrolateral approaches to thoracic spine, 115–​17 vertebral artery injury in cervical fracture dislocation, 18–​19 following cervical foraminotomy, 107 in odontoid fracture type II, 7, 8 vitamin B12 deficiency, 112, 247 warfarin, ATCCS and, 38 West Nile virus, 247 Wiltse classification system, 200 Zika virus, 244

263

264

 

26