A Practical Guide to Care of Spinal Cord Injuries : Clinical Questions and Answers [1 ed.] 9789819945412, 9789819945429

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A Practical Guide to Care of Spinal Cord Injuries Clinical Questions and Answers Hyun-Yoon Ko

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A Practical Guide to Care of Spinal Cord Injuries

Hyun-Yoon Ko

A Practical Guide to Care of Spinal Cord Injuries Clinical Questions and Answers

Hyun-Yoon Ko Parkside Rehabilitation Hospital Busan, Korea (Republic of) Department of Rehabilitation Medicine Pusan National University College of Medicine Yangsan, Korea (Republic of)

ISBN 978-981-99-4541-2    ISBN 978-981-99-4542-9 (eBook) https://doi.org/10.1007/978-981-99-4542-9 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Singapore Pte Ltd. The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore

To my parents, who have always been my source of strength and inspiration. To my mentors, who have generously shared their expertise and wisdom with me. To my patients, who have entrusted me with their care and taught me so much. And, of course, to my dear wife Insun, whose unwavering love and support have sustained me throughout this journey.

Preface

Spinal cord injuries are among the most life-altering events an individual can encounter, profoundly impacting not only their physical health but also their emotional, psychological, and social well-being. Despite remarkable advancements in spinal cord medicine over the years, numerous challenges persist. As healthcare professionals, it is our responsibility to continually refine our knowledge and skills to deliver the best care possible for patients with spinal cord injuries. This new book, “A Practical Guide to Care of Spinal Cord Injuries: Clinical Questions and Answers,” builds upon the foundation set by the first and second editions of “Management and Rehabilitation of Spinal Cord Injuries,” offering an interactive approach to learning about spinal cord medicine. Designed for a diverse range of healthcare professionals, including rehabilitation medicine physicians, neurologists, neurosurgeons, orthopedic surgeons, and others involved in treating spinal cord injury patients, this book encourages intellectual thinking, learning, and practical application of knowledge. The question-and-answer format fosters an engaging learning experience, promoting readers to think critically about the intricacies of spinal cord injuries. This book aims to provide a comprehensive and progressive approach to acquiring knowledge about spinal cord medicine, focusing on intellectual thinking and learning through understanding the questions and applying logical reasoning to formulate the desired answers. This new book, comprised of 42 chapters, explores various aspects of spinal cord medicine, concentrating on clinical and practical content. In particular, one of my objectives is to assist readers in deepening their understanding of spinal cord anatomy and its relevance to clinical practice. With this knowledge, readers will be better equipped to interpret and approach clinical symptoms, ultimately leading to improved patient care. The chapters on psychological challenges and adaptation in spinal cord injury rehabilitation, as well as emergencies and acute care in chronic spinal cord injury patients, emphasize the importance of addressing the often-overlooked psychosocial and emotional challenges faced by patients during the rehabilitation process and equipped healthcare professionals to handle potential emergencies in chronic spinal cord injury patients. I hope that this book serves as a valuable resource for healthcare professionals looking to expand their understanding of spinal cord medicine and enhance their ability to provide comprehensive care for spinal cord injury patients. As you navigate the complex and ever-evolving field of spinal cord vii

Preface

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medicine, I believe that this guide will prove to be a valuable and practical tool that not only deepens your knowledge but also cultivates intellectual curiosity and dedication to offering the best care possible for those living with spinal cord injuries. I extend my gratitude to the numerous colleagues, mentors, and experts who have contributed to the field of spinal cord medicine and have been instrumental in shaping my understanding and approach to patient care. Their passion and dedication have been a source of inspiration and a driving force behind the continued advancement of our collective knowledge. Together, let us work toward expanding our understanding, honing our skills, and making a meaningful difference in the lives of our patients. With great excitement and anticipation, I present to you “A Practical Guide to Care of Spinal Cord Injuries: Clinical Questions and Answers.” May this book serve as a catalyst for growth, understanding, and compassionate care for all those who commit themselves to the treatment and care of spinal cord injury patients. Busan, Korea (Republic of) April 2023

Hyun-Yoon Ko

Contents

1 U  nderstanding Spinal Cord Injuries: A Historical and Clinical Perspective������������������������������������������������������������������   1 References������������������������������������������������������������������������������������������  17 2 C  linical Perspectives on Spinal Cord Development����������������������  19 References������������������������������������������������������������������������������������������  34 3 N  euroanatomical Overview to Understand the Complexities of Spinal Cord Function������������������������������������  37 References������������������������������������������������������������������������������������������  72 4 A  ssessing and Predicting Function After Spinal Cord Injuries������������������������������������������������������������������������������������  75 References������������������������������������������������������������������������������������������  81 5 B  iomechanics of the Spine and Spinal Cord and Pathophysiology of Spinal Cord Injuries ������������������������������  83 References������������������������������������������������������������������������������������������  99 6 K  inematics-Related Understanding for Enhancing Extremity Muscle Functionality After Spinal Cord Injuries ������ 101 References������������������������������������������������������������������������������������������ 115 7 E  ssential Laboratory Tests for Managing Spinal Cord Injuries������������������������������������������������������������������������������������ 117 References������������������������������������������������������������������������������������������ 133 8 U  nderstanding Pharmacokinetics and Pharmacotherapeutics in the Management of Spinal Cord Injuries������������������������������������������������������������������������ 135 References������������������������������������������������������������������������������������������ 176 9 A  ssessment and Diagnosis of Traumatic Spine Fractures������������ 181 References������������������������������������������������������������������������������������������ 195 10 U  nderstanding the Role of Imaging Studies in the Management of Spinal Cord Injuries�������������������������������������� 197 References������������������������������������������������������������������������������������������ 213 11 I dentifying and Assessing Spinal Cord Lesions: Clinical Approach���������������������������������������������������������������������������� 215 References������������������������������������������������������������������������������������������ 228 ix

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12 S  tandardizing Spinal Cord Injury Assessment and Classification ���������������������������������������������������������������������������� 229 References������������������������������������������������������������������������������������������ 251 13 E  pidemiology and Demographics of Spinal Cord Injuries���������� 253 References������������������������������������������������������������������������������������������ 268 14 S  pinal Shock: Understanding the Phenomenon and Reflex Recovery Patterns �������������������������������������������������������� 271 References������������������������������������������������������������������������������������������ 281 15 E  arly Intervention and Care for Traumatic Spinal Cord Injuries������������������������������������������������������������������������������������ 283 References������������������������������������������������������������������������������������������ 302 16 U  nderstanding Nontraumatic Spinal Cord Disorders����������������� 307 References������������������������������������������������������������������������������������������ 336 17 U  nderstanding Neural Tube Defects: Abnormalities in Spinal Cord Development ���������������������������������������������������������� 341 References������������������������������������������������������������������������������������������ 347 18 U  nderstanding Incomplete Spinal Cord Syndromes�������������������� 349 References������������������������������������������������������������������������������������������ 364 19 U  nderstanding Cauda Equina and Conus Medullaris Injuries�������������������������������������������������������������������������� 367 References������������������������������������������������������������������������������������������ 378 20 U  nderstanding Syringomyelia and Chiari Malformations���������� 381 References������������������������������������������������������������������������������������������ 392 21 A  utonomic Dysfunction in Spinal Cord Injuries: Anatomy and Clinical Assessment�������������������������������������������������� 395 References������������������������������������������������������������������������������������������ 413 22 C  ardiovascular Challenges in Spinal Cord Injury Rehabilitation ���������������������������������������������������������������������������������� 415 References������������������������������������������������������������������������������������������ 427 23 M  anaging Autonomic Dysreflexia: Clinical Insights and Strategies ���������������������������������������������������������������������������������� 431 References������������������������������������������������������������������������������������������ 445 24 B  lood Pressure Stabilization in Spinal Cord Injuries: A Focus on Orthostatic Hypotension and Supine Hypertension������������������������������������������������������������������������������������ 447 References������������������������������������������������������������������������������������������ 463 25 P  reventing and Managing Venous Thromboembolism in Spinal Cord Injuries�������������������������������������������������������������������� 467 References������������������������������������������������������������������������������������������ 481

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26 R  espiratory Care and Intervention Strategies for Spinal Cord Injuries������������������������������������������������������������������ 483 References������������������������������������������������������������������������������������������ 516 27 M  anaging Neurogenic Lower Urinary Tract Dysfunction in Spinal Cord Injuries�������������������������������������������������������������������� 519 References������������������������������������������������������������������������������������������ 554 28 N  eurogenic Bowel Dysfunction and Gastrointestinal Complications in Spinal Cord Injuries������������������������������������������ 559 References������������������������������������������������������������������������������������������ 583 29 U  nderstanding and Managing Sexual Dysfunction in Spinal Cord Injuries�������������������������������������������������������������������� 587 References������������������������������������������������������������������������������������������ 607 30 P  reventing and Managing Pressure Injuries in Spinal Cord Injuries�������������������������������������������������������������������� 611 References������������������������������������������������������������������������������������������ 630 31 A  bnormal Temperature Control After Spinal Cord Injuries������ 633 References������������������������������������������������������������������������������������������ 642 32 N  eurogenic Heterotopic Ossification in Spinal Cord Injuries������������������������������������������������������������������������������������ 643 References������������������������������������������������������������������������������������������ 656 33 U  nderstanding Spasticity and Contractures in Spinal Cord Injuries�������������������������������������������������������������������� 659 References������������������������������������������������������������������������������������������ 679 34 U  nderstanding Electrolyte Imbalances in Spinal Cord Injuries������������������������������������������������������������������������������������ 681 References������������������������������������������������������������������������������������������ 695 35 M  etabolic Syndrome and Health Concerns in Spinal Cord Injuries������������������������������������������������������������������������������������ 697 References������������������������������������������������������������������������������������������ 714 36 P  ain in Spinal Cord Injuries: Taxonomy and Management�������� 719 References������������������������������������������������������������������������������������������ 732 37 P  ediatric Spinal Cord Injuries: Assessment and Management������������������������������������������������������������������������������ 735 References������������������������������������������������������������������������������������������ 758 38 S  pinal Cord Injury in the Elderly and Aging of Spinal Cord Injuries�������������������������������������������������������������������� 761 References������������������������������������������������������������������������������������������ 772

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39 C  o-occurring Conditions of Traumatic Brain Injury and Spinal Cord Injury ������������������������������������������������������������������ 775 References������������������������������������������������������������������������������������������ 782 40 U  nderstanding and Managing Neurological Deterioration in Spinal Cord Injuries�������������������������������������������� 785 References������������������������������������������������������������������������������������������ 790 41 P  sychological Challenges and Adaptation in Spinal Cord Injury Rehabilitation�������������������������������������������� 793 References������������������������������������������������������������������������������������������ 804 42 E  mergencies and Acute Care in Chronic Spinal Cord Injury Patients������������������������������������������������������������������������ 807 References������������������������������������������������������������������������������������������ 819 Index��������������������������������������������������������������������������������������������������������  823

Contents

1

Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

Abstract

The chapter begins by discussing the historical perspectives of spinal cord injuries, including the early treatment methods and outcomes, and how medical science and clinical practice regarding spinal cord injuries have evolved over time. It then moves on to discuss the impact of spinal cord injuries on various bodily systems, including the somatic and autonomic nervous systems, and the resulting physical, psychological, and social challenges that individuals with spinal cord injuries face. The chapter also highlights the improvements in medical care for spinal cord injury patients, including the decrease in medical complications and increase in life expectancy. However, it also notes that the gap in life expectancy between those with spinal cord injuries and the general population has widened, and this poses challenges for the management of medical problems in the acute, subacute, and chronic phases of spinal cord injuries. The chapter emphasizes the importance of understanding the management of medical problems in the acute and subacute phases of spinal cord injuries, including the physical changes and complications that can arise. It also highlights the need to address the physical, psychological, and social challenges that spinal cord injury patients face in the chronic phase, particularly in light of the aging population with spinal cord injuries. Overall, the chapter provides a histori-

cal and clinical perspective on spinal cord injuries and the associated physiological changes and complications. It is a valuable resource for healthcare professionals involved in the care of individuals with spinal cord injuries. 1. What is the significance of the Edwin Smith Papyrus in the history of medical science and spinal cord injuries? The Edwin Smith Papyrus, also known as the Edwin Smith Surgical Papyrus, is a significant document in the history of medical science from the pre-Greek era. It is the only known surviving copy of an ancient treatise on trauma surgery, dating back to 3000– 2500 BC, and is recognized as both the oldest surviving text of medical literature and the oldest known surgical document in the world. In January 1862, Mr. Edwin Smith purchased this document from an Egyptian dealer named Mustafa Agha in Luxor or Thebes. However, Smith left the papyrus untouched as he focused on tomb exploration (Ganz 2014; Hughes 1988; Lifshutz and Colohan 2004) (Fig. 1.1). Following his death in 1906, his daughter, Miss Leonora Smith, donated the unread text to the New  York Historical Society. In 1920, historian James Breasted was commissioned to translate the papyrus. Dr. Breasted, a renowned Egyptologist, completed the translation and published it in 1930 under the patronage of the New  York

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 H.-Y. Ko, A Practical Guide to Care of Spinal Cord Injuries, https://doi.org/10.1007/978-981-99-4542-9_1

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1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

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Fig. 1.1 (a) The Edwin Smith Surgical Papyrus, Column VIII.  It is one of the 46 columns of the original Edwin Smith Papyrus that have been preserved. Written in hieratic, a more rapid, cursive form of hieroglyphic signs, the columns have undergone only minor changes since they

were photographed and published, along with hieroglyphic transliterations of each. (b) The title page of Breasted’s translation of the Edwin Smith Surgical Papyrus in 1930. (Adapted from Breasted (1930))

Historical Society (Breasted 1930; Lifshutz and Colohan 2004; Moore 2011). The papyrus was housed in the Brooklyn Museum from 1938 to 1948 before being presented to the New York Academy of Medicine by both the museum and the New  York Historical Society. The original papyrus is currently preserved in the Rare Book Room of the Library of the New York Academy of Medicine.

Almost all general discussions of spinal cord injuries begin by referencing the Edwin Smith Papyrus (Ganz 2014; Hughes 1988; Lifshutz and Colohan 2004) (Fig.  1.2). The documented spinal cord injury cases present severe injuries with a grim prognosis (Brawanski 2012; Breasted 1930). Ancient Egyptian physicians regarded spinal cord injuries as “an ailment not to be treated” (Hughes 1988; van Middendorp et  al. 2010). The two cases of spinal cord injuries are described in “Case 31. Dislocation of a cervical vertebra” and “Case 33. A crushed cervical vertebra” (Breasted 1930; Howorth and Petrie 1964) (Fig.  1.3). Egyptian surgeons differentiated between patients with open wounds or sprains of the cervical vertebrae that did not involve the spinal cord (case 29, 30, 32) and those with spinal dislocations and fractures who had lost power and sensation in all four limbs (case 31

2. What insights does it provide into ancient Egyptian medicine’s understanding and treatment of spine injuries, including spinal cord injuries? The Edwin Smith Papyrus includes descriptions of 48 cases of war injuries, offering valuable insight into ancient Egyptian medicine (Lifshutz and Colohan 2004). Six of these cases involve spinal injuries and two specifically concern spinal cord injuries.

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective Fig. 1.2 (a) Egyptian papyrus roll acquired by Edwin Smith in Luxor or Thebes in January 1892. Smith quickly recognized its medical significance. After his death in 1906, his daughter donated the papyrus to the New York Historical Society. The roll, measuring 32.5–33 cm in height and composed of 12 sheets, is now unrolled and preserved between glass sheets. With a current length of 4.68 m and at least one column missing, its original length exceeded 5 m. (b) Plate X and XI of the Edwin Smith papyrus, featuring five cervical spinal injury cases in hieratic script. (Adapted from Hughes (1988) and van Middendorp et al. (2010), with permission)

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and 33). They noted that such patients would ­experience priapism and incontinence of urine and semen (Silver 2003). 3. What was the condition of spinal cord injury patients during World War I, and what were the common complications that led to death in patients with spinal cord injuries? How has medical technology improved the treatment of spinal cord injuries? Prior to World War I, European medicine, particularly in Germany, led the world in the field of neurology. Historically, there had been an unfortunate military tradition of maltreatment, unpreparedness, and scandals

in hospitals, dating back to the Napoleonic Wars, Crimean War, and Boer War. During the Balkan War of 1912–1913, a staggering 95% of patients died (Sutton 1973). American military surgeon Harvey Cushing reported that during World War I, 80% of spinal cord injury patients died within 2 weeks of their injury. He discovered that only cases with “partial” lesions survived (Silver 2005; Guttman 1976a). These soldiers did not die from their immediate injury but from subsequent complications, such as those affecting the urinary tract, kidney, and cardiopulmonary system. Although complete spinal cord lesions are among the most life-altering injuries, therapeutic nihilism is

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

4 Fig. 1.3 (a) Case 31 (cervical vertebra dislocation), X 13–16. Translation: If thou examine a man having a dislocation in a vertebra of his neck, shouldst thou find him unconscious of his two arms and his two legs on account of it, while his phallus is erected on account of it, and urine drops from his member without his knowing it; his flesh had received wind; his two eyes are blood-shot; it is a dislocation of a vertebra of his neck extending to his backbone which causes him to be unconscious of his two arms and his two legs. If, however, the middle vertebra of his neck is dislocated, it is an emissio seminis which befalls his phallus. (b) Case 33 (crushed cervical vertebra), XI 9–12. Translation: If thou examine a man having a crushed vertebra in his neck and thou findest that one vertebra has fallen into the next one, while he is voiceless and cannot speak; his falling head downward has caused that one vertebra crush into the next one; and shouldst thou find that he is unconscious of his two arms and his two legs because of it. (Adapted from Breasted (1930))

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no longer justified due to advancements in medical technology related to spinal cord injuries, such as antibiotics, mechanical ventilators, and treatment for urinary tract system issues.

4. How did World War I contribute to the establishment of the first spinal unit in the UK? Hospitals were better organized during World War I, leading to the establishment of

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

the first spinal unit in the UK.  Pioneering work in this area was conducted by Henry Head (1861–1940), George Riddoch (1888– 1947), and Gordon Holmes (1876–1965). Treatment of patients with traumatic spinal cord injuries took place at the King George V and Empire Hospitals, followed by the Royal Star & Garter Home. Holmes oversaw all neurological cases in France, working at a base hospital, likely No. 13. He arranged for patients to be transferred under Head’s care at The London Hospital, who then coordinated their transfer to either the Royal Star & Garter Home or the Empire Hospital, which served as a spinal unit. At the time, physical therapy was not a recognized specialty as it is today, but various treatments such as massage, electricity, hydrotherapy, and manipulation were used to treat patients. Following the end of the war, military hospitals contracted, and specialist units, including spinal units, were closed (Silver 2003). 5. Who is credited with developing the first spinal unit? The turning point in the history of spinal cord injuries is often attributed to Donald Munro (Beneš 1968). Before the establishment of the Unit at Stoke Mandeville in 1944, there was a pattern of treatment in US Veterans’ Hospitals, where Munro’s work was recognized (Silver 2003). Munro (Donald Munro, 1889–1973) created the first spinal unit in 1936, paving the way for spinal cord injury treatment. He started his first spinal unit at Boston City Hospital in 1936 and later managed the Veterans’ Service at Cushing Hospital during World War II.  Munro graduated from Harvard and became the first surgical resident in genitourinary surgery at Boston City Hospital. While he was not the only one to realize the importance of careful nursing in preventing bedsores and urinary infections, he was a pioneer in frequently changing the position of paralyzed patients and inventing tidal drainage of the bladder to prevent urinary tract infections (Beneš 1968). After World War II, the US government established the

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first comprehensive spinal cord injury unit at Hines Veterans Administration Hospital in suburban Chicago, following the British model (Silver 2003). 6. What was the mortality rate for spinal cord injury patients during World War II, and what approach did the British medical research council recommend for managing spinal cord injuries during World War II? During World War II, the mortality rate for spinal cord injury patients remained around 80% (Sutton 1973). There was no organized effort to treat these injuries at the time, leading to high mortality rates for those with cervical injuries resulting in tetraplegia and an extremely shortened life expectancy for paraplegics (Sutton 1973). World War II spurred the development of modern treatments in the UK, with Guttmann’s role marking a significant milestone in spinal cord injury care. Although spinal units existed in the UK, treatment was not successful during the war. Suprapubic cystotomy was widely practiced and used during World War II in the UK, the Soviet Union, other European countries, and by the American Army (Sutton 1973). This method was advised for treating urinary retention in spinal cord injury patients before serious infection occurred due to catheterization (Sutton 1973). The British Medical Research Council (MRC) recommended a more aggressive approach to managing spinal cord injuries during World War II, which included guidelines for examining patients with peripheral nerve or nerve root lesions (Medical Research Council 1943). The MRC’s Peripheral Nerve Committee, chaired by George Riddoch, decided that war casualties with spinal cord injuries should be treated in special units (Sutton 1973). Guttmann, not yet working in spinal injuries, was sent with orthopedic surgeon Frank Holdsworth (1904–1969) to visit Dr. Munro and learn from his methods to establish spinal units in the UK based on Munro’s ideas. Holdsworth opened a unit in Sheffield,

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1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

and Guttmann opened one at Stoke Mandeville (Silver 2003). 7. When and where was the first specialized spinal cord injury unit established in the UK? In 1943, a spinal unit was set up at the Ministry of Pensions Hospital, Stoke Mandeville, Aylesbury. The Stoke Mandeville Hospital, a specialized spinal cord injury unit, opened in 1944 in Aylesbury, England, under the direction of Dr. Ludwig Guttmann (later Sir Ludwig Guttmann) (1899–1980) (Silver 2003). In 1952, the specialized spinal cord injury unit at Stoke Mandeville Hospital became the National Spinal Injuries Centre, part of the British National Health Service. Guttmann, Frankel, and their contemporaries developed a comprehensive approach to acute management and long-term rehabilitation for spinal cord injuries. Guttmann introduced sports such as wheelchair polo and archery into his rehabilitation program early on. In 1948, he started the National Stoke Mandeville Games, which evolved into the International Stoke Mandeville Games in 1952 (ISCoS 2022). These games were the precursor to the Paralympic Games, which eventually became a recognized and integral part of the Olympic Movement (Silver 2003). In 1955, doctors from various countries who accompanied their teams to the Stoke Mandeville International Games began to meet informally to discuss their clinical work and research. As these meetings grew larger and more formal, the International Paraplegia Medical Society (now ISCoS) was founded in 1961 (ISCoS). 8. What is the purpose of model system spinal cord injury centers in the United States? Specialized centers for spinal cord injury, dedicated to treating patients with these injuries, have significantly increased life expectancy for patients, allowing for the development of specialized rehabilitation and lifelong care approaches. Since the establishment of spinal cord injury centers in the United States and Great Britain, there

has been rapid medical advancement in the field (Guttman 1976b). In the UK, including Ireland, the treatment and management of spinal cord injury patients are centralized in 12 specialized centers (Stoke Mandeville, Oswestry, Sheffield, Southport, Middlesborough, Wakefield, Cardiff, Stanmore, Salisbury, Glasgow, Belfast, and Dublin). In the United States, following Dr. Guttmann’s positive experience, leading spinal cord injury specialists advocated for the creation of regional Model System Spinal Cord Injury Centers to demonstrate the benefits of a system approach to spinal cord injury care. Consequently, the federal government funded the Regional Centers in 1971. The National Spinal Cord Injury Statistical Center (NSCISC), centered on the American Model Spinal Cord Injury Center, began collecting data in 1973, initially gathering data on approximately 15% of newly developed spinal cord injuries in the United States and 57.4% of all surviving individuals with spinal cord injuries in the country. The impact of the American Spinal Injury Association (ASIA), established in 1973, on spinal cord injury management and the model systems is significant (Ragnarsson 2013). There are 14 model systems and five follow-up centers. Each Model System Spinal Cord Injury Center is designed to meet five basic criteria: (1) a system of emergency care and early referral, (2) coordination of acute medical/surgical care, (3) rehabilitation management beginning at the onset of acute care, (4) vocational evaluation, counseling, and placement, and (5) a system of lifetime follow-up care. 9. What are the two types of horns that gray matter forms in nerve cells, how is gray matter divided, and what are its main components? The spinal cord’s gray matter forms the sensory dorsal and motor ventral horns of nerve cells. It comprises numerous interwoven nerve fibers, including myelinated axons and unmyelinated fibers. The gray matter consists of symmetrical crescent-shaped masses

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

connected by a tissue bridge or commissure, which encloses the central canal. Divided into ten zones or laminae, labeled from I to X from dorsal to ventral, the gray matter structure includes the dorsal horn containing laminae I–VI and laminae VII–X located at the base of the ventral horn and the central area of the dorsal horn (Afifi and Bergman 2005; Blumenfeld 2010; Rexed 1954) (Fig. 1.4). 10. Why is gray matter more susceptible to mechanical trauma than white matter? In spinal cord injuries, how does damage to the gray matter typically manifest? Traumatic spinal cord injuries can lead to damage in the gray matter, white matter, nerve roots, or any combination thereof. Since the gray matter is more vascular, it is considered more susceptible to mechanical trauma (Thron 2016) (Fig.  1.5). Depending

7

on the trauma’s impact intensity, gray matter damage typically extends one or two segments rostral and caudal to the injured spinal cord segment but can be more extensive if the spinal cord blood supply is disrupted. Pathological studies on spinal cord trauma reveal a higher involvement of gray matter than white matter (Kakulas 1987). In both nontraumatic lesions, such as degenerative cervical myelopathy, and traumatic spinal cord injuries, gray matter lesions precede white matter lesions. If these lesions expand, symptoms and signs of central cord syndrome may be induced. A stenotic spinal a

Dorsal

b

Ventral Fig. 1.4  Rexed’s laminae of the gray matter. The lamina IX is the ventral horn of the gray matter including motor nuclei.

Fig. 1.5  There is distinctly higher density of arterioles and capillaries in the gray matter of the spinal cord compared to the white matter in axial microangiograms at levels T9 (a) and L5 (b). asa anterior spinal artery. (Adapted from Thron (2016), with permission)

8

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

canal can lead to central hematomyelia, gray matter hematoma formation, and eventual white matter compression of anterior or lateral corticospinal tracts (Hashmi et al. 2018; Avila and Hurlbert 2021). Although a spinal cord injury or lesion may show evidence of an upper motor neuron lesion, when the ventral gray matter of the ventral horn (Rexed lamina IX) is affected, it results in segmental denervation muscle atrophy and altered reflexes due to motor neuron damage. 11. What is the clinical definition of a spinal cord injury and how does it differ from the anatomical definition? The spinal cord, a central nervous system structure, extends from the cervicomedullary junction to the tip of the conus medullaris. However, clinically, a spinal cord injury encompasses both the spinal cord and the cauda equina. The spinal cord’s mean length ranges from 41 to 43  cm in females and 45 cm in males (Bican et al. 2013). 12. What types of lesions can occur due to traumatic spinal cord injury? How do high-velocity impact spinal traumas affect the spinal nerve root? A traumatic spinal cord injury can result in upper motor neuron lesions due to spinal cord damage or lower motor neuron lesions caused by cauda equina injury. The spinal cord contains ventral horn motor neurons, which give rise to the motor unit representing the lower motor neuron, and is surrounded by spinal nerve roots that correspond to each spinal cord segment or the proximal segmental nerve roots (Fig. 1.6). Consequently, most traumatic spinal cord injuries involve some degree of lower motor neuron lesion at the site of injury or proximal or distal segments. High-velocity impact spinal trauma can lead to central or peripheral avulsion injuries to the spinal nerve root (Moran et al. 2005) (Fig. 1.7). 13. What are the possible consequences of spinal fractures resulting in spinal cord injuries? Spinal trauma, such as fractures resulting in spinal cord injury, does not typically

result in clear or sharp injuries like severing the spinal cord with a knife. Spine fractures can cause multiple mechanical insults to the spinal cord and spinal canal, including widespread segmental physical damage from fractured bone fragments, abnormal load on the spinal cord parenchyma, hemorrhage in the spinal canal, and root avulsion injuries. In traumatic spinal cord injuries, lower motor neuron lesion-type neural injuries can be observed in proximal or distal segments to the epicenter of trauma, in addition to the affected spinal cord segment(s). Initially, the proximal segment to the trauma epicenter is identified as the neurological level of injury. In cases of spinal cord injury related to these traumas, the lower the neurological level of injury, the more likely a lower motor neuron-type neurogenic bladder is to occur, although a hyperreflexic or overactive detrusor may accompany it, as the neurological level of injury is proximal to the level of the conus medullaris and the epiconus. 14. Why is understanding the neuroanatomical region and pattern of neurological dysfunction important in spinal cord injuries or lesions? Understanding the precise neuroanatomical region associated with neurological dysfunction, as well as the pattern of neurological dysfunction is essential for effective diagnosis and management of spinal cord injuries or lesions (Tator and Koyanagi 1997). The organization of motor and sensory areas in the spinal cord, known as the homunculus, is not as clearly defined as it is in the brain. The efferent and afferent neural networks within the spinal cord are densely organized within a narrow structure. The white matter of the spinal cord contains each nerve pathway, characterized by its distinct anatomical features in a laminated fashion. 15. What is the organization of ascending and descending tracts in the white matter and posterior column of the spinal cord? How are motor neurons of the ventral horn of the gray matter organized?

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

a

9

b

Fig. 1.6  Topographical relationship between spinal cord and nerve roots. (a) Each spinal cord segment is surrounded by the segmental nerve root and proximal segmental nerve roots, except the upper cervical segments. (b) The lower the spinal cord segment, the more proximal

a

Fig. 1.7  Central and peripheral mechanism of nerve root avulsion. (a) Central mechanism of root avulsion is the result of longitudinal or transverse movement of the spinal cord following direct spinal trauma. Flexion of the spinal cord within the spinal canal induces avulsion of the root-

nerve roots are surrounding the segment. ISNCSCI International Standards for Neurological Classification of Spinal Cord Injury, CMS conus medullaris syndrome, CES cauda equina syndrome

b

lets. (b) Peripheral avulsion occurs when an external traction force is present and the fibrous supports around the rootlets are avulsed. The epidural sleeve can be pulled out of the spinal canal, creating a pseudomeningocele. (From Moran et al. (2005), with permission)

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1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

All ascending or descending white matter tracts have rostral segment fibers medially and caudal segment fibers laterally. However, in the posterior column, the caudal segment fibers are medial and the rostral segment fibers are lateral, since the fasciculus cuneatus and fasciculus gracilis are located laterally and medially, respectively. Furthermore, the motor neurons of the ventral horn of the gray matter organize the motor neurons of the proximal-distal part and the extensors-­ 18. flexors in the medial-lateral and anterior-posterior areas, respectively. The somatotopic organization of ascending and descending tracts in the white matter, posterior column, and ventral horn motor neurons of the spinal cord is described in detail in Chap. 3. 16. What is sacral sparing, and why is it considered the most critical modality in evaluating spinal cord injuries? Various factors play a role in predicting and determining neurological dysfunction in spinal cord injuries, but sacral sparing is considered the most critical modality among the various neurological signs used for evaluation. Sacral sparing is defined as the presence of any one of the following: voluntary anal contraction, pinprick sensation or light touch sensation at one or both S4–S5 dermatomes (anal mucocutaneous junctions), or deep anal pressure (ASIA 2019; Kirshblum et al. 2016). If all three sensory modalities (pinprick, light touch, and deep anal pressure) and voluntary anal contraction are absent, motor sacral sparing is identified by the presence of voluntary contraction of the external anal sphincter upon digital rectal examination (Zariffa et al. 2012). 17. What is the difference between motor sacral sparing and positive sensory sacral sparing? How does sacral sparing help differentiate between complete and incomplete spinal cord injuries in the ISNCSCI? Conventionally, if there is no voluntary anal contraction, but pinprick, light touch, or deep anal pressure is present, it is referred to as positive sensory sacral sparing. The definition of sacral sparing has proven to be the

most reliable indicator of completeness (Waters et  al. 1991). It is intuitive because, for sacral sparing to be present, some signals must have traversed the entire length of the spinal cord, as one would expect with incomplete conduction block. In the ISNCSCI, sacral sparing serves as a key neurological presentation that differentiates complete and incomplete spinal cord injuries. What are the two divisions of the motor system? What are upper motor neurons, and what role do they play in movement? The motor system is anatomically divided into an upper motor neuron system and a lower motor neuron system (Fig. 1.8). Upper motor neurons are first-order neurons that transmit electrical pulses for movement, and several descending upper motor neuron tracts coordinate movement (Emos and Agarwal 2022). Motor neurons innervate skeletal muscles and have cell bodies in the spinal cord and brainstem. Areas of the brain, such as the cerebral cortex and red nucleus, project to motor neurons, exerting a facilitatory or inhibitory action. These neurons projecting to motor neurons are called “upper motor neurons.” The anterior horn cells and their peripheral axons, which innervate striated muscle, make up the anatomical and physiological units referred to as “lower motor neurons”(Carpenter 1994; Yew et al. 1996).

19. What are the three motor systems for upper motor neurons? What is the difference between the pyramidal and extrapyramidal systems? Upper motor neurons project to lower motor neurons in the brainstem and spinal cord, either synapsing directly with lower motor neurons or terminating at nearby interneurons. There are three motor systems for upper motor neurons: corticospinal, extrapyramidal, and cerebellar. Projections in the spinal cord include the corticospinal tract, rubrospinal tract, tectospinal tract, reticulospinal tracts, and vestibulospinal tract (Yew et al. 1996). The corticospinal tract originates from the cerebral cortex’s pyramidal cells,

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

a

11

Motor cortex

b

Internal capsule

Peripheral nerve

Brainstem

Upper motor neuron

Spinal cord Motor neuron

Nerve root

Neuromuscular junction Muscle fiber

Interneuron Anterior horn cell Lower motor neuron

Peripheral nerve Motor endplate

Fig. 1.8 (a) Anatomical concepts of the upper motor neuron and lower motor neurons. (b) Anatomical components of the lower motor neuron (motor unit)

with axons traveling through ipsilateral structures sequentially: corona radiata, posterior limb of the internal capsule, cerebral peduncle of the midbrain, central pons, and pyramids of the medulla (Emos and Rosner 2022). The extrapyramidal system primarily consists of specific nuclei, the basal ganglia, including the caudate, globus pallidus, subthalamus, and putamen. Other extrapyramidal system structures are the thalamus, red nucleus, pons, and medullary reticular formation (Lance 1984) (Fig. 1.9). Clinically, “extrapyramidal” distinguishes between the clinical effects of basal ganglia damage and damage to the classic “pyramidal” pathway (Lee and Muzio 2022). Generally, descending fibers passing through the tegmentum rather than the medullary pyramid are considered components of the extrapyramidal system. However, no real dichotomy exists between pyramidal and extrapyramidal systems since the cortex,

which gives rise to all descending tract systems, is anatomically, functionally, and inextricably interconnected with the basal ganglia (Noback et  al. 2005). Table  1.1 shows the extent of descending tracts along the spinal cord and whether fibers cross to the opposite side or remain uncrossed. 20. What is a motor unit? Motor neurons send axons out of the spinal cord or brainstem, branching as they approach skeletal muscle. Each terminal branch forms a neuromuscular junction with a single skeletal muscle fiber through the nerve root and peripheral nerve. The motor neuron and muscle fibers constitute a single functional unit called the motor unit. 21. What is the Babinski reflex, and what does its recurrence indicate? How are the Chaddock’s sign and Oppenheim’s sign

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

12

eb

r Ce

Fig. 1.9 Descending tracts. The sequence includes the cerebral cortex to striatum, globus pallidus, thalamus, supplementary, premotor, and motor cortices originating the corticospinal, corticorubrospinal , corticoreticulospinal, and corticobulbar tracts originate. (Adapted from Noback et al. (2005))

ra x te

or lc

Caudate nucleus Ventral anterior and ventral lateral thalamic nuclei

Putamen Globus pallidus

Nucleus ruber Rubrospinal tract Reticular formation

Corticobulbar fibers

Reticulospinal tracts Corticospinal tract

Table 1.1  Summary of descending tracts: pyramidal and extrapyramidal tracts Tract Lateral corticospinal Anterior corticospinal Rubrospinal Tectospinal Medial reticulospinal Lateral reticulospinal Medial vestibulospinal Lateral vestibulospinal

Origin Primary motor and premotor areas Primary motor and premotor areas Red nucleus Superior colliculus Reticular formation in pons Reticular formation in medulla Medical vestibular nucleus Lateral vestibular nucleus

Extent in the spinal cord Laterality Entire length Cross at medulla Up to upper thoracic cord Entire length Cervical cord Entire length Entire length Up to upper thoracic cord Entire length

Uncrossed at medulla, but cross gradually at lower segments Cross at midbrain Cross at midbrain Uncrossed Crossed and uncrossed Uncrossed Uncrossed

Adapted from Yew et al. (1996)

performed, and what do they mimic? What is the Hoffmann’s sign, and how is it performed? Damage to descending motor pathways can result in a loss of spinal reflex modulation. The Babinski reflex, a reliable upper motor neuron sign, is commonly observed in

neonates but decreases as descending motor pathways mature (Emos and Rosner 2022). The recurrence of this reflex strongly indicates damage to the pyramidal tract (Emos and Rosner 2022; van Gijn 1995). In cases of pyramidal tract lesions, the segmental downward reaction of the toes disappears, flexion

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

synergy may be disinhibited, and the extensor hallucis longus muscle can be recruited into the leg’s flexion reflex (van Gijn 1995). The Babinski’s sign is performed by stroking the lateral sole of the foot from heel to toe with a firm, painless stimulus. A positive sign occurs when the big toe extends, along with the extension and fanning of the remaining toes. Babinski mimicking signs that elicit abnormal plantar responses include the Chaddock’s sign and Oppenheim’s sign. The Chaddock’s sign is triggered by stroking the lateral malleolus, while the Oppenheim sign is elicited by applying pressure on the medial side of the tibia. The Hoffmann’s sign, a testable upper extremity reflex, is performed by stabilizing a patient’s middle finger and quickly flicking the tip. The reflex is positive if the fingers and thumb flex (Emos and Rosner 2022). Pathological reflex signs, such as clonus, can be found in the ankle and patella. Clonus is elicited by rapidly extending the ankle for ankle clonus and quickly moving the patella downward for patellar clonus (Dimitrijevic et al. 1980; Emos and Rosner 2022). 22. What are superficial reflexes, and why are they challenging to analyze? Superficial reflexes are motor reactions in response to light stimulation of overlying skin. Examples include the abdominal reflex and cremasteric reflex. A decreased intensity of superficial reflexes can indicate an upper motor neuron lesion. However, analyzing these reflexes may be challenging, as they can be absent in healthy individuals and reemerge in patients with upper motor neuron lesions (Dick 2003; Emos and Rosner 2022). 23. What are the clinical signs of lower motor neuron lesions? How does the level of spinal cord injury affect the type of motor neuron damage experienced by patients? Depending on the level of spinal cord injury, patients may exhibit clinical signs of lower motor neuron lesions, such as flaccid weakness, absent or hypoactive deep

13

tendon reflexes, and muscle atrophy. Although motor neurons in the thoracic spinal cord’s ventral horn may be affected following injury, motor neuron damage in the thoracic segments typically has little functional impact because the muscles of the upper and lower extremities are spared (Anderberg et  al. 2007; Peckham et  al. 1976). In the lumbosacral spinal cord, lower motor neuron damage becomes more common due to injuries to the surrounding nerve roots of the conus medullaris and cauda equina (Fig.  1.10). A retrospective study analyzing cases of complete thoracolumbar spinal cord injury found that patients with neurological injuries above level T10 predominantly experienced upper motor neuron-type injuries. In contrast, those with injuries below level T12 mainly exhibited flaccid paralysis (Doherty et  al. 2002). 24. How has the life expectancy for individuals with spinal cord injuries changed over time? What factors influence the life expectancy of individuals with spinal cord injuries compared to the general population? The incidence of medical complications after spinal cord injury has decreased, and life expectancy for individuals with spinal cord injuries has increased. However, since the mid-1980s, the increase in life expectancy for this group has slowed and plateaued (DeVivo et al. 2018; Middleton et al. 2012; Shavelle et  al. 2015). As the general population’s life expectancy gradually increases, the gap between individuals with spinal cord injuries and the general population is estimated to widen. For reference, life expectancy in the United States increases by 0.08% per year, excluding the impacts of COVID-­19 (US life expectancy 1950–2022 2022) (Fig. 1.11). A British study on longterm survival after traumatic spinal cord injury found that the estimated life expectancy after spinal cord injury improved significantly between the 1950s and 1980s, plateaued in the 1990s and 2000s, and then

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

14 Fig. 1.10 The relationship between the conus medullaris and nerve toots surrounding the conus medullaris and arrangement pattern of the nerve roots

Life Expectancy from Birth (Years)

Historical

Current (79.05)

80.00 78.00 76.00 74.00 72.00 70.00 68.00 66.00

Annual % Change

Historical

Current

0.40 0.20 0.00 -0.20

1950

1960

1970

1980

1990

2000

2010

2020

Fig. 1.11  The current life expectancy for U.S. in 2022 is 79.05  years. All 2020 and later data are United Nations projection and do not include any impacts of the

COVID-­ 19 virus. (Retrieved from https://www.macr o t r e n d s . n e t / c o u n t r i e s / U S A / u n i t e d -­s t a t e s / life-­expectancy)

saw slight improvement again since 2010. The estimated life expectancy compared to the general British population ranged from 18.1% to 88.4%, depending on factors such as ventilator dependency, neurological level of injury, injury completeness, age, and gender (Ridler 2019; Savic et  al. 2017)

(Fig. 1.12). Life expectancy for individuals with spinal cord injuries varies based on statistical methods, highlighting the need for further research to determine the precise difference in life expectancy between this group and the general population (DeVivo et al. 2018).

1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

15

Years 70

60 50

50

48.8

43.2

40 36 30

30.5

30.8

25.5

24.6 20.7

20

19.7 16.2

10

10.7

0

50.8

37.7 31.1 26.8

51.7

53.2 49

44.9

39.4 32.7 28.5

19.7

21.1

1960-1969

1970-1979

59.8

57.6

55.2

52.4

50.3

50.8

43.6

45

45.3

36.8 32.3

38.2 33.7

38.4 33.9

24.7

25.9

26.1

1980-1989

1990-1999

2000-2009

47 40.1 35.5 27.7

14.4

1943-1949

1950-1959

General populaon

AIS D

Para ABC

C5-8 ABC

C1-4 ABC

2010-2014

Venlated

Fig. 1.12  Trends in life expectancy by study decades for a 20-year-old male first year survivor, expressed in remaining years of life compared to the remaining years

in the general population for England and Wales for the relevant time period. (Modified from Savic et al. (2017), with permission)

25. What are the key areas that need to be evaluated once a patient with spinal cord injury is stabilized, and what are some examples of secondary complications or medical problems resulting from spinal cord injuries? Once a patient’s emergency life-support needs have been addressed or their medical condition has stabilized, a thorough evaluation must be conducted in several key areas: (1) neurological level and extent of injury; (2) orthopedic spine injuries; (3) cardiovascular impairment or complications; (4) respiratory complications related to neurological injury or associated chest injury; (5) genitourinary complications; (6) gastrointestinal complications; (7) associated injuries or complications involving the head, chest, abdomen, and extremities; and (8) other significant medical history (Abrams and Ganguly 2015; Bauman et  al. 2012; Burns 1998; Gorman 2011; Sezer et  al. 2015). Spinal cord injuries disrupt communication between the brain and spinal cord, affecting end organs and limbs and leading to sensory,

motor, and autonomic dysfunction. These injuries have a wide-ranging impact on the entire body system, resulting in various secondary complications or medical problems, as outlined in Table 1.2. 26. Which key issues are related to the organ system and rehabilitation in spinal cord injuries? What is the mnemonic for remembering the spinal cord injury-­ related problem list? Spinal cord injuries can lead to a variety of complications, which can be broadly categorized into issues related to the organ system or those concerning rehabilitation. Some of the key problems that may arise include neurological evaluation, mobility or immobility, bladder and bowel function, cardiovascular system-related issues like blood pressure, respiratory system, extremity issues, skin conditions, social challenges, and psychological complications. To aid in remembering these important aspects of spinal cord injury management, refer to the mnemonic “N-I-BB-L-E-S” provided in Table 1.3.

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1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

Table 1.2  Clinical care issues in spinal cord injuries System Neurological Cardiovascular Hemostasis Respiratory Gastrointestinal

Genitourinary

Skin Musculoskeletal Psychological Others

Problems Motor/sensory paralysis, physical dysfunctions, spasticity Neurogenic shock, orthostatic hypotension, autonomic dysreflexia Deep vein thrombosis (venous thromboembolism), pulmonary embolism Atelectasis, pneumonia, ventilation failure, mechanical ventilation, tracheostomy, difficult weaning of mechanical ventilation Neurogenic bowel, fecal impaction, constipation, gastroesophageal reflux, stress ulcer, ileus, occult acute abdomen, cholecystitis, cholelithiasis, superior mesenteric artery syndrome Neurogenic bladder, urinary tract infection, vesicoureteral reflux, urinary stones, epididymitis, nocturnal polyuria, neurogenic sexual dysfunction, erectile dysfunction, male fertility problem, pregnancy Pressure injuries Spasticity, contracture, heterotopic ossification Anxiety, depression, suicide Poikilothermia, pain

Table 1.3  Mnemonic-based problem list for people with spinal cord injuries: N-I-B-B-L-E-S System Neurological Immobility, mobility Bladder/Bowel

Blood pressure

Lung

Extremities

Skin, Social, Psychological

Issues •  Neurological evaluation and classification •  Function evaluation •  Mobility evaluation •  Rehabilitation goal setting • Evaluation of neurogenic lower urinary tract function •  Urinary tract infection •  Dysfunctional defecation • Ileus •  Stress ulcer • Constipation •  Other GI complications •  Low resting blood pressure •  Orthostatic hypotension •  Autonomic dysreflexia •  Supine hypertension • Postvoid syncope, postdefecation hypotension, postprandial hypotension • Pneumonia • Atelectasis •  Ventilator care •  Deep vein thrombosis • Fracture •  Heterotopic ossification •  Pressure injury, burn wound •  Depression, anxiety, suicidal ideation, suicide •  Limited participation, difficult discharge

Management • ISNCSCI •  Mobility/functional training

•  Anticholinergic medication •  Clean intermittent catheterizations • Antibiotics •  Bowel program • H2 blocker

•  •  •  • 

Beware of noxious stimuli below NLI Nonpharmacological measures Head-up while sleeping Slow voiding

•  •  •  •  • 

Mechanical ventilation Incentive spirometer Secretion management LMWH prophylaxis IVC filter, etc.

•  Pressure injury management • Counseling •  SSRI medication

ISNCSCI International Standards for Neurological Classification of Spinal Cord Injury, NLI neurological level of injury, LMWH low molecular weight heparin, IVC inferior vena cava, SSRI selective serotonin reuptake inhibitor

References

27. What are the neurological manifestations of spinal cord complications related to COVID-19 or its vaccine? What are the potential mechanisms underlying these complications, and what are some ­examples of COVID-19-associated spinal cord issues? Spinal cord complications associated with the coronavirus infectious disease of 2019 (COVID-19) and its vaccine have been extensively documented in a range of studies (Bax et  al. 2021; Dario et  al. 2021; Hsiao et al. 2021; Kahan et al. 2021; Sampogna et al. 2020). The neurological manifestations of these complications include weakness, sensory deficits, autonomic dysfunction, and ataxia (Mondal et al. 2021). Several potential mechanisms have been proposed to underlie these complications, such as direct invasion, cytokine storm, coagulopathy, and autoimmune responses (Garg et al. 2021; Sampogna et  al. 2020). A variety of COVID-19associated spinal cord issues have been identified, including acute transverse myelitis, acute necrotizing myelitis, spinal cord infarction, neuromyelitis optica spectrum disorder, hypoxic myelopathy, SARS-CoV-2 myelitis, acute disseminated encephalomyelitis, MOG antibody-related myelitis, and spinal epidural abscess (Bax et  al. 2021; Dario et  al. 2021; Garg et  al. 2021; Hsiao et  al. 2021; Kahan et al. 2021; Mondal et al. 2021).

References Abrams GM, Ganguly K.  Management of chronic spinal cord dysfunction. Continuum (Minneap Minn). 2015;21:188–200. Afifi AK, Bergman RA.  Functional neuroanatomy: text and atlas. 2nd ed. New York: Lange Medical Books/ McGraw-Hill; 2005. American Spinal Injury Association (ASIA). International Standards for Neurological Classification of Spinal Cord Injury. Revised 2019. Richmond: ASIA; 2019. Anderberg L, Aldskogius H, Holz A. Spinal cord injury-­ scientific challenges for the unknown future. Ups J Med Sci. 2007;112:259–88. Avila MJ, Hurlbert RJ. Central cord syndrome redefined. Neurosurg Clin N Am. 2021;32:353–63.

17 Bauman WA, Korsten MA, Radulovic M, et  al. 31st g. Heiner sell lectureship: secondary medical consequences of spinal cord injury. Top Spinal Cord Inj Rehabil. 2012;18:354–78. Bax F, Gigli GL, Iaiza F, et al. Spontaneous spinal cord ischemia during COVID-19 infection. J Neurol. 2021;268:4000–1. Beneš V.  Spinal cord injury. Baltimore: Williams and Wilkins Co.; 1968. Bican O, Minagar A, Pruitt AA.  The spinal cord: a review of functional neuroanatomy. Neurol Clin. 2013;31:1–18. Blumenfeld H. Neuroanatomy through clinical cases. 2nd ed. Sunderland: Sinauer Associates; 2010. Brawanski A.  On the myth of the Edwin Smith papyrus: is it magic or science? Acta Neurochir. 2012;154:2285–91. Breasted JH. Edwin Smith surgical papyrus in facsimile and hieroglyphic transliteration with translation and commentary. Chicago: University of Chicago Oriental Institute Publications; 1930. Burns S.  Review of systems. In: Hammond MC, editor. Medical care of persons with spinal cord injury. Washington, DC: Department of Veterans Affairs; 1998. p. 17–22. Carpenter MB.  Upper and lower motor neurons. In: Downey JA, Myers SJ, Gonzalez EG, et  al., editors. The physiological basis of rehabilitation medicine. 2nd ed. Boston: Butterworth-Heinemann; 1994. Dario A, Innamorato M, Frigerio G. Spinal cord stimulation and COVID-19 pandemic: an Italian experience. Minerva Anestesiol. 2021;87:1054–5. DeVivo MJ, Savic G, Frankel HL, et  al. Comparison of statistical methods for calculating life expectancy after spinal cord injury. Spinal Cord. 2018;56:666–73. Dick JP.  The deep tendon and the abdominal reflexes. J Neurol Neurosurg Psychiatry. 2003;74:150–3. Dimitrijevic MR, Nathan PW, Sherwood AM.  Clonus: the role of central mechanisms. J Neurol Neurosurg Psychiatry. 1980;43:321–32. Doherty JG, Burns AS, O’Ferrall DM, et al. Prevalence of upper motor neuron vs lower motor neuron lesions in complete lower thoracic and lumbar spinal cord injuries. J Spinal Cord Med. 2002;25:289–92. Emos MC, Agarwal S. Neuroanatomy, upper motor neuron lesion. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Emos MC, Rosner J.  Neuroanatomy, upper motor nerve signs. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Ganz JC.  Edwin Smith papyrus case 8: a reappraisal. J Neurosurg. 2014;120:1238–9. Garg RK, Paliwal VK, Gupta A.  Spinal cord involvement in COVID-19: a review. J Spinal Cord Med. 2021;46:390–404. Gorman PH.  The review of systems in spinal cord injury and dysfunction. Continuum (Minneap Minn). 2011;17(3. Neurorehabilitation):630–4.

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1  Understanding Spinal Cord Injuries: A Historical and Clinical Perspective

Guttman L.  Spinal cord injuries. Comprehensive management and research. 2nd ed. London: Blackwell Science Ltd; 1976a. Guttman L.  Historical background. In: Guttman L.  Spinal cord injuries: comprehensive management and research. 2nd ed. London: Blackwell Scientific Publication; 1976b. p. 1–8. Hashmi SZ, Marra A, Jenis LG, Patel AA.  Current concepts: central cord syndrome. Clin Spine Surg. 2018;31:407–12. Howorth MB, Petrie JG. Injuries of the spine. Baltimore: The Williams & Wilkins Company; 1964. Hsiao YT, Tsai MJ, Chen YH, et  al. Acute transverse myelitis after COVID-19 vaccination. Medicina (Kaunas). 2021;57:1010. Hughes JT. The Edwin Smith surgical papyrus: an analysis of the first case reports of spinal cord injuries. Paraplegia. 1988;26:71–82. ISCoS.  The history of ISCoS. https://www.iscos.org.uk/ the-­history-­of-­iscos. Accessed 7 Oct 2022. Kahan J, Gibson CJ, Strauss SB, et  al. Cervical spinal cord infarction associated with coronavirus infectious disease (COVID)-19. J Clin Neurosci. 2021;87:89–91. Kakulas BA.  The clinical neuropathology of spinal cord injury. A guide to the future. Paraplegia. 1987;25:212–6. Kirshblum SC, Botticello AL, Dyson-Hudson TA, et  al. Patterns of sacral sparing components on neurologic recovery in newly injured persons with traumatic spinal cord injury. Arch Phys Med Rehabil. 2016;97:1647–55. Lance JW.  Pyramidal and extrapyramidal disorders. In: Shahani BT, editor. Electromyography in CNS disorders: central EMG. Boston: Butterworth; 1984. Lee J, Muzio MR.  Neuroanatomy, extrapyramidal system. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Lifshutz J, Colohan A.  A brief history of therapy for traumatic spinal cord injury. Neurosurg Focus. 2004;16:E5. Medical Research Council (Nerve Injuries Committee). Aids to the examination of the peripheral nervous system. Memorandum No. 45 (superseding War Memorandum No. 7). London: Her Majesty’s Stationery Office; 1943. Middleton JW, Dayton A, Walsh J, et al. Life expectancy after spinal cord injury: a 50-year study. Spinal Cord. 2012;50:803–11. Mondal R, Deb S, Shome G, et al. COVID-19 and emerging spinal cord complications: a systematic review. Mult Scler Relat Disord. 2021;51:102917. Moore W.  The Edwin Smith papyrus. BMJ. 2011;342:d1598. Moran SL, Steinmann SP, Shin AY. Adult brachial plexus injuries: mechanism, patterns of injury, and physical diagnosis. Hand Clin. 2005;21:13–24.

Noback CR, Strominger NL, Demarest RJ, et  al. The human nervous system: structure and function. 6th ed. Totowa: Humana Press; 2005. Peckham PH, Mortimer JT, Marsolais EB.  Upper and lower motor neuron lesions in the upper extremity muscles of tetraplegia. Paraplegia. 1976;14:115–21. Ragnarsson KT.  G. Heiner sell distinguished lecture: American Spinal Injury Association (ASIA) 40th anniversary: beginnings, accomplishments and future challenges. Top Spinal Cord Inj Rehabil. 2013;19:153–71. Rexed B. A cytoarchitectonic atlas of the spinal cord in the cat. J Comp Neurol. 1954;100:297–379. Ridler C.  Insights into life expectancy after spinal cord injury. Nat Rev Neurol. 2019;13:258. Sampogna G, Tessitore N, Bianconi T, et al. Spinal cord dysfunction after COVID-19 infection. Spinal Cord Ser Cases. 2020;6:92. Savic G, DeVivo MJ, Frankel HL, et al. Long-term survival after traumatic spinal cord injury: a 70-year British study. Spinal Cord. 2017;55:651–8. Sezer N, Akkus S, Ugurlu FG. Chronic complications of spinal cord injury. World J Orthop. 2015;6:24–33. Shavelle RM, DeVivo MJ, Brooks JC, et al. Improvements in long-term survival after spinal cord injury? Arch Phys Med Rehabil. 2015;96:645–51. Silver JR.  History of the treatment of spinal injuries. New  York: Springer Science+Business Media, LLC; 2003. Silver JR.  History of the treatment of spinal injuries. Postgrad Med J. 2005;81:108–14. Sutton NG. Injuries of the spinal cord: the management of paraplegia and tetraplegia. Chichester: Butterworths; 1973. Tator CH, Koyanagi I. Vascular mechanisms in the pathophysiology of human spinal cord injury. J Neurosurg. 1997;86:483–92. Thron AK. Vascular anatomy of the spinal cord. 2nd ed. Switzerland: Springer; 2016. U.S. life expectancy 1950–2022. https://www.macrotrends.net/countries/USA/united-states/life-expectancy. Accessed 11 Sept 2022. van Gijn J.  The Babinski reflex. Postgrad Med J. 1995;71:645–8. van Middendorp JJ, Sanchez GM, Burridge AL.  The Edwin Smith papyrus: a clinical reappraisal of the oldest known document on spinal injuries. Eur Spine J. 2010;19:1815–23. Waters RL, Adkins RH, Yakura JS. Definition of complete spinal cord injury. Paraplegia. 1991;29:573–81. Yew DT, Kwong WH, You MC.  Basic neuroanatomy. London: World Scientific Publishing Co.; 1996. Zariffa J, Kramer JL, Jones LA, et  al. Sacral sparing in SCI: beyond the S4–S5 and anorectal examination. Spine J. 2012;12:389–400.

2

Clinical Perspectives on Spinal Cord Development

Abstract

The chapter aims to provide a comprehensive understanding of the various stages of human spinal cord and brain development. It discusses the different phases of embryonic development and the developmental disorders associated with each stage. One of the challenges in studying spinal cord development is that the regulatory mechanisms involved in cell migration and differentiation are not yet fully understood, particularly in humans. As a result, much of the information available comes from animal experiments. The chapter describes the early stages of embryonic development, which includes the first 8 weeks after fertilization. This period is divided into 23 Carnegie stages, each of which marks a specific developmental milestone. The chapter explains that all components of the central and peripheral nervous system are derived from cells of the embryonic ectoderm. The earliest derivatives of the ectoderm are the neural plate and neural crest, which give rise to all neural cell types. The chapter discusses the folding of the neural plate, primary and secondary neurulation, and the formation of all neural cell types along the anteroposterior and dorsoventral axes that form the central nervous system. Overall, the chapter aims to provide a detailed understanding of spinal cord development from a clinical perspective, with a focus on the embryonic stages. This information can be useful for clinicians and researchers working

with patients who have spinal cord injuries or developmental disorders. 1. How can the terminologies related to human developmental stages be explained, particularly those concerning the embryonic period and staging, gestational age, fetal period and staging, and pregnancy or obstetric staging? The embryonic period, defined as the first 8 weeks of development after fertilization, consists of 23 Carnegie stages (O’Rahilly and Müller 2010; ten Donkelaar et al. 2014a). These stages are based on the embryo’s external features and are not reliant on chronological age or size. Following the embryonic period, the fetal period extends until delivery; however, no satisfactory morphological staging system exists for this phase (ten Donkelaar et al. 2014a). Gestational age is calculated from the first day of the last menstrual period, with the number of gestational or menstrual weeks exceeding the postfertilization weeks, also known as fertilization age, by two. The gestational or pregnancy period is divided into three trimesters (Standring 2016). The first two trimesters each span 12 weeks, while the third trimester covers weeks 24 to delivery. The perinatal period lasts from the end of week 24 to 7 days after birth. Neonates born before 37 weeks are considered preterm (or premature), while those delivered after 42  weeks are deemed

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 H.-Y. Ko, A Practical Guide to Care of Spinal Cord Injuries, https://doi.org/10.1007/978-981-99-4542-9_2

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2  Clinical Perspectives on Spinal Cord Development

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Fig. 2.1  Human development timeframes and defined terminologies. Embryonic development, as shown in the upper scale, is measured from the point of fertilization.

The clinical estimation of pregnancy, depicted in the lower scale, is calculated from the last menstrual period. (Adapted from Standring (2016))

postterm (Standring 2016). Figure  2.1 illustrates the various timescales of human development and the associated terminologies.

The primitive streak enlarges and lengthens, with the rostral end thickening to form Hensen’s node, also known as the primitive node of Hensen (ten Donkelaar et al. 2014a). The primitive streak serves as an entry point for cells to invaginate, proliferate, and migrate, ultimately forming the extraembryonic mesoderm, endoderm, and intraembryonic mesoderm. Nowadays, the term gastrulation is used more broadly to describe the developmental phase from the end of cleavage to the formation of an embryo with a defined axial structure (Collins and Billett 1995; ten Donkelaar et al. 2014a).

2. What is gastrulation and what germ layer does it establish? Gastrulation is a developmental process responsible for the formation of the mesoderm, the third germ layer, which gives rise to muscles, bones, blood vessels, and other organs (Hawryluk et al. 2012). During the second week after fertilization, a bilaminar embryonic disc forms inside the amniotic cavity, composed of an outer epiblast layer adjacent to the amniotic cavity and an inner hypoblast layer, which is later replaced by the endoderm, adjacent to the primary yolk sac. The embryonic disc migrates ventrally, creating the primitive (primary) streak. Gastrulation starts with the formation of the primitive streak in the epiblast’s caudal region at around 14 or 15 days. By the end of the first 3 weeks of development, the three germ layers (ectoderm, mesoderm, and endoderm) are established, serving as the foundation for the various organs and systems of the body. 3. What is the function of the primitive streak during gastrulation?

4. What is the notochord and what role does it play in embryonic development? Another critical event during the second week is the formation of the notochord, a cylindrical structure derived from mesodermal cells that defines the embryo’s midline and serves as a rigid axis for development (Hawryluk et  al. 2012). The notochord secretes inductive signals from the overlying ectoderm that are essential for nervous system formation. Prenotochordal cells, which form the notochord, migrate from the primitive streak and move rostrally toward the prechordal plate, creating the notochordal

2  Clinical Perspectives on Spinal Cord Development

process, a notochord precursor. The notochordal process first intercalates with the hypoblast to form the notochordal plate (Hawryluk et al. 2012) (Fig. 2.2). 5. What is neurulation and when does it take place? Following gastrulation, the neural plate, an ectodermal thickening that is the precursor to the spinal cord and brain, begins to develop around day 20 after fertilization (Sadler 2005). Within 24 h, the neural plate a

b

c

d

Fig. 2.2  Development of the notochord. (a) and (b) depict coronal views through the bilaminar disc. During gastrulation, epiblast cells invaginate at the primitive pit and primitive streak, forming the definitive endoderm and mesoderm. Prenotochordal cells also invaginate and migrate as far rostral as the prechordal plate. (c) Prenotochordal cells intercalate with the hypoblast, creating the notochordal plate. (d) The notochordal plate detaches from the endoderm and forms a tube known as the definitive notochord. (Adapted from Hawryluk et al. (2012), with permission)

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cells rapidly proliferate and fold to form the neural groove. As the neural plate develops, mesoderm condenses on each side of the ­notochord to form paired somites in longitudinal rows on each side of the neural groove. Starting from day 20, somites first develop in the rostral area, later becoming the future occipital bone, and proceed caudally. Over the next 10 days, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and approximately 5–7 or 8–10 coccygeal somites are formed, totaling up to around 44 pairs extending to the coccyx level (ten Donkelaar et al. 2014a). Neurulation is the process of folding the neural plate into the neural tube, which later differentiates into the spinal cord and brain, eventually forming the central nervous system (Mancall and Brock 2011; Sadler 2005; Standring 2016). Between days 22 and 23, the neural groove deepens, and the neural folds converge in the dorsal midline to form the neural tube. Closure of the neural groove starts at the area of the third or fourth somite, later becoming the cervicomedullary junction, and proceeds rostrally and caudally simultaneously (Figs.  2.3 and 2.4). Eventually, the first occipital pair and the caudal 5–7 coccygeal pairs will regress. Closure of the neural tube takes 4–6  days. Neurulation, the process of neural tube formation that will become the spinal cord and brain, occurs between the 18th and 27th day. This event requires several days and must be coordinated simultaneously at the rostral and caudal ends. 6. What is the difference between primary and secondary neurulation? At which point in development does the closure of the neural tube begin? What are neuropores and when do they close? The development of the central nervous system begins during the third week after fertilization, starting with neurulation. Primary neurulation involves the folding and closure of the neural plate to form the neural tube. The process of folding the neural plate, creating a neural groove, and eventually forming the neural tube by combining both neural plates

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22

a

b

c

d

Fig. 2.3  Development of the neural crest, neural tube, and somites in a human embryo (dorsal view). (a) Stage 8

(23 days), (b) stage 9 (25 days), (c) stage 10 (28 days, 7 somites), (d) stage 10 (10 somites). (Adapted from ten Donkelaar et al. (2014a))

differs in timing for each part. In human embryos, the closure of the neural tube generally starts at the level of the future cervical region and proceeds both rostrally and caudally. This process, known as primary neurulation, extends the spinal cord to the S4/S5 level (Singh and Munakomi 2022). Primary neurulation occurs in the mid-region of the neural plate and progresses cranially and caudally, resembling a zipper. The neural tube closure takes 4–6  days. During closure, the rostral and caudal regions that have not yet fused are called neuropores. Cranial and caudal neuropores remain open to the amniotic fluid until closure, which occurs at approximately 25 and 27 days, respectively. Prolonged contact with amniotic fluid can be destructive to neural tissue (Hawryluk et al. 2012).

Secondary neurulation follows the formation of the neural tube (Singh and Munakomi 2022). Unlike the more rostral elements of the spinal cord, the conus medullaris and the filum terminale form through the process of secondary neurulation (Hawryluk et al. 2012). Secondary neurulation only involves the formation of the most caudal part of the conus medullaris, the filum terminale, and a focal dilation of the central canal known as the ventriculus terminalis. The more caudal spinal cord segments develop through the process of canalization, rather than neurulation (O’Rahilly and Müller 2002; ten Donkelaar et  al. 2014a). The caudal part of the neural tube forms not through fusion of the neural folds, but from the caudal eminence, which involves the connection and fusion of mesodermal cells (Sadler 2005). Secondary neurulation is the continuing formation of the sacrocaudal part of the spinal cord without direct involvement of the surface ectoderm or

7. What is the caudal eminence and how does it contribute to the formation of the caudal part of the neural tube?

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23

a

time. However, there is some discrepancy in the literature regarding the level of the caudal neuropore at the beginning and end of closure (Mancall and Brock 2011).

b

9. What are the roles of median and lateral hinge points in the formation of the neural tube? What are the consequences of cranial and caudal neuropore closure failure during primary neurulation? During embryonic development, the correct formation and closure of the neural tube are crucial for a healthy spinal cord. Both median and lateral hinge points play a significant role in the folding and closure of the neural tube, and any defects along the embryo can lead to spinal cord abnormalities (Copp and Greene 2013). When the cranial and caudal neuropores, which are the unfused regions at the head and tail ends of the neural tube, fail to close during primary neurulation, it results in severe conditions such as anencephaly and spina bifida, respectively (Hawryluk et al. 2012).

c

d

Fig. 2.4  Development of the neural crest, neural tube, somites, spinal cord, and spinal nerves in a human embryo (transverse sections). Sensory neurons originate from the alar plate, while motor neurons develop the basal plate. The alar plate and the basal plate are bounded by sulcus limitans. (a) Approximately 19  days, (b) approximately 20  days, (c) approximately 26  days, and (d) 1  month. (From Noback et al. (2005))

without the intermediate phase of a neural plate (O’Rahilly and Müller 2006). 8. When does the closure of the neural tube complete, and when do the rostral and caudal neuropores close? What is the posterior neuropore? The closure of the neural tube forms the basic structure of the spinal cord, completing around postconception day 30 when the embryo is about 4 mm long. The rostral neuropore closes within a few hours at a­ pproximately 29 days (stage 11), while the caudal neuropore closes around a day later (stage 12). At stage 12, secondary neurulation begins and ends. An opening in the central canal, known as the posterior neuropore, is typically closed by this

10. What are some abnormal conditions that can result from neurulation failure, and how do they differ from each other? The location of the defect determines the severity and type of the neurulation failure. Some of the abnormal conditions that may occur include craniorachischisis totalis, where the entire neural tube remains unfused along the dorsal midline; cranioschisis or anencephaly, in which the neural tube fuses dorsally to form the spinal cord but fails to do so in the brain; and spina bifida or spinal dysraphism, where local regions of the spinal neural tube are not fused, or the vertebral neural arches fail to form properly (Copp and Greene 2013; Greene and Vopp 2014; Mancall and Brock 2011) (Fig. 2.5). A summary of the different malformations caused by neurulation failure can be found in Table 2.1. 11. What is the role of neuroepithelial cells in the development of the spinal cord? The initial structure of the neural tube consists of a single layer of neuroepithelial

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a Entire neural tube remains open

Herniated brain tissue

Herniated arachnoid mater

Craniorachischisis

b

Anencephaly

c

Meningoencephalocoele

Open spinal cord

Cranial meningocoele Dura and arachnoid mater

Dura and arachnoid mater Spinal cord

Channel open due to incomplete vertebral arch Myelocoele

Subarachnoid space containing CSF Spinal cord

Subarachnoid space containing CSF Meningomyelococle

Meningocoele

Fig. 2.5  Malformations resulted from failure of neurulation. (a) Total failure of neurulation, (b) failure of rostral neurulation, (c) failure of caudal neurulation. (Adapted from Mancall and Brock (2011)) Table 2.1  Definitions of terminology related to neurulation failure Terms of malformation Cranioschisis Inionschisis Rachischisis Myelomeningocoele Meningocoele Spinal dysraphism Spina bifida Spina bifida occulta

Definition Neural folds, corresponding to future brain, do not fuse and fail to differentiate, invaginate, and separate from surface ectoderm. Failure of neural tube to differentiate properly and close in the occipital and upper spinal region. Neural folds corresponding to future spinal cord do not fuse and fail to differentiate, invaginate, and separate from surface ectoderm. Dura, arachnoid, and neural tissue protrude from spinal canal through spina bifida defect in the posterior midline neural arches. Dura and arachnoid protrude from spinal canal through spina bifida defect in posterior midline neural arches. Failure of part of neural tube to close. Defect in the posterior midline neural arch. Vertebral arches of a single vertebra fail to fuse.

cells, also known as the germinal neuroepithelium or the matrix layer. As this layer thickens, its nuclei become organized into multiple layers. Neuroepithelial cells con-

tribute to the formation of primitive nerve cells called neuroblasts as the neural tube closes. These neuroblasts create a new layer within the developing spinal cord, referred

2  Clinical Perspectives on Spinal Cord Development

25

to as the mantle layer (Hawryluk et  al. 2012). 12. How do the mantle layer and marginal zone develop in the spinal cord? Cell division (mitosis) occurs on the inner ventricular side of the cell layer, with migrating cells forming a second layer around the ­original neural tube. This second layer, called the mantle layer or intermediate zone, thickens as more cells from the germinal neuroepithelium—now known as the ventricular zone—are added. The mantle layer, situated between the ventricular zone and the marginal zone, surrounds the primitive spinal cord and arises from numerous neuroepithelial cell divisions (ten Donkelaar et  al. 2014a). The mantle layer eventually becomes the gray matter of the spinal cord, while the marginal zone transforms into the white matter of the mature spinal cord. 13. What are the alar plate and basal plate, and what do they contribute to in the spinal cord? As development continues, more neuroblasts are added to the mantle layer, leading to dorsal and ventral thickening. The dorsal thickening is referred to as the alar plate

(future sensory areas of the spinal cord), while the ventral thickening is called the basal plate (future motor area of the spinal cord). The alar plates and incoming dorsal roots form the sensory (afferent) part of the spinal cord, while the basal plate and its exiting ventral roots create the motor (efferent) part (Fig. 2.6). In the thoracic and upper lumbar regions of the spinal cord, an additional lateral swelling occurs in the gray matter, known as the intermediate horn, containing nerve cells of the sympathetic nervous system (Hawryluk et al. 2012). Motor neurons, forming the nuclei of the ventral gray columns, appear in the uppermost spinal segments around embryonic day 27 and progress caudally, reaching the cervical enlargement site by day 30. Dorsal root ganglion cells are also present during this time (Table 2.2). Dorsal root fibers enter the spinal gray matter early in development, and the subdivisions of the ventral gray column become evident before the end of the sixth week. The entire spinal cord contains medial motor neurons, which later innervate axial muscles, while visceral motor neurons are found in the intermediolateral column in thoracic and upper lumbar segments (Tomlinson et al. 1973).

Roof plate Primitive ependymal layer (matrix cell layer) (ventricular zone) Oval bundle Dorsal spinal nerve root Spinal (dorsal root) ganglion Fibers of ventral spinal nerve root

Cells of mantle layer (intermediate zone) forming anterior horn of gray matter

Spinal nerve trunk

Floor plate

Notochord

Marginal layer (zone)

Fig. 2.6  Detailed illustration of the cervical region in a human embryo, depicting the development of the spinal cord, ventral and dorsal spinal nerve roots. (Adapted from Mancall and Brock (2011))

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2  Clinical Perspectives on Spinal Cord Development

Table 2.2  Timeline of neuron origin in the human spinal cord

a

Neuron Motor neurons  Cervical cord  Thoracic cord  Lumbar cord Intermediate zone Dorsal horn (substantia gelatinosa) Dorsal root ganglion cells Ascending tract neurons  Contralaterally projecting neurons  Ipsilaterally projecting neurons

Time of neuron origin 3.5–5.7 weeks of development 4.1–5.7 weeks of development 4.1–5.7 weeks of development Fourth to fifth week 6.7–7.4 weeks of development Fourth to fifth week 4.1–5.7 weeks of development 5.8–6.6 weeks of development

b

Adapted from ten Donkelaar et  al. (2014a), with permission

14. When do the differentiating motor neurons start to gather outside the ventral neuroepithelium? The onset of postmitotic cell migration from the ventral neuroepithelium and the differentiation of the earliest spinal cord neurons, the ventral horn motor neurons, are marked by the formation of a cluster of differentiating cells. These differentiating motor neurons begin to gather outside the ventral neuroepithelium around gestational week 4.5 and significantly increase in number by gestational week 5.0. For approximately a week, the young motor neurons stay close to the ventral neuroepithelium, creating an ­unsegregated cell mass in the developing ventral horn (Fig. 2.7). 15. What comprises the immature muscular system during the development of arm and leg buds? At what gestational week do nerve fibers enter the primordial muscles? During gestational week 4.5, arm and leg buds emerge, while the immature muscular system consists of axial myotomes and mesenchymal limb primordia. It is possible that outgrowing motor axons establish contact

Fig. 2.7 (a) Accumulation of the earliest motor neurons (red line) in a GW4.5 embryo, (b) expansion of the unsegregated mass of motor neurons in a GW3.0 embryo. (Adapted from Altman and Bayer (2001), with permission)

with primordial muscle masses as early as gestational week 5.0 (Altman and Bayer 2001). Trunk muscles and shoulder muscles (levator scapulae, trapezius, deltoid, teres major) become visible in the embryo during gestational week 5.5. Motor neuron segregation continues to progress in the gestational week 6.5 embryo (Altman and Bayer 2001; ten Donkelaar et  al. 2014b). By gestation week 7, nerve fibers penetrate the primordial muscles and simple nerve endings can be found among myoblasts in human embryos (Altman and Bayer 2001; Bayer and Altman 2002).

2  Clinical Perspectives on Spinal Cord Development

16. What are somitomeres, and how do they contribute to the development of the embryo? A clustering of cells and thickening of the mesodermal layer on either side of the embryo’s midline arise from the paraxial mesoderm, leading to the formation of the first pair of somitomeres. In the cranial region, the first seven somitomeres contribute to the development of head musculature, while the remaining somitomeres transform into somites (Webster and de Wreede 2016). The first somites emerge on day 20, with subsequent somites appearing at a rate of three pairs per day. Somites develop from cranial to caudal and are situated lateral to the neural tube. By the end of week 5, a full set of somites has formed, comprising 4 occipital, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 8–10 coccygeal pairs. The first occipital and last five to seven coccygeal somites degenerate, leaving approximately 37 of the original 42–44 pairs of somites (Webster and de Wreede 2016). Cells within each somite differentiate and migrate into ventral and dorsal groups of cells called the dermamyotome and sclerotome, respectively (Fig. 2.8). 17. What are dermamyotome and sclerotome, and how do they form? How does the development of skeletal muscle fibers occur in relation to the development of neural structures? The dermamyotome, located in the dorsolateral part of the somite, is divided into two

Fig. 2.8  A condensation of cells around the somitocoel separates to form dermamyotomes and sclerotomes. The dermamyotome further subdivides into dermatome and myotome. (Adapted from Webster and de Wreede (2016))

27

groups: the myotome and the dermatome. The development of skeletal muscle fibers from myotomes and limb bud mesenchyme occurs parallel to neural structure development. Myofibrils appear in human myoblasts during the fifth week, with cross striations becoming visible at 7 weeks. Between the fifth and sixth weeks, a myotome divides into a dorsal epaxial part, or epimere, and a ventrolateral hypaxial part called the hypomere (ten Donkelaar et  al. 2014b). Medial cells within the myotome form the epaxial musculature of the back, while lateral cells create the hypaxial muscles, such as the intercostal and abdominal muscles, which make up the ventrolateral body wall. Lateral cells also migrate to the limb buds, forming limb musculature (Webster and de Wreede 2016). At gestational week 7, nerve fibers enter primordial muscles, and simple nerve endings are present among myoblasts in human embryos. The ventromedial part of the somite forms the sclerotome, consisting of cells that develop into vertebrae, intervertebral discs, ribs, and connective tissues (Webster and de Wreede 2016). A single vertebral bone is formed by the combination of the caudal part of the sclerotome from one somite and the dorsal part of the adjacent somite (Kaplan et al. 2005; Webster and de Wreede 2016). 18. When does the ventriculus terminalis develop and where is it initially located? Between days 43 and 48, the ventriculus terminalis, which is the future site of the conus medullaris, develops. Initially, it is situated at the level of the second coccygeal vertebra. At 3 months, the spinal cord appears similar to that of an adult, occupying the entire spinal canal. Until this point, the mantle layer has a shape characteristic of mature gray columns, and the dorsal and ventral horns are connected by an isthmus, including the central canal lined by ependymal cells. The nerve fibers of the marginal layer are unmyelinated, and by the mid-gestation period, myelination begins to generate white matter in the spinal cord. At the end of the embryonic age of 8 weeks, the

2  Clinical Perspectives on Spinal Cord Development

28

spinal cord still extends to the end of the vertebral column. 19. What is the process of regression, and how does it relate to the formation of the filum terminale and cauda equina? Regression refers to the process of filum terminale and cauda equina formation and the migration of the conus medullaris to its adult level at the L1–L2 intervertebral body. During the fetal period, it ascends to lumbar levels due to the disproportionate growth of the spinal cord and the vertebral column. Up to the 11th gestational week, the length of the spinal cord corresponds to that of the ­vertebral column. Subsequently, the “ascensus medullae” begins, the filum terminale forms, and the lower spinal nerves demonstrate progressive obliquity due to the growth difference between the spinal cord and the vertebral column (ten Donkelaar et  al. 2014b). The caudal neural tube regresses, and the ventriculus terminalis is obliterated, allowing it to rise within the spinal canal. By 18 weeks, it reaches the level of the L4 vertebral body, initially ascending relatively quickly. The rise then slows, with the tip of the spinal cord at the L2–L3 interspace at birth, reaching the adult level of the L1–L2 interspace within the first 3 postnatal months. As the neural tube ascends, a fibrous band remains between the ventricularis medullaris and the tip of the coccygeal vertebrae, which becomes the filum terminale. During this ascent, the nerve roots originally exiting the spinal canal opposite their segmental origin of the spinal cord lengthen, forming the cauda equina (Keegan and Garrett 1948). 20. How do the positions of spinal cord segments, nerve roots, and bony structures differ in more caudal spinal cord segments? What are the cervical and lumbar enlargements, and when do they first appear in the embryo? The discrepancy between the position of spinal cord segments with their nerve roots and corresponding bony structures, caused by different growth rates during embryonic

development, becomes more evident in the more caudal spinal cord segments. The nerve roots connected to the lower lumbar, sacral, and coccygeal spinal cord segments must travel longer distances before reaching the corresponding intervertebral foramina to pass through. As the nerve roots descend to their corresponding vertebral level, they become more oblique from rostral to caudal, such that the lumbar and sacral nerves descend almost vertically to reach their exit points. The difference between the spinal cord segment and the corresponding vertebra increases in the caudal segment (Fig. 2.9). These long spinal nerve roots surrounding the filum terminale form the cauda equina, with the most caudal segments being the most central. The spinal cord has an uneven contour due to the presence of cervical and lumbar enlargements associated with the spinal nerves for the upper and lower extremities. The enlargements first appear in the embryo at the time of limb formation. In adults, the spinal cord is four times longer than at birth, with its weight increasing from 7 to 90 g or more, and its volume from 6 to almost 80 mL in adults. The spinal cord is an approximately cylindrical structure, with an average length of 45 cm in males and slightly less than 43 cm in females. 21. How do spinal nerves relate to the segmental organization of the body? The distribution of spinal nerves is based on an original segmental organization where each nerve is composed of fibers associated with skin, muscles, and connective tissue originating from a body segment (Heimer 1983). There are 31 pairs of spinal nerves, each supplying a body segment derived from an embryonic somite. Somites form from cranial to caudal and are positioned lateral to the neural tube. The formation of somites begins on day 20, with the first four somite pairs belonging to the occipital region, followed by 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and approximately 3–6 or 8–10 coccygeal somites over the next 10  days (ten Donkelaar et  al. 2014b; Webster and de Wreede 2016).

2  Clinical Perspectives on Spinal Cord Development

a

b

29

c

Fig. 2.9  The relationship between the spinal cord and the vertebral column at various stages of development. (a) Approximately at the third month, (b) end of the fifth

month, (c) in the newborn. (Adapted Heimer (1983), with permission)

22. What are the roles of the ventromedial sclerotome and dorsolateral dermamyotome in the formation of body structures? Each somite further divides into a ventromedial sclerotome, which contributes to the formation of the vertebral column, and a dorsolateral dermamyotome, which forms myotomes and dermatomes (Fig. 2.8). During the fifth and sixth weeks of development, myotomes separate into a dorsal epaxial portion (epimere) and a ventrolateral hypaxial portion (hypomere) (ten Donkelaar et al. 2014b). Medial cells within the myotome form the epaxial back muscles, while lateral cells form the hypaxial muscles, such as the ­intercostal and abdominal muscles. Some lateral cells also migrate to the limb buds and contribute to limb musculature (ten Donkelaar et  al. 2014a; Webster and de Wreede 2016).

Metamerism, or the segmental organization of the body, is more evident in the thoracic region, where sensory innervation fields are easier to identify than motor innervation fields (McLachlan 1990). The dermatome, the area of the body surface supplied by nerve fibers from a single dorsal root ganglion (Standring 2016), is thought to appear in early limb buds in a pattern similar to that observed in adult thoracic segments. Figure 2.10 presents a schematic of the ventral (preaxial) and dorsal (postaxial) axial lines in the upper and lower extremities, showing areas without sensory overlap (Biller et  al. 2017; Vanderah and Gould 2016). Cervical dermatomes have an orderly distribution in the upper extremity, but limb outgrowth distorts the dermatomes along the ventral axial line, causing the C4 dermatome to lie above T2 at the sternal angle and positioning the C5 dermatome adjacent to the T1 dermatome.

23. What is metamerism, and how does it manifest in the thoracic region? How do dermatomes appear in early limb buds, and how are they affected by limb outgrowth?

30

2  Clinical Perspectives on Spinal Cord Development

Fig. 2.10  Sensory distribution of the spinal segments to the skin of the upper and lower extremities and schematic drawing of the ventral and dorsal axial lines. (From Medical Research Council (1956))

24. How do the preaxial and postaxial borders relate to the formation of the upper and lower extremities? The lower extremity is an extension of the trunk, and most caudal dermatomes primarily supply the perineum rather than the foot (Felten et al. 2016). In both upper and lower extremities, limb buds initially have a cranial (cephalic) border, referred to as the preaxial border, and a caudal border, called the postaxial border. In the upper extremities, the thumb and little finger form on the preaxial and postaxial borders, respectively. In contrast, the great toe and tibia are positioned along the preaxial border, while the little toe and fibula lie along the postaxial border in the lower extremities. 25. How does the rotation of the upper and lower extremities affect the arrangement of dermatomes in the limbs? What is the impact of the medial rotation of the lower extremity on the dermatomes and borders of the lower limb? By the end of the embryonic period at 8 weeks, the upper extremities have rotated

90° laterally (Fig.  2.11), while the lower extremities have undergone a 180° medial rotation. This rotation leads to a spiral arrangement of dermatomes in the lower extremities, with more pronounced changes in distal segmental dermatomes compared to proximal segmental dermatomes (Fig. 2.12). The medial rotation of the lower extremity reverses the preaxial and postaxial borders, causing the great toe and tibia to be carried medially, and the little toe and fibula laterally. As a result, the tibial border becomes the original preaxial border, and the fibular border becomes the postaxial border of the lower limb. Consequently, the great toe is supplied by nerves from a more rostral dermatome (L4) than the little toe (S1). 26. How does metamerism manifest in the innervation of skeletal muscles? Metamerism also appears in the innervation of skeletal muscles. Few muscles originate from a single somite, with the adductor pollicis and some small deep back muscles possibly having monosegmental innervation.

2  Clinical Perspectives on Spinal Cord Development

a

b

31

c

Fig. 2.11  Formation of the upper limb dermatomes during embryonic development. (a) The longitudinal axis of the limb buds is transverse to the long axis of the embryonic body. (b) Dermatomes of the upper limb in an

embryo. (c) The preaxial border becomes the lateral border with the external rotation of the embryonic upper limb. (Adapted from Bhuiyan et al. (2018))

Fig. 2.12  Changes in ventral dermatome pattern during limb development with limb rotation. Rotation of the lower limb results in a reversal of the preaxial and postaxial borders, producing a spiral arrangement of dermatomes. Spinal nerve segments on the anterior surface of the lower extremity extend medially and inferiorly; the great toe is supplied by nerves from a more rostral derma-

tome (L4) than the little toe (S1). The lower extremity is an extension of the trunk, and the most caudal dermatomes (sacral and coccygeal) supply the perineum, not the foot. Cervical dermatomes maintain a relatively orderly distribution to the upper extremity with minimal rotation. (Adapted from Felten et al. (2016))

2  Clinical Perspectives on Spinal Cord Development

32

Other muscles receive nerve fibers from 2 to 5 ventral roots, particularly in the upper and lower extremities (Keegan and Garrett 1948). 27. What is a dermatome and how is it related to motor innervation? A dermatome is the area of skin supplied by the sensory fibers of a single spinal nerve. It is essential to recognize that there is significant overlap between adjacent dermatomes. While the segmental organization in terms of motor innervation is less apparent, the muscles beneath a specific skin area are generally innervated by approximately the same segments as the overlying skin (Heimer 1983). 28. How do different sensory modalities overlap in dermatomes, and why is evaluating pain and temperature in sensory testing potentially more meaningful? How does the overlap of adjacent dermatomes affect the area of sensory loss following spinal cord or nerve root injury? Dermatomes overlap to varying degrees, with pain and temperature overlapping less than touch. Along the midline, there is an overlap of sensory fibers that can extend from 25 to 40 mm (Kellgren 1939). Since the overlap of touch is wider than that of pain and temperature, evaluating pain and temperature in sensory testing may provide more clinically meaningful information. Due to the varying extent of overlap between adjacent dermatomes, the area of sensory loss resulting from spinal cord or nerve root injury is always smaller than the actual area of dermatomes. 29. What role do sclerotome cells play in the formation of the spine, and when does this process begin? How do the cranial and caudal halves of the somite contribute to the formation of the intervertebral disc and vertebral body? The formation of the spine is primarily driven by the cells of the sclerotome. In the fourth week of development, these cells migrate toward and around the notochord and neural tube. As the sclerotomes encircle

the notochord and neural tube, each level separates into a cranial area with loosely packed cells and a caudal area with densely packed cells. The intervertebral disc forms between these two layers of cells. Segmentation of the stacked somites occurs through the loosely packed cells in the cranial half of each somite. The cranial half develops into the disc space and annulus fibrosus, while the caudal, densely packed half of the somite forms the vertebral body. Eventually, the notochord regresses and becomes the nucleus pulposus within the annulus fibrosus (Kaplan et al. 2005) (Fig. 2.13). 30. When does the corticospinal tract reach the level of the pyramidal decussation, and when does pyramidal decussation complete? The corticospinal tract, a late-developing descending tract, reaches the level of the pyramidal decussation at the end of the embryonic period, or at 8 weeks of development (ten Donkelaar 2000; Müller and O’Rahilly 1990). Pyramidal decussation is completed by 17 weeks of gestation, with the rest of the spinal cord being invaded by 19 weeks (lower thoracic cord) and 29 weeks (lumbosacral cord) of gestation (Humphrey 1960). Early-developing fiber tracts generally undergo myelination before later-­ appearing tracts (Kinney et  al. 1988; ten Donkelaar et al. 2014a). 31. What are the rules governing the chronological and topographical sequences of CNS myelination during the first 2 years after birth? Postnatal myelination in the human central nervous system (CNS) is a complex and intricately timed process. It begins during the fetal period and continues into adulthood, with significant changes occurring within the first 2 postnatal years (Kinney et  al. 1988). Several rules govern the chronological and topographical sequences of CNS myelination during the first 2 years after birth: proximal pathways myelinate earlier and faster than distal pathways, sensory pathways pre-

References

33

a

b

c

d

Fig. 2.13 (a) Transverse section through a 4-week embryo. The arrows indicate the dorsal growth of the neural tube and the simultaneous dorsolateral movement of the somite remnant, leaving behind a trail of sclerotomal cells. (b) Diagrammatic frontal section of this embryo showing that the condensation of sclerotomal cells around the notochord consists of a cranial area of loosely packed cells and a caudal area of densely packed cells. (c) Transverse section through a 5-week embryo showing the condensation of sclerotomal cells around the notochord

and neural tube, which forms a mesenchymal vertebra. (d) Diagrammatic frontal section illustrating that the vertebral body forms from the cranial and caudal halves of two successive sclerotomal masses. The intersegmental arteries now cross the bodies of the vertebrae, and the spinal nerves lie between the vertebrae. The notochord is degenerating except in the region of the intervertebral disc, where it forms the nucleus pulposus. (Adapted from Moore et al. (2013), with permission)

cede motor pathways, and projection pathways develop before associative pathways (Kinney et al. 1988).

observed at less than 16 weeks of gestation. Unlike in many mammals, myelination in humans extends into the postnatal developmental period. The earliest myelinated structure is the medial longitudinal fascicles in the upper cervical spinal cord at 20 weeks, with the corticospinal tract being the last to undergo myelination during the first year after birth (Armand 1982; Weidenheim et al. 1996). The process of myelin formation takes several years, but the exact time of completion remains unknown. Table  2.3 illustrates the development of myelination of the main fiber tracts in the human spinal cord.

32. When is the first myelination of axons in the human spinal cord observed, and when do the medial longitudinal fascicles in the upper cervical spinal cord undergo myelination? Myelin formation on the nerve fibers of the spinal cord only occurs in the middle of the fetal period and is believed to be associated with the differentiation of glioblasts into oligodendrocytes. In humans, the first myelination of axons in the spinal cord is

2  Clinical Perspectives on Spinal Cord Development

34

Table 2.3  Timeline of myelination in major fiber tracts of the human spinal cord First evidence of myelin basic protein staining

Onset of reactive gliosis

Onset of myelination

GW 14

GW 20

 Gracilis fascicle

GW 16

GW 20

 Dorsal spinocerebellar tract  Ventral spinocerebellar tract  Spinothalamic tract Descending tracts  Vestibulospinal tract

GW 20

GW 26

At GW 33, myelination well advanced throughout At GW 33, wedge area myelinating GW 33

GW 20

Later than dorsal spinocerebellar tract

Late third trimester

GW 20

GW 33

Late-term neonate

GW 9.5

GW 33

 Reticulospinal tract Corticospinal tracts  Lateral corticospinal tract  Anterior corticospinal tract

GW 9.5

By GW 20, first sign of reactive gliosis in medial vestibulospinal tract Comparable to vestibulospinal tracts At birth few glia present

After birth

At birth few glia present

After birth

Fiber tract Ascending tracts  Cuneate fascicle

GW 33

GW gestational weeks. Adapted from ten Donkelaar et al. (2014b), with permission

References Altman J, Bayer SA.  Development of the human spinal cord: an interpretation based on experimental studies. 1st ed. New York: Oxford University Press; 2001. Armand J.  The origin, course and termination of corticospinal fibers in various mammals. Prog Brain Res. 1982;57:329–60. Bayer SA, Altman J. Atlas of human central nervous system development series. The spinal cord from gestational week 4 to the 4th postnatal month. New York: CRC Press; 2002. Bhuiyan PS, Rajgopal L, Shyamkishore K, editors. Inderbir Singh’s textbook of human neuroanatomy. 10th ed. New Delhi: Jaypee Brothers Medical Publisher; 2018. Biller J, Gruener G, Brazis P.  DeMyer’s the neurologic examination: a programmed text. 7th ed. New  York: McGraw-Hill Education; 2017. Collins P, Billett FS.  The terminology of early development: history, concepts, and current usage. Clin Anat. 1995;8:418–25. Copp AJ, Greene ND.  Neural tube defects-disorders of neurulation and related embryologic processes. Wiley Interdiscip Rev Dev Biol. 2013;2:213–37.

Felten DL, O’Banion MK, Maida MS.  Netter’s atlas of neuroscience. 3rd ed. London: Elsevier; 2016. Greene ND, Vopp AJ.  Neural tube defects. Annu Rev Neurosci. 2014;37:221–42. Hawryluk GW, Ruff CA, Fehlings MG.  Development and maturation of the spinal cord: implications of molecular and genetic defects. Handb Clin Neurol. 2012;109:3–30. Humphrey T. The development of the pyramidal tracts in human fetuses, correlated with cortical differentiation. In: Tower DB, Schadé JP, editors. Structure and function of the cerebral cortex. Amsterdam: Elsevier; 1960. Heimer L. The human brain and spinal cord. Functional neuroanatomy and dissection guide. New  York: Springer; 1983. Kaplan KM, Spivak JM, Bendo JA.  Embryology of the spine and associated congenital abnormalities. Spine J. 2005;5:564–76. Keegan JJ, Garrett FD.  The segmental distribution of the cutaneous nerves in the limbs of man. Anat Rec. 1948;102:409–37. Kellgren JH. On the distribution of pain arising from deep somatic structures with charts of segmental pain areas. Clin Sci. 1939;4:35–46. Kinney HC, Brody BA, Kloman AS, et  al. Sequence of central nervous system myelination in human infancy.

References II.  Patterns of myelination in autopsied infants. J Neuropathol Exp Neurol. 1988;47:217–34. Mancall E, Brock DG. Gray’s clinical neuroanatomy: the anatomic basis for clinical neuroscience. Philadelphia: Elsevier; 2011. McLachlan JC. Development of the dermatome pattern in the limb. Chin Anat. 1990;3:41–9. Medical Research Council. Aids to the investigation of peripheral nerve injuries. War memorandum nerve injuries committee, No. 7. 2nd ed. London: Her Majesty’s Stationery Office; 1956. Moore KL, Persaud TVN, Torchia MG.  The developing human clinically oriented embryology. 9th ed. Philadelphia: Elsevier; 2013. Müller F, O’Rahilly R.  The human rhombencephalon at the end of the embryonic period proper. Am J Anat. 1990;189:127–45. Noback CR, Strominger NL, Demarest RJ, et  al. The human nervous system: structure and function. 6th ed. Totowa: Humana Press; 2005. O’Rahilly R, Müller F. The two sites of fusion of the neural folds and the two neuropores in the human embryo. Teratology. 2002;65:162–70. O’Rahilly R, Müller F. The embryonic human brain. An atlas of developmental stages. 3rd ed. Hoboken: John Wiley & Sons, Inc.; 2006. O’Rahilly R, Müller F.  Developmental stages in human embryos: revised and new measurements. Cells Tissues Organs. 2010;192:73–84. Sadler TW. Embryology of neural tube development. Am J Med Genet C Semin Med Genet. 2005;135C:2–8. Singh R, Munakomi S.  Embryology, neural tube. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022.

35 Standring S, editor. Gray’s anatomy. 41st ed. Philadelphia: Elsevier; 2016. ten Donkelaar HJ. Development and regenerative capacity of descending supraspinal pathways in tetrapods: a comparative approach. Adv Anat Embryol Cell Biol. 2000;154:1–145. ten Donkelaar HJ, Yamada S, Shiota K, et al. Overview of the development of the human brain and spinal cord. In: ten Donkelarr HJ, Lammens M, Hori A, editors. Clinical neuroembryology. Development and developmental disorders of the human central nervous system. 2nd ed. Heidelberg: Springer; 2014a. ten Donkelaar HJ, Itoh K, Hori A.  Development and developmental disorders of the spinal cord. In: ten Donkelarr HJ, Lammens M, Hori A, editors. Clinical neuroembryology. Development and developmental disorders of the human central nervous system. 2nd ed. Heidelberg: Springer; 2014b. Tomlinson BE, Irving D, Rebeiz JJ. Total numbers of limb motor neurons in the human lumbosacral cord and an analysis of the accuracy of various sampling procedures. J Neurol Sci. 1973;20:313–27. Vanderah TW, Gould DJ. Nolte’s the human brain. 6th ed. London: Elsevier; 2016. Webster S, de Wreede R. Embryology at a glance. 2nd ed. West Sussex: John Wiley & Sons, Ltd; 2016. Weidenheim KM, Bodhireddy SR, Rashbaum WK, et  al. Temporal and spatial expression of major myelin protein in the human fetal spinal cord during the second trimester. J Neuropathol Exp Neurol. 1996;55:734–45.

3

Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Abstract

The spinal cord is a crucial component of the central nervous system that facilitates communication between the brain and other parts of the body. Accurate localization of lesions and interpretation of clinical manifestations necessitate an in-depth comprehension of spinal cord anatomy. This chapter starts with a detailed overview of the protective meningeal layers surrounding the spinal cord, including the dura mater, arachnoid mater, and pia mater, which support and protect the spinal cord. The spinal cord features cervical, lumbar, and sacral enlargements responsible for limb innervation. The cervical enlargement supplies nerves to the upper limbs, while the lumbar and sacral enlargements supply nerves to the lower limbs. The spinal cord comprises outer white matter and inner gray matter. The outer white matter includes ascending and descending tracts, transmitting sensory and motor information between the brain and the body. The inner gray matter comprises nerve cell bodies, responsible for processing sensory information and generating motor output. The central canal, filled with cerebrospinal fluid, is encompassed by gray matter featuring dorsal, ventral, and lateral horns. A comprehensive comprehension of spinal cord anatomy, internal and external, is crucial for interpreting pathological findings, clinical manifestations, and lesion localization. The chapter empha-

sizes the significance of a thorough knowledge of the spinal cord’s anatomy for effective treatment of spinal cord injuries and understanding spinal cord function. 1. What are the unique features of the first cervical and coccygeal nerves regarding their dorsal roots and dermatomal presentation? How do sensory and motor roots form, and what are the typical numbers of filaments in ventral and dorsal roots? At which levels of the spinal cord do the ventral roots carry preganglionic autonomic fibers, and where do these fibers originate from? The human nervous system contains 31 spinal nerves, each corresponding to a specific spinal cord segment. These spinal nerves comprise a sensory root and a motor root, originating from the anterolateral and posterolateral surfaces of the spinal cord, respectively, at each segmental level (Standring 2016). Notably, the first cervical and coccygeal nerves lack a dorsal root and do not display a dermatomal presentation. Each sensory and motor root is formed by the union of three or more small rootlets, also known as root filaments. The ventral root typically consists of 4–7 filaments emerging from the spinal cord at the anterolateral sulcus, whereas the dorsal root enters the cord at the posterolateral sulcus and is composed of 4–10 filaments. At every level of the spinal cord, motor neurons give rise to the ventral root,

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 H.-Y. Ko, A Practical Guide to Care of Spinal Cord Injuries, https://doi.org/10.1007/978-981-99-4542-9_3

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3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

while at the T1–L2 and S2–S4 levels, these roots also carry preganglionic autonomic fibers originating from the intermediolateral nucleus (Standring 2016). The dorsal root houses the central process of bipolar sensory neurons located in the dorsal root ganglion. 2. What is the significance of unmyelinated axons in the ventral roots, and what percentage of the total ventral root axon population do they represent? Interestingly, some primary sensory afferents, particularly those of visceral origin, enter the spinal cord via the ventral root but ultimately terminate in the dorsal horn. Ventral roots contain a large number of unmyelinated axons, accounting for 27% of the total ventral root axon population (Coggeshall et al. 1975). While the function of these unmyelinated axons remains unclear, it is likely that a significant proportion serves a sensory purpose. 3. What structures and cells are included in the nerve root coverings, and how do they protect the nerve roots? How does the lack of a dural covering in the subarachnoid space impact the susceptibility of nerve roots to injury? Nerve roots are enveloped by a thin layer of arachnoid cells enclosing the nerve’s endothelial compartment, which includes myelinated and unmyelinated nerve fibers, Schwann cells, and endoneurial blood vessels. In each intervertebral foramen, the dura mater forms dural sleeves and blends with the epineurium of each spinal nerve. The nerve roots, surrounded by the pia mater, traverse the subarachnoid space until reaching their respective dural sleeves, which emerge from the anterolateral surface of the dural sac (Standring 2016). Notably, nerve roots in the subarachnoid space lack a dural covering and are devoid of an epineurial layer, rendering them more susceptible to injury compared to spinal nerves. 4. What are the key differences between the dura mater of the brain and the spinal cord?

The primary distinction between the meninges of the brain and spinal cord lies in the characteristic features of the dura mater. While the brain’s dura mater has two layers, the periosteal (outer dura mater) and the meningeal (inner dura mater) layers, the spinal cord’s dura mater only has one layer. The epidural space separates the periosteal and meningeal layers of the brain’s dura mater. The outer dura mater serves as the skull’s periosteum, while the inner dura mater extends into the falx cerebri, dividing the two cerebral hemispheres in the midsagittal plane, and forms the tentorium cerebelli between the occipital lobes and cerebellum. Located between the inner dura mater and the arachnoid, the brain’s subdural space is a thin layer. However, the spinal dura mater and arachnoids are densely packed, leaving virtually no space (Fig. 3.1). The brain’s epidural space lacks adipose tissue and nerve roots. In contrast, the epidural space in the spine, which separates the spinal dura mater (equivalent to the inner dura mater surrounding the brain), contains the Batson venous plexus, intraspinal veins, and adipose tissue. 5. How are the anterior and posterior spinal nerve roots connected to the spinal nerve? Where does the spinal dura mater attach to the bone, and where does the dural sac terminate? The anterior and posterior spinal nerve roots share a common dural sleeve, continu-

Fig. 3.1  The meningeal layers of the spinal cord. Unlike the brain, the space between the dura mater and the arachnoid of the spinal cord is narrow

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

ous with the spinal nerve’s epineurium at the intervertebral foramen. Unlike the cranial cavity, where the dura mater is attached to the skull’s periosteum, the spinal dura mater forms a tubular sac that securely attaches to the bone only at the foramen magnum’s margin. The dural sac terminates at the second sacral vertebra level. 6. What is the average length of the spinal cord in females and males, and what structures are involved in spinal cord injuries from a clinical perspective? The spinal cord, while simpler in structure and function than the brain, constitutes around 2% of the entire human nervous system. It measures 41–43  cm in females and 45  cm in males from the cervicomedullary junction to the conus medullaris tip (Bican et al. 2013). Anatomically, the spinal cord is the central nervous system structure between the cervicomedullary junction and the conus medullaris tip. However, clinically, spinal cord injuries encompass both the spinal cord and the cauda equina. The cauda equina, a bundle of lumbar and sacral nerve roots, is located below the conus medullaris tip in the spinal canal (Barson 1970). The filum terminale anchors the spinal cord caudally. 7. How do the spinal cord segments differ in terms of weight, length, and diameter? There are 31 spinal cord segments, each with distinct quantitative measures, from the first cervical to the fifth sacral spinal cord segment. Each segment weighs about 1 g, but their lengths vary by region: approximately 25 mm in the midthoracic spinal cord, 12 mm in the midcervical spinal cord, and 10 mm in the midlumbar spinal cord (Ko et al. 2004). The T6 spinal cord segment is the longest, averaging 22.4 mm in length, while the longest segments in the cervical and lumbar spinal cord are C5 and L1, respectively, with average lengths of 15.5 mm (Ko et al. 2004). The anteroposterior diameter of each spinal cord segment is relatively uniform at 6–8 mm, but the lateral diameters differ. The cervical and lumbar enlargements have larger

39

diameters than other spinal cord parts, with their quantitative features determined by lateral diameters (Ko et al. 2004) (Fig. 3.2). 8. What distinguishes the gray matter in thoracic and upper lumbar segments from the cervical and middle or lower lumbar segments? How does the amount of white matter change along the length of the spinal cord, and which region has the smallest white matter content? The spinal cord features two symmetrical enlargements that contain segments responsible for limb innervation. The cervical enlargement (C5–T1) gives rise to the brachial plexus, while the lumbar enlargement (L2–S3) forms the lumbosacral plexus. The spinal cord is composed of an outer white matter, housing ascending sensory and descending motor tracts, and an inner gray matter containing nerve cell bodies. Gray matter volume is most prominent in the cervical and lumbar regions due to increased neuron numbers in upper and lower extremities. In contrast, white matter volume gradually decreases in a craniocaudal direction (Fig.  3.3). The thoracic and upper lumbar a

b

Fig. 3.2 (a) Sagittal diameter and (b) lateral diameter of each segment of spinal cord. (Adapted from Ko et  al. (2004), with permission)

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40

segments feature a unique lateral horn, housing autonomic preganglionic motor neurons. The gray matter encircles a central canal— an extension of the fourth ventricle—lined with ependymal cells and filled with cerebrospinal fluid. The cervical region has the most developed white matter, which gradually decreases in size at successive caudal levels of the spinal cord (Breig and el-Nadi 1966; Breig et al. 1966; Holmes et al. 1996). White matter content diminishes in caudal sections as long ascending and descending pathways contain fewer axons at increasingly caudal levels, making the sacral spinal cord possess the smallest amount of white matter. 9. What is the role of denticulate ligaments in the spinal cord, and how many pairs of denticulate ligaments are there? Three ligament-like structures, which are pia mater extensions, support the spinal cord. Two denticulate ligaments, one on each side, extend from the midlateral aspect of the spinal cord through the subarachnoid space and attach laterally to the dura. These ligaments span from the cervicomedullary junction to the conus medullaris tip at the first lumbar vertebra’s lower border (Bican et  al. 2013). Figure 3.4 illustrates a diagram of the spinal cord, dura, and connective tissue, including

Fig. 3.3 Cross-­ sectional mean area and white and gray matter areas of each segment of the spinal cord. (Adapted from Kameyama et al. (1996))

the denticulate ligaments. There are 20 or 21 pairs of denticulate ligaments. 10. What are the alar and basal plates, and what do they form in the spinal cord? What is the order of neuron development in the spinal cord? The neural tube thickens as nuclei form multiple layers. The ventricular zone is cre-

Fig. 3.4  Spinal cord, dura, and connective tissue. 1 dura, 2 arachnoid membranes, 3 attachment of the septum and extent of the arachnoid, 4 connective tissue septum for fixating the spinal cord, 5 epipial subarachnoidal tissues, 6 vessels in the epipial network, 7 trabecular membrane, 8 denticulate ligament. (From Nix (2017), with permission)

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

ated when the inner ventricular side of this cell layer forms the mantle layer or intermediate zone and gradually thickens. The mantle layer, lying between the ventricular zone and the marginal zone, surrounds the primitive spinal cord and arises from numerous neuroepithelial cell divisions (ten Donkelaar et  al. 2014). The gray matter of the spinal cord is formed from the mantle layer, while the marginal zone eventually becomes the white matter. The mantle layer has two distinct paired regions: the dorsal thickening, known as the alar plate (future sensory areas), and the ventral thickening, called the basal plate (future motor area). The alar plates and dorsal roots form the sensory part of the spinal cord, while the basal plate and ventral roots form the motor part. Spinal ganglia originate from the neural crest (ten Donkelaar et  al. 2014). Motor neurons are the first neurons to develop during spinal cord development, followed by neurons in the intermediate zone and, finally, dorsal horn neurons (Bayer and Altman 2002). 11. How does the spinal cord change during fetal development concerning its position relative to the vertebral column? At 3 months, the spinal cord resembles the adult spinal cord, except that it extends the entire length of the spinal canal, and the spinal nerves pass through the intervertebral foramina at their spinal cord origin level. However, by the third fetal month, the vertebral column and dura mater grow faster than the spinal cord, causing spinal cord segments to eventually lie higher than their corresponding vertebrae. The growth difference between the spinal cord and vertebrae stretches the long lumbar and sacral roots during development, ultimately forming the cauda equina. In the caudal segments, the distance between the spinal cord segment and corresponding vertebra increases. At birth, the spinal cord ends at the level of vertebra L3, but it only extends to the L2 vertebra in adults. 12. What occurs during the “ascensus” phase of spinal cord development? Where does

41

the spinal cord end in newborns and adults? During the 11th gestational week, the “ascensus” begins, which is marked by the formation of the filum terminale and the increased obliquity of the lower spinal nerves due to the displacement between the spinal cord and the vertebral column. This occurs as a result of the disproportionate growth of the spinal cord and vertebral column. The tip of the spinal cord ascends to the lumbar spinal level, forming the cauda equina. In newborns, the spinal cord ends at the L3 vertebra level, while in adults, it typically ends at the L1 or L2 vertebra level. The most common termination site for the conus medullaris in adults is the L1–L2 disc space. Below the tip of the conus medullaris, the lumbar and sacral nerve roots of the cauda equina are arranged laterally to medially around the filum terminale, with L2 roots being the most lateral and S4–S5 roots being the most medial (De Vloo et al. 2016). 13. What is the epiconus, and which spinal cord segments does it typically include? The rostral extent of the conus medullaris lacks a clear anatomical landmark. The area of the spinal cord immediately rostral to the conus medullaris is called the epiconus, which usually consists of spinal cord segments from L4 to S2 (Baehr and Frotscher 2012; Toribatake et al. 1997) (Fig. 3.5). 14. What is a “tract” in the context of nerve fibers? How does a “fasciculus” differ from a “tract”? Nerve fibers sharing a common origin and destination come together to form a “tract.” These tracts may not always create well-­defined bundles, as fibers from one tract can intertwine with fibers from adjacent tracts (Fig.  3.6). A “fasciculus” is a collection of fibers, which can contain multiple tracts (Heimer 1983). 15. What is a spinal cord segment, and how many segments are present in the adult spinal cord? A spinal cord segment refers to a section of the spinal cord situated between the

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42

attachment points of the ventral and dorsal rootlets for a single pair of spinal nerves (Fig. 3.7). With 31 pairs of spinal nerves in the adult spinal cord, there are consequently 31 spinal cord segments.

Fig. 3.5  Epiconus, conus medullaris, and cauda equina. (Adapted from Baehr and Frotscher (2012)) Fig. 3.6  The figure shows that the axons of the adjacent tracts are intermingled

16. What is a dermatome, and what are some alternative definitions? A dermatome is generally defined as the skin area supplied by a single spinal nerve through both rami (Standring 2016). Other ­definitions include the skin area supplied by a single posterior nerve root and its ganglion (Haymaker and Woodhall 1953; Bonica and Loeser 2001) or one spinal cord segment (Schuenke et al. 2016), or the tissue within a

Fig. 3.7  Spinal cord segment

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

somite that forms part of the dermis (Anthoney 1994; Lee et al. 2008). The latter term is not utilized after metameric segmentation in the mature spinal cord. 17. In which spinal segments do adjacent spinal nerves overlap the most? What is the difference in overlap when testing pain and temperature versus touch? Dermatomes typically extend around the body from the posterior to the anterior midline. The upper half of each zone is supplemented by the spinal nerve above, and the lower half by the spinal nerve below. The skin areas supplied by dorsal rami do not exactly correspond to those supplied by ventral rami, differing in width and position. Dermatomes of adjacent spinal nerves overlap considerably, particularly in segments least affected by limb development (T2 to L1). In some regions, such as the upper anterior thoracic wall, cutaneous nerves supplying adjacent areas may not originate from consecutive spinal nerves, resulting in minimal overlap (Mancall and Brock 2011). Although the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) designates 28 key sensory points, dermatomes often overlap to varying

Fig. 3.8  Diagram of the position of the nipple in the sensory skin fields of the third, fourth, and fifth thoracic spinal cord segments or roots, showing the overlap of the

43

extents. However, the overlap is less for pain and temperature than for touch, making it easier to detect a small sensory deficit by testing pain sensitivity rather than touch (Heimer 1983). Sensory fiber overlap along the midline can reach 25–40  mm (Kellgren 1939). For example, the upper half of dermatome T4 is innervated not only by fibers from T4 but also by fibers from T3, while the lower half of T4 is additionally innervated by T5 (Fig. 3.8). 18. What is a myotome? A myotome refers to a group of muscles innervated by motor axons from a specific spinal root. It is a segmental mass of mesoderm in a vertebrate embryo that differentiates into skeletal muscle. This group of muscles originates from a single somite and is innervated by a single spinal nerve segment. Figure  3.9 illustrates the redistribution of motor units that form the dermatome and myotome (Baehr and Frotscher 2012). 19. How is the peripheral innervation of spinal nerves organized based on somite segmentation, and what is the relationship between the motor innervation and dermatome?

cutaneous areas. The overlap of adjacent dermatomes is usually greater for touch than for pain. (Adapted from Waxman (2010))

44

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

a

b

Fig. 3.9  Redistribution of afferent and efferent nerve fibers to the dermatome and myotome. (a) The sensory fibers of a single spinal cord segment are recombined to supply a specific segmental regions of the skin (derma-

tome). (b) Each muscles is supplied by a single peripheral nerve originating from multiple anterior roots or spinal cord segments (myotome). (Adapted from Baehr and Frotscher (2012))

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

The peripheral innervation of the spinal nerves reflects an original segmental organization, with each spinal nerve composed of fibers related to the region of the skin, muscles, or the connective tissue that develops from a body segment (somite) (Heimer 1983). The segmental organization of the motor innervation is less obvious compared to the dermatome. The muscles that lies deep to a certain area of the skin are usually innervated by approximately the same segments as the overlying skin (Baehr and Frotscher 2012; Heimer 1983) (Fig. 3.10). Most muscles receive nerve fibers from two to five ventral roots, particularly in the upper and lower extremities. However, few muscles have been derived from a single somite. The adductor pollicis and some of the small deep back muscles may have a monosegmental innervation (Keegan and Garrett 1948). 20. What is the basis for distinguishing between white matter and gray matter, and what is the appearance of myelin sheath and how does it affect the appearance of white matter? What is the structure of gray matter in the spinal cord? The distinction between white matter and gray matter is based on the structure of the nerve cells comprising these regions. Many axons are surrounded by a myelin sheath, which has a white, glistening appearance, so areas containing mostly bundles of myelinated axons appear white and are called white matter. Myelin staining can darken the white matter (Heimer 1983). Conversely, gray matter consists of nerve cell bodies embedded in a delicate network of nerve processes and unmyelinated fibers. In the spinal cord, gray matter is centrally located and exhibits a characteristic H-shaped appearance in cross sections. The crossbar of the “H,” known as the commissural gray matter, encloses the central canal. Macroscopically, gray matter can be divided into ventral and dorsal horns, with an intermediate zone between them. 21. How is the white matter of the spinal cord divided, and what structures are responsible for the division?

45

The white matter of the spinal cord is generally divided into anterior (ventral), posterior (dorsal), and lateral funiculi by the ventral and dorsal horns of the gray matter (Nolte and Angevine 2013) (Fig. 3.11). In the cervical and upper thoracic regions, the posterior intermediate sulci are subdivided into fasciculi gracilis and cuneatus. The white matter surrounding the gray matter primarily contains the propriospinal fibers of the spinal cord, also known as fasciculi proprius. 22. What are the main components of the ascending tracts and descending tracts in the spinal cord? In ascending tracts, the anterolateral funiculus houses the anterior and lateral spinothalamic tracts, while the lateral funiculus contains the posterior and anterior spinocerebellar and spino-olivary tracts. The posterior funiculus includes two fasciculi: fasciculus gracilis and fasciculus cuneatus (Bican et al. 2013; Patestas and Gartner 2006; Schuenke et al. 2016). As for descending tracts, the lateral corticospinal tract, rubrospinal tract, and lateral reticulospinal tract are located within the lateral funiculus. The anterior funiculus contains the anterior corticospinal tract, reticulospinal tract, vestibulospinal tract, and tectospinal tract (Fig.  3.12). The primary ascending and descending tracts are summarized in Table 3.1. 23. What are the primary roles of the spinal cord’s ascending tracts, and what are the main components of both ascending and descending tracts along with their respective functions? The ascending tracts primarily convey sensory information to higher relay nuclei within the main sensory pathway (e.g., thalamus) or supply sensory input (mainly proprioceptive) to the cerebellum. Most ascending tracts consist of second-order sensory afferents originating from neurons in the gray matter, primarily from the dorsal horn. An exception is the posterior columns, where the fasciculus cuneatus and gracilis consist of primary sensory afferents from

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46

Biceps brachii m.

C7

C8

Triceps brachii m. Pronator teres m.

Brachioradials m.

Thenar muscles

Hypothenar muscles

C6

C7

C8

Vastus lateralis m. Vastus medalis m. Triceps surae m.

Tibialis anterior m.

Extensor hallucis longus m.

Peroneus longus m. Peroneus brevis m.

Extensor digitorum brevis m. L4

L5

S1

Fig. 3.10  The dermatomes (blue hatched areas) and underlying myotomes roughly match. (Adapted from Baehr and Frotscher (2012))

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47

Posterior median septum Posterior intermediate sulcus Central canal Posterior (or dorsal) gray horn

Posterolateral sulcus Posterior funiculi

Intermediate gray zone Lateral funiculus Lateral gray horn

Ventral (or anterior) horn

Anterior funiculi Commissural gray maer Anterolateral sulcus Anterior white commissure

Anterior median fissure (anterior sulcus)

Fig. 3.11  Subdivisions of the white matter and gray matter. The white matter is composed of three funiculi. The gray matter is divided into two horns and an intermediate zone. Rexed’s laminae of the gray matter are shown on the right

a

Fig. 3.12  The approximate positions of ascending (a) and descending tracts (b) in the spinal cord. Most important ascending tracts are spinothalamic tracts (anterior and lateral), tracts of the posterior funiculus (fasciculus cuneatus and fasciculus gracilis), and spinocerebellar tracts (anterior and posterior). The descending tracts of the spi-

b

nal cord are divided into two motor systems: lateral motor system (anterior and lateral corticospinal tract and rubrospinal tract) and medial motor system (reticulospinal tract, tectospinal tract, and vestibulospinal tract). (From Schuenke et al. (2016))

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Table 3.1  Summary of main ascending (a) and descending (b) tracts of the spinal cord Crossed/ uncrossed

Tract Origin (a) Ascending tracts Fasciculus gracilis Dorsal root ganglia below T6 Fasciculus Dorsal root ganglia cuneatus above T6 Posterior Clarke’s nucleus spinocerebellar

Termination Nucleus gracilis (medulla) Nucleus cuneatus (medulla) Cerebellum

U

Anterior spinocerebellar

Cerebellum

C

Thalamus (ventral posterior nucleus) Thalamus (ventral posterior nucleus)

C

Proprioception and vibration Proprioception and vibration Proprioceptive, pressure, and touch input to the cerebellum Proprioceptive, pressure, and touch input to the cerebellum Pain and temperature

C

Light touch and pressure

Medial and lateral motor nuclei at all levels

C (85–90%)

Medial and lateral motor nuclei in cervical and upper thoracic levels

U

Skilled movements mediated by distal limb muscles Descending motor input to motor neurons that innervate neck musculature

Spinal neurons primarily at cervical levels

C

Bilateral reticular formation (pons and medulla) Superior and inferior colliculi

Spinal neurons for trunk and proximal limb musculature Motor neurons for neck muscles

C and U

Ipsilateral vestibular nuclei (medulla)

Spinal neurons for trunk musculature

U

Preganglionic sympathetic neurons in intermediolateral nucleus (T1–L2) Preganglionic parasympathetic neurons in the intermediolateral nucleus (S2–S4)

C and U

Descending sympathetic outflow to entire body

C and U

Parasympathetic supply to the distal colon, rectum, bladder, and sexual organs

Anterior horn especially lumbosacral Lateral Rexed laminae I, III, spinothalamic IV, and V Anterior Rexed laminae I, III, spinothalamic IV, and V (b) Descending tracts Pyramidal system  Lateral Layer V neurons in corticospinal the contralateral motor cortex (major)  Anterior Layer V neurons in corticospinal contralateral motor cortex Extrapyramidal system  Rubrospinal Contralateral red nucleus (midbrain)  Reticulospinal

 Tectospinal

 Vestibulospinal

Central autonomic tract  Sympathetic Hypothalamus and brainstem nuclei

 Parasympathetic

Hypothalamus and brainstem nuclei

U U

C

Main function

Posture and locomotion primarily flexor activities (small tract in man) Posture and locomotion, respiration, modulation of pain, vasomotor tone Reflexic head movements toward visual and auditory stimuli Posture and locomotion primarily extensor activities

Adapted from Critchley and Eisen (1997), with permission

dorsal root ganglia. These afferents enter the spinal cord and ascend to the medulla without synapsing in the dorsal horn (Critchley and Eisen 1997). The ascending tracts

include: (1) the posterior column-medial lemniscal system, which transmits sensory information on vibration and proprioception through the fasciculus cuneatus and gracilis;

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

(2) the anterolateral system, which transmits nociceptive, thermoreceptive, and tactile information via the anterior and lateral spinothalamic tracts, spinoreticular tract, etc.; and (3) the cerebellar input system, responsible for proprioceptive sensibility of the upper and lower limbs via the posterior spinocerebellar tract, cuneocerebellar tract, and smaller tracts such as ventral and rostral spinocerebellar tracts (Bican et  al. 2013; Patestas and Gartner 2006). The descending pathways are organized into: (1) the lateral motor system, responsible for contralateral limb movement through the lateral corticospinal tract and rubrospinal tract, and (2) the medial motor system, controlling bilateral trunk muscles, head/neck positioning, balance, and other posture- and gait-­related movements via the anterior corticospinal tract, medial and lateral vestibulospinal tract, reticulospinal tract, and tectospinal tract (Patestas and Gartner 2006) (Fig. 3.13). 24. How does lamination occur in the embryonic spinal cord? What is the arrangement of axons within the cervical spinal cord? Are tracts of ascending and descending short fibers laminated?

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During the development of the embryonic spinal cord, early nerve fibers create tracts that are subsequently covered by additional, similarly formed fibers. This results in the formation of layers within individual fiber tracts (Blumenfeld 2010). Ascending fibers originating from lower segments of the spinal cord overlap with pre-existing fibers in higher segments. In the cervical spinal cord, for example, a layered arrangement can be observed, with axons from cervical origins situated deeper than those from thoracic, lumbar, and sacral origins. The latter are positioned more superficially (Fig.  3.14). This lamination is not commonly observed in tracts composed of ascending and descending short fibers, such as the fasciculi proprius. 25. How is lamination observed in long descending tracts of the spinal cord? Long descending tracts of the spinal cord also exhibit lamination, with earlier descending fibers being enveloped by white matter from fibers that form later. In the larger lateral corticospinal tracts, fibers that terminate at the level of the cervical cord are positioned more medially, while those that terminate at the

Fig. 3.13  Ascending and descending tracts corresponding to white matter functional subgroups

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3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Fig. 3.14  Schematic diagram of the segmental organization of fibers in the dorsal funiculus, the lateral spinothalamic tract, and the lateral corticospinal tracts. The

probable cross-sectional areas of these tracts are schematically enlarged. (Adapted from Standring (2016), with permission)

lumbosacral levels are situated more laterally (Armand 1982; Moore and Dalley 1999).

spinal cord? Where are the fasciculi proprii located? What is the primary function of Lissauer’s tract? In the spinal cord, two key association structures connect various segments: the fas-

26. What are the two association structures connecting different segments within the

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51

ciculi proprii and Lissauer’s tract. The fasciculi proprii can be found in all three funiculi, typically located near the gray matter. On the other hand, Lissauer’s tract is a wedge-­ shaped white matter structure situated between the gray matter’s dorsal horn and the spinal cord’s surface, primarily functioning as a propriospinal pathway.

descending fibers typically reach only one or two root levels, the fasciculi proprii also contain long fibers connecting the cervical and lumbar spinal cord. These fibers transmit excitatory and inhibitory impulses to anterior horn motor neurons, contributing to the coordinated movement of extensors and flexors during locomotion (Kahle 2015).

27. Where are the majority of propriospinal fibers found in the spinal cord, and what is the fasciculi proprius? What is the function of interneurons in the spinal cord? What is the significance of the long fibers in the fasciculi proprii for locomotion? The white matter surrounding the gray matter of the spinal cord contains the majority of propriospinal fibers, which include the fasciculi proprius, an intersegmental fiber. Interneurons facilitate the propagation of impulses across multiple segments, either on the same or opposite side. The fasciculi proprii, located next to the gray matter and present in all three funiculi, are the association pathways of ascending and descending fibers that connect different segments within the spinal cord (Fig. 3.15). While ascending and

28. What is Lissauer’s tract, and where is Lissauer’s tract located? What is the role of the substantia gelatinosa neurons in Lissauer’s tract? Lissauer’s tract, also known as the dorsolateral tract, is a funiculus located between the apex of the dorsal horn and the surface of the spinal cord. It surrounds the incoming dorsal root fibers and is present throughout the spinal cord, with greater development in the upper cervical regions. Compared to the rest of the white matter, the tract consists of fine myelinated and unmyelinated axons. Many of these axons are branches from the lateral bundles of the dorsal roots, which bifurcate into ascending and descending branches upon entering the spinal cord. These branches travel within Lissauer’s tract for one or two segments and give off collaterals that terminate on and around neurons in the dorsal horn. The tract also contains propriospinal fibers, including short axons of small substantia gelatinosa neurons that re-enter the dorsal horn (Mancall and Brock 2011).

Fig. 3.15  Fasciculi proprii. The fasciculi proprii is the association pathways the ascending and descending fibers that connect different segments within the spinal cord immediately adjacent to the gray matter

29. What is the gray commissure and what is its function? What are the different parts of the gray matter and what are their functions? The central gray matter is made up of symmetrical crescent-shaped masses that are connected by a tissue bridge, known as the gray commissure, which contains the central canal. The gray commissure is a thin strip of gray matter that crosses the midline, connecting the left and right halves of the gray matter. Crossing fibers that are symmetrical are called commissures, while those that are asymmetrical are called decussations. The gray matter is divided into ventral and dorsal columns or

52

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

horns by an imaginary transverse line through the central canal (Fig. 3.11). The ventral gray columns contain nerve cells and axons that exit the spinal cord in ventral roots to innervate skeletal muscles. The ventral gray column is largest at the cervical and lumbar enlargement, where it contains cells of motor neurons for muscles of the extremities. The dorsal gray columns contain the main receptive zones for afferent impulses from the dorsal roots. The dorsal column is directed posterolaterally and is separated from the posterolateral sulcus by an important thin layer of white matter, the Lissauer’s tract. 30. What is the intermediolateral cell column and what is its function? The third horn is present only in the thoracic and upper lumbar spinal cord, which is the intermediolateral (or lateral) horn containing neurons of the autonomic nervous system. Two prominent cell columns in the intermediate gray are the intermediolateral and intermediomedial cell columns (Fig.  3.16). The intermediolateral cell column in the thoracic and upper lumbar spinal cord, from T1 to L2, receives visceral afferent impulses and contains cell bodies of preganglionic sympathetic, visceral efferent neurons. These axons emerge in the ventral roots (Afifi and Bergman 2005; Clifton et al.

Fig. 3.16  Intermediolateral and intermediomedial cell columns of the intermediate horn in the gray matter of the thoracic spinal cord. (Adapted from Kiernan and Rajakumar (2014))

1976). The corresponding intermediolateral cell column as the sacral parasympathetic nucleus is in S2–S4. 31. What are interneurons, and what is their role in the spinal cord? What are propriospinal neurons, and how do they differ from other interneurons in the spinal cord? The gray matter is mainly composed of nerve cells, neuroglia cells, and blood vessels. It also contains numerous interweaving nerve fibers, including axons with myelin sheaths and many that are unmyelinated. The majority of neurons in the gray matter of the spinal cord and the rest of the central nervous system are interneurons that perform integrative functions. The interneurons are also known as association neurons or intercalated neurons. The interneurons in the spinal cord have short to medium-length axons that either remain in the same segment (intrasegmental interneurons), project into adjacent segments (intersegmental interneurons), or run to the opposite side of the spinal cord (commissural interneurons) (Critchley and Eisen 1997) (Fig.  3.17). Neurons that connect different segments within the spinal cord are also known as propriospinal neurons. The interneurons are intercalated in various reflex loops and intrinsic neuron circuits. They also serve as mediators in relationships between long descending pathways and spinal motor and sensory mechanisms or between peripheral afferent fibers and spinal cord neurons leading to long ascending pathways (Heimer 1983). 32. What is the Rexed laminae, and what are they used for? The Rexed laminae are a system of 10 zones or laminae (I–X) labeled in the gray matter, which were identified in 1952 by Bror Rexed. The laminar maps of the gray matter of the spinal cord were provided for the studies of cytoarchitecture (size, density, and morphology) of neurons based on a fundamental anatomical nomenclature for the spinal cord gray matter of cats by Rexed

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53

Funicular neuron Lissauer’s tract

Commissural neuron

Associa on neuron Interneuron

Fasciculus proprius Motor neuron Fig. 3.17  Intrinsic neurons and various connections. Interneurons are also called intercalated or internuncial neurons. (Adapted from Baehr and Frotscher (2012))

(Afifi and Bergman 2005; Blumenfeld 2010; Rexed 1952, 1954). 33. What is the role of the substantial gelatinous (lamina II) in the gray matter of the spinal cord? Lamina I, also called the marginal zone, is a thin layer of gray matter that covers the substantia gelatinosa, lamina II is the sub-

stantia gelatinosa. The substantia gelatinosa can be regarded as laminae II and III (Heimer 1983). Laminae III to VI are the body of the dorsal horn; lamina VII roughly corresponds to the intermediate gray matter including Clarke’s nucleus, but also includes large extensions into the ventral horn; lamina VIII comprises some of the interneuronal zones of the ventral horn, while lamina IX consists

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54

of the clusters of motor neurons embedded in the ventral horn; lamina X is the zone of gray matter that surrounds the central canal (Afifi and Bergman 2005; Blumenfeld 2010; Rexed 1952, 1954; Vanderah and Gould 2016) (Fig. 3.18). Laminae I to IV are located in the dorsal horn. Rexed lamina I is the tip of the dorsal horn. Each dorsal and intermediate horn contains two anatomically distinct nuclei, the substantia gelatinosa (lamina II) and the nucleus dorsalis (Clarke’s nucleus, lamina VII) (Zeman and Innes 1963). The rest of the gray matter dorsal horn forms the so-called nucleus proprius (laminae III and IV), these are ill-defined nuclei. Lamina II, the substantia gelatinosa, is the part of the spinal gray matter with the highest neuronal density. The substantia gelatinosa present in all segments of the spinal cord is prominent, since it contains few elements stained with dyes for staining myelin sheathes, and many cells are very small (Golgi II). The small cells are interneurons that have a prominent role in modifying the perception of pain. Their axons synapse immediately with larger neurons in the nucleus proprius, which adjoin the nucleus, and lead to axons to the lateral spinothalamic tract (Bican et  al. 2013). Laminae III and IV (together as the nucleus proprius) receive light touch and position

input. Lamina VI receives mechanical input from the skin and joints (Afifi and Bergman 2005; Bican et  al. 2013; Blumenfeld 2010; Rexed 1952, 1954). 34. What is the function of the intermediate zone, and what does it contain? What is the role of the nucleus dorsalis in the gray matter of the spinal cord, and where is it located? The intermediate zone presents in the thoracic and upper lumbar segments. It contains preganglionic autonomic neurons for the sympathetic nervous system that receive input from hypothalamic and brainstem nuclei via the descending central autonomic tract. Lamina VII of the gray matter in the thoracic and upper lumbar segments includes the nucleus containing cells projecting from preganglionic sympathetic fibers and cells of the nucleus dorsalis (Clarke’s nucleus), which form the posterior spinocerebellar tract (Rexed and Brodal 1951). The nucleus dorsalis occupies a medial area near the base of the dorsal horn in the T1 to L2 segments of the spinal cord. Other visceral efferent neurons are located in the S2 to S4 segments of the spinal cord and form a parasympathetic efferent column lateral to the central gray matter and central canal in the intermediate zone of the

Region

Central canal

Dorsal horn

Intermediate zone

Ventral horn Gray maer surrounding the central canal

Fig. 3.18  Rexed’s laminae of the gray matter and their region and nuclei

Nuclei

Laminae

Marginal zone

I

Substana gelanosa

II

Nucleus proprius

III, IV

Neck of dorsal horn

V

Base of dorsal horn

VI

Clarke’s nucleus, intermediolateral nucleus

VII

Commissural nucleus

VIII

Motor nuclei

IX

Grisea centralis

X

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

spinal cord (Afifi and Bergman 2005; Blumenfeld 2010; Vanderah and Gould 2016).

55

sections, lying along the entire length of the spinal cord or part of the segments. Characteristic cell column of the various cell groups are the substantia gelatinosa, nucleus posteromarginalis, nucleus proprius, nucleus dorsalis (Clarke’s column), lateral cervical nucleus, and intermediolateral and intermediomedial nuclei (Afifi and Bergman 2005; Blumenfeld 2010; Heimer 1983). The substantia gelatinosa is in most of the apex of the dorsal horn, where it consisted mainly of small neurons and unmyelinated or small myelinated fibers. The nucleus posteromarginalis consists of a thin layer of cells covering the tip of the dorsal horn. The axons of the large- and medium-sized cells join the spinothalamic tract, which also receives contributions from other cell groups, including the nucleus proprius and the intermediate gray. Neurons of nucleus proprius at the base of the dorsal horn are the source of spinocerebellar tract. The cell column of the nucleus dorsalis is in T1–L2, which form the dorsal

35. How are neurons in the ventral gray column arranged, and what is their innervation pattern? Neurons in the ventral gray column (lamina IX) are somatotopically arranged, with the more medially located neurons innervating the axial and proximal limb muscles, and the more laterally located neurons innervating the distal limb muscles. More anteriorly located neurons innervate extensor muscles, while more lateral neurons innervate flexor muscles (Craw 1928) (Fig. 3.19). 36. What are the characteristic cell groups and their locations within the spinal cord’s gray matter, and how do they contribute to various sensory and motor functions? The gray matter consists of a large number of neurons and their processes. These various cell groups are identified in cross a

b

Fig. 3.19  Somatotopical arrangement of neurons of the ventral gray column. (a) The more medial neurons innervate the axial and proximal limb muscles, and the more lateral neurons innervate the distal limb muscles. More

ventral neurons innervate the extensor muscle and more lateral neurons innervate the flexor muscles. (b) The diagram is showing distribution of the motor neurons in the caudal section of the C8 segment

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spinocerebellar tract. The nuclei of the lateral cervical nucleus are located in C1 and C2 segments. The lateral cervical nucleus is a relay nucleus in one of the ascending tracts for touch and pressure sensitivity. Preganglionic visceral motor neurons of the sympathetic nervous system are located in the intermediate gray of T1–L2. Sacral parasympathetic preganglionic visceral motor neurons are located in the intermediate gray of the S2–S4 (Afifi and Bergman 2005; Vanderah and Gould 2016) (Table 3.2). 37. What is the anatomical organization of the motor neurons in the ventral horns of the spinal cord? The ventral horns of the spinal cord contain large alpha-motor neurons that innervate striated muscle and smaller gamma-motor neurons that innervate muscle spindles. Those of the gamma-motor neurons innervate the intrafusal fibers of muscle spindles, hence they are also referred to as fusimotor neurons. Neurons of the ventral gray column are somatotopically arranged. These cell groups belong to longitu-

dinally arranged cell columns of varying length. One of the medial cell columns, which innervates trunk and neck muscles, is present throughout the spinal cord, while the lateral columns, innervating the muscles of the limbs, are present only in the cervical and lumbar enlargements (Craw 1928; Heimer 1983; Vanderah and Gould 2016). 38. At what week of gestation does the lateral corticospinal tract reach the lumbosacral spinal cord during human embryonic development? During human embryonic development, the pyramidal tract reaches the level of the pyramidal decussation at 13 weeks of gestation. Subsequently, there is a prolonged waiting period before the pyramidal decussation is completed 2 weeks later  (Fig.  3.20). The lateral corticospinal tract reaches the cervical spinal cord between 14 and 16 weeks of gestation and invades the caudal regions of the spinal cord at later stages of development, reaching the low thoracic spinal cord at 17 weeks and the lumbosacral spinal cord at

Table 3.2  Important subdivisions of spinal cord gray matter: their segmental levels and function

Marginal zone

Levels All

Rexed laminae I

Substantia gelatinosa

All

II

Lateral gray column

Nucleus proprius Nucleus proprius Nucleus dorsalis Nucleus dorsalis Clarke’s nucleus Intermediolateral nucleus

All All All All T1–L2 T1–L2

III IV V VI VII VII

S2–S4

VII

Anterior gray column

Intermediolateral nucleus (sacral parasympathetic nucleus) Commissural nucleus Medial motor nuclei

All All

VIII IX

Lateral motor nuclei

C5–T1 and L2–S3

IX

Nucleus Posterior gray column

Main function Modulate nociceptive sensory input Some spinothalamic tract cells Modulate nociceptive sensory input Modulate transmission of pain and temperature information Sensory processing Origin of main secondary sensory afferents to higher centers (e.g., spinothalamic tract) Origin of posterior spinocerebellar tract Origin of preganglionic sympathetic fibers Origin of preganglionic parasympathetic fibers Motor neurons Motor neurons innervating trunk musculature Motor neurons innervating upper and lower limb musculature

Modified from Critchley and Eisen (1997), Kaiser et al. (2019), and Vanderah and Gould (2016)

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Fig. 3.20  Diagram of the lengthening of the human corticospinal tract. The earliest descending corticofugal fibers penetrate the basal ganglia and form the internal capsule between GW 8.5 and GW 9.5. The volume of the corticospinal tract increases greatly between GW 13 and GW 18. At about GW 18, or shortly thereafter, the fibers

of the corticospinal tract that form the pyramids split into two descending components, the larger contralaterally projecting lateral corticospinal tract, and the smaller ipsilateral projecting ventral corticospinal tract. (From Altman and Bayer (2001))

27 weeks (Altman and Bayer 2001; Armand 1982; ten Donkelaar et al. 2004) (Fig. 3.21).

and 3.23). The smaller the size or length of the motor neuron column of a muscle, the less likely it is to be damaged, but the degree of damage can be more serious once injured (Elliott 1942; Sharrard 1955). Sharrard’s study on the victims of poliomyelitis may be useful in predicting the degree of weakness of the lower extremity muscles and the possibility of muscle strength recovery of each muscle over time in incomplete spinal cord injuries or spinal cord diseases. Based on the study, muscle groups with large cell columns such as hip flexors, hip adductors, or quadriceps are more likely to recover than other muscle groups.

39. What is the anatomical characteristic that affects the difference between the degree of motor paralysis and the degree of recovery of motor function of muscles in case of partial damage to a spinal cord segment? How can Sharrard’s study on the victims of poliomyelitis be useful in predicting the degree of weakness of lower extremity muscles in spinal cord injuries or diseases, and which muscle groups are more likely to recover in the event of spinal cord injuries or diseases based on Sharrard’s study? The size of the motor neuron group and length of the motor neuron column in the same or adjacent spinal cord segments affect the difference between the degree of motor paralysis and the degree of recovery of motor function of muscles in the event of partial damage to a spinal cord segment (Figs. 3.22

40. How is the somatotopic organization of the gray matter in the laminae II–III of the cervical spinal cord related to the early symptoms of spinal cord conditions such as syringomyelia? The arrangement of the gray matter dorsal horn in the cervical spinal cord of animals such

58

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Fig. 3.21  The spinal outgrowth of the human corticospinal tract for 14, 19, 26, 29, 31, and 37 gestational weeks. Light reds show the outgrowth of the anterior corticospi-

nal tract and reds show the outgrowth of the lateral corticospinal tract. (From Altman and Bayer (2001))

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59

(mm) 25 22

Qd

Had

23

20

20 16

15

10

22

8

8

TA

TP

14

14

Calf

Bcp

16

15

9

5

0 EHL

Hab

Foot

MH

TFL

HFx

Fig. 3.22  Length of the motor neuron cell column of the muscles in the leg. (Modified from Sharrard (1955))

Fig. 3.23  Approximate location in the transverse plane and longitudinal extent of the anterior horn cell groups innervating muscles, in the lumbosacral segments of the human spinal cord. Note the S1 cluster of triceps surae, hamstrings, and gluteals and the S2–3 cluster of quadri-

ceps, hip flexors, and adductors. Based on clinicopathological studies of poliomyelitis. (From Hsu et al. (2008). This Figure from Hsu et  al. (2008) was modified from Sharrard (1955))

as cats and monkeys has been studied and it has been confirmed that there is a somatotopic organization of the forelimbs (Altman and Bayer 2001; Brown and Fuchs 1975; Nyberg and Blomqvist 1985; Whitsel et al. 1970) (Fig. 3.24). This organization is in the order of palm-fingerhand and dorsum of the forearm from medial to lateral, adjacent to the central canal. This somatotopic arrangement provides an anatomical basis to explain the appearance of paresthesia and pain in the hand and fingers first, which

are common early symptoms of syringomyelia. For example, in case of syrinx formation in the C7 segment (marked with a light red arrow in the C7 segment in Fig.  3.24), paresthesia and pain of the palm and middle finger appear initially, and as syrinx dilatation gradually increases, abnormal sensory symptoms may spread to the hand dorsum and forearm. 41. How does the spinothalamic tract transmit a variety of sensations, including pain,

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3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Fig. 3.24  Somatotopic organization of cutaneous afferents in laminae II–III of the cervical and upper thoracic spinal cord of the cat. Sensory fibers from the dorsal skin, arm, forearm, and hand are arranged in a lateral to medial order. Digit II, III, and IV are represented in a rostral-to-­ caudal order. (Adapted from Altman and Bayer (2001))

temperature, touch, pressure, tickling, itching, sexual sensations, and muscle fatigue? What happens to touch and pressure sensations when the spinothalamic nerve fibers are severed on the one side? How do small or early lesions of the spinal commissures affect pain and temperature sensations versus tactile perception? The axons within the anterior spinothalamic tract are located in the anterior funiculus of the spinal cord, while the axons of the lateral spinothalamic tract reside in both the anterior and lateral funiculi. These two tracts are often collectively called the anterolateral system. The lateral spinothalamic tract serves as the pathway for pain and temperature sensations, as well as transmitting impulses

related to tickling, itching, sexual sensations, and muscle fatigue. The anterior spinothalamic tract is responsible for light touch and pressure sensations. The spinothalamic tract is composed of fibers that cross in the anterior white commissure, which allows for communication between the right and left halves of the spinal cord. In the anterior spinothalamic tract, the axons of the first-order neurons initially branch in a T-shaped pattern. After entering Lissauer’s tract, which is part of the posterior column, these axons descend 1–2 segments and ascend 2–15 segments before entering and synapsing in the dorsal horn of gray matter with the second-order neurons (Baehr and Frotscher 2012). The axons of these second-­ order neurons cross within the anterior white commissure and ascend in the opposite anterior funiculus. Touch and pressure sensations are expressed bilaterally and remain unaffected when the nerve fibers of the spinothalamic system are severed on the one side. Small or early lesions of the spinal commissures, such as in syringomyelia, can eliminate pain and temperature sensations transmitted by the lateral spinothalamic tract, but they do not impair tactile perception transmitted by the anterior spinothalamic tract. This is because pain and temperature sensations are carried more posteriorly compared to touch sensation (Fig. 3.25). Within the lateral spinothalamic tract, the axons of the first-order neurons synapse with the second-order neurons as soon as they enter the gray matter of the spinal cord. Additionally, the axons of these secondorder neurons cross the midline in the anterior white commissure at the same level of the spinal cord and then ascend in the opposite lateral funiculus (Fig. 3.26). 42. To which areas of the cerebral cortex do the fibers of the lateral and anterior spinothalamic tracts project? The fibers within the lateral spinothalamic tract, which transmit pain and temperature sensations, ultimately connect to the second-

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Fig. 3.25  Small or early lesions involving the spinal commissures affect pain and temperature sensations transmitted by the lateral spinothalamic tract, but do not impair

61

tactile perception transmitted by the anterior spinothalamic tract because pain and temperature sensations are carried further posteriorly compared to touch sensation

a

b

Fig. 3.26  Central connections of the anterior spinothalamic tract (a) and the lateral spinothalamic tract (b). (Adapted from Schuenke et al. (2016))

ary somatosensory area (S2), insula, and anterior cingulate gyrus (area 24) within the cerebral cortex. Notably, there is a prominent projection to the primary somatosensory cortex (area 3). In contrast, the anterior spinothalamic tract, responsible for transmitting light touch and pressure sensations, primarily projects to the primary somatosensory cortex (S1) and has a sparse projection to the

secondary somatosensory cortex (Strominger et al. 2012) (Fig. 3.27).

(S2)

43. What are the two major ascending tracts of the dorsal funiculus, and what separates them? What sensations do the dorsal columns convey? The dorsal funiculus comprises two major ascending tracts: the fasciculus gracilis and

62

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

a

b

Fig. 3.27  Final projection of the lateral and anterior spinothalamic tracts. (a) The lateral spinothalamic tract finally projects to the secondary somatosensory area (S2), insula, and interior cingulate gyrus (area 24) of the cere-

bral cortex. (b) The anterior spinothalamic tract projects mainly to the primary somatosensory cortex (S1). (Adapted from Strominger et al. (2012))

the fasciculus cuneatus, collectively known as the dorsal columns. These tracts are separated by a posterior intermediate sulcus (septum) (Fig.  3.11). The dorsal columns are characterized by a high percentage of myelinated fibers that convey proprioceptive, exteroceptive, and vibratory sensations to higher levels in the nervous system.

ties. Consequently, it is absent in the spinal cord below the midthoracic level. The cell bodies of the first neurons for both the fasciculus gracilis and cuneatus are situated in the dorsal root ganglion. Their highly myelinated fibers enable rapid impulse conduction. These fibers travel uncrossed to the dorsal column nuclei (nucleus gracilis and cuneatus) in the posterior aspect of the caudal medulla oblongata. The axons of the second-­order neurons, following the nucleus gracilis and cuneatus cross the midline as internal arcuate fibers, forming the medial lemniscus. This structure ascends through the brainstem to the ventral posterolateral nucleus in the thalamus and the postcentral gyrus of the parietal lobe (Schuenke et  al. 2016; Standring 2016).

44. What is the role of the fasciculus gracilis and the fasciculus cuneatus in the spinal cord? The fasciculus gracilis, which originates at the caudal end of the spinal cord, lies medial to the fasciculus cuneatus in the upper spinal cord. It is responsible for transmitting sensations from the lower half of the body, including the lower thoracic, lumbar, and sacral regions, to the brain. The fasciculus cuneatus, which begins at the midthoracic level, is located more laterally and carries proprioceptive input from the upper extremi-

45. How are the fasciculi within the dorsal funiculus organized somatotopically and topographically?

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

The fasciculi within the dorsal funiculus are organized somatotopically: the lower limb is represented in the fasciculus gracilis, the upper limb in the fasciculus cuneatus, and the trunk in an intermediate position between them. Topographically, sacral fibers are innermost, followed by lumbar, thoracic, and cervical fibers. Furthermore, sensory modality organization exists within the dorsal columns (Standring 2016), with pressure and vibration fibers being most superficial and touch and position fibers located in deeper layers (Fig. 3.28). 46. What is the main function of the spinocerebellar tracts? How is the somatotopic organization of the anterior and posterior spinocerebellar tracts similar? The spinocerebellar tracts, situated in the spinal cord’s lateral funiculus, do not convey information to the cerebral cortex (via the thalamus) like other ascending spinal cord tracts. Instead, they transmit information to the cerebellum, which is not consciously perceived. These tracts provide afferent input for unconscious proprioception, which is crucial for coordinating motor activities like running or cycling. They are the primary source of input for the cerebellum and con-

63

vey feedback information about limb movement and spinal interneuron activity during locomotion. The anterior and posterior spinocerebellar tracts share a similar somatotopic organization, with the fibers of the lower segments being superficial. The posterior spinocerebellar tract carries information from the trunk and lower extremities since Clarke’s column tapers rostrally and does not extend beyond the lowest cervical segment. Proprioceptive and exteroceptive information from the upper extremities travel in primary afferent fibers of the fasciculus cuneatus, which synapse with their corresponding second-order neurons in the medulla’s accessory cuneatus nucleus (Baehr and Frotscher 2012; Mancall and Brock 2011). 47. What is the primary role of the posterior spinocerebellar tract? How does the anterior spinocerebellar tract function differently from the posterior spinocerebellar tract? While both the anterior and posterior spinocerebellar tracts transmit proprioceptive and exteroceptive information, they serve distinct functions. The posterior spinocerebellar tract carries modality-specific and space-specific information for the fine coordination of individual limb muscles. In contrast, the anterior spinocerebellar tract conveys information from large receptive fields encompassing various limb segments, lacks discrimination between different modalities, and is responsible for the coordinated movement and posture of the entire lower extremity (Mancall and Brock 2011). 48. What type of information is primarily conveyed by the ascending fibers of the fasciculus gracilis and cuneatus, and is it different from the spinocerebellar tract? The ascending fibers of the fasciculus gracilis and cuneatus, located in the dorsal funiculus, primarily focus on conscious proprioception (position sense and kinesthesia) and exteroceptive information, including vibration (Fig. 3.29).

Fig. 3.28  Schematic somatotopic organization of the spinal cord levels and sensory modalities in the posterior funiculus

49. What are the locations and pathways of the posterior and anterior spinocerebellar

64

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Fig. 3.29  Position of fibers of different somatosensory modalities including conscious proprioception and unconscious proprioception. (Adapted from Baehr and Frotscher (2012))

tracts, and where do they terminate in the cerebellum? The posterior spinocerebellar tract is situated laterally to the lateral corticospinal tract. Originating from Clarke’s nucleus in lamina VII at levels T1(C8)–L2(L3), this uncrossed tract contains second-order sensory afferents and can be found at the dorsal periphery of the lateral funiculi (Afifi and Bergman 2005; Mai and Paxinos 2011). The tract extends into the brainstem and enters the cerebellar vermis’ rostral and caudal parts via the ipsilateral inferior cerebellar peduncle. In comparison, the smaller and less pronounced anterior spinocerebellar tracts are located at the lateral funiculi’s periphery, immediately anterior to the posterior spinocerebellar tract. These tracts’ cells of origin are found in laminae V to VII of the lumbosacral cord. The anterior spinocerebellar tract ascends both ipsilaterally and contralaterally, primarily terminating contralaterally in the anterior cerebellar vermis (Mancall and Brock 2011).

50. How are the descending tracts divided based on their location in white matter? The primary descending tracts include the corticospinal tract, rubrospinal tract, reticulospinal tracts, and vestibulospinal tracts (Fig. 3.30). These tracts are classified into lateral and medial (or anteromedial) motor systems based on their location in the white matter. The lateral motor system comprises the lateral corticospinal tract and rubrospinal tract, descending in the posterior portion of the lateral white matter funiculus. The anteromedial motor system consists of the anterior corticospinal tract, vestibulospinal tract, medial (pontine) reticulospinal tract, and tectospinal tract. Lateral system fibers mainly terminate in laterally placed interneurons in the intermediate gray matter, associated with the posterolateral part of the anterior horn and motor neurons that innervate limb muscles essential for skilled movements. In contrast, the anteromedial system is closely related to medially placed interneurons and motor neurons, which control both limb and axial mus-

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65

Fig. 3.30  Major descending motor tracts and schematic diagram of upper motor neuron and lower motor neuron system

cles crucial for postural activity and gross movement (Heimer 1983) (Fig. 3.31). 51. What are the functions of the lateral corticospinal tract and the anterior corticospinal tract? Additionally, could you explain the differences between the pyramidal tract and the extrapyramidal tract? Descending tracts can be categorized into pyramidal tracts (lateral and anterior corticospinal tracts and corticobulbar tract), extrapyramidal tracts, and the central autonomic tract (Fig.  3.32). The corticospinal tract is

often referred to as the pyramidal tract because its fibers pass through the medulla oblongata’s anterior part in an area called the pyramids (Snell 2010; Strominger et  al. 2012). This term typically includes not only corticospinal fibers but also corticobulbar fibers that diverge above this level and terminate in association with cranial motor nuclei (Mancall and Brock 2011). The term extrapyramidal tracts refer to all other descending tracts that do not pass through the pyramid. While the term extrapyramidal is imprecise, it is still commonly used.

66

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Anterior corcospinal trac

Lateral corcospinal tract Olivospinal tract Rubrospinal tract Vesbulospinal tract

Reculospinal tract Tectospinal tract Descending somatosensory fiber

Annulospiral fiber (Ia)

Semilunar fasciculus

Golgi fiber (Ib)

1

fiber

fiber

Fig. 3.31  Synapses of the descending tracts on motor neurons in the anterior horn. The fibers in the lateral system synapse with the posterolaterally located motor neu-

rons in the anterior horn, and the anteromedial system is more closely related to medially placed motor neurons. (Adapted from Baehr and Frotscher (2012))

Fig. 3.32  Hierarchical classification of the descending tracts of the white matter of the spinal cord according to their primary function. (From Steinmetz et al. (2022), with permission)

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

The corticospinal tract is the largest and most crucial descending tract of the human spinal cord due to its importance in voluntary motor control. Occupying neurons in the medullary pyramids’ parts, the corticospinal tracts form the spinal components of the pyramidal system (Coppola 1973; Dumitru and Lang 1986). Approximately 40% of the ­corticospinal tract fibers are formed in the primary motor cortex of the frontal lobes (in the precentral gyrus, Brodmann area 4), with the remainder occurring in other cortical regions of the frontal and parietal lobes. About 85–90% of the corticospinal tract fibers decussate at the medulla oblongata’s lower end, while the rest pass uncrossed into the spinal cord (Armand 1982). Of the 20% uncrossed fibers, 5% join the lateral corticospinal tract, and the remaining 15% form the uncrossed anterior corticospinal tract in the anterior funiculus of white matter. The decussating fibers form the lateral corticospinal tracts, occupying lateral funiculi between the fasciculi proprius and the posterior spinocerebellar tracts. Over half of the axons of the lateral corticospinal tracts terminate in the cervical and upper thoracic spinal cord, and only one-fourth reach the lumbosacral segments (Armand 1982). The lateral corticospinal tract controls voluntary movements on the opposite side. Some fibers synapse directly with motor neurons supplying distal limb muscles and mediate skilled movements (Critchley and Eisen 1997; Lawrence and Kuypers 1968). The anterior corticospinal tract fibers terminate at motor neurons or interneurons in the medial portions of the anterior horn or intermediate gray matter, primarily influencing the activity of motor neurons for axial muscles. Many of them cross in the anterior white commissure before synapsing, but others do not. Most of the anterior corticospinal tract fibers terminate in the cervical and thoracic segments, possibly playing a unique role in controlling the neck and shoulder muscles. Damage to this tract typically does not result in apparent weakness, possibly due to the bilateral distribution of fibers from the con-

67

tralateral tract (Vanderah and Gould 2016). The corticospinal tract is also organized somatotopically, with cervical fibers in the corticospinal tract being most medial and sacral fibers most lateral (Armand 1982; Moore and Dalley 1999). 52. What are the four recognized tracts of the extrapyramidal system, and what are their functions? Numerous brainstem nuclei send axons into the spinal cord, forming components of the extrapyramidal system, which preceded the pyramidal tracts in development. The main sources of the spinal portions of this system are vestibular nuclei, red nuclei, superior colliculi, and the brainstem reticular formation. There are four recognized tracts of this system on both sides of the human spinal cord: tectospinal, vestibulospinal, reticulospinal, and rubrospinal tracts. The tectospinal tract, originating from the midbrain, is involved in coordinating head and eye movement. The vestibulospinal tract arises from the lateral and medial vestibular nuclei and participates in head and neck position and balance. The reticulospinal tract, arising from the brainstem reticular formation, plays a role in automatic posture and walking-related movements by modulating spinal reflexes. The rubrospinal tract, which arises from the red nucleus in the midbrain, decussates within the brainstem and is thought to affect muscle tone in distal extremities. 53. How are descending tracts involved in maintaining posture and voluntary motor function, and how do they reinforce movement tone in a specific direction? Can you explain the classification of flexor-biased and extensor-biased tracts and the regional differences in white matter associated with these tracts? The descending tracts in the lateral funiculus are categorized as flexor-biased tracts, which strengthen flexor tone, and include the lateral corticospinal tract, rubrospinal tract, and medullary reticulospinal tract. On the

68

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

other hand, the pontine reticulospinal tract and the lateral and medial vestibulospinal tracts, located in the anteromedial funiculus, are classified as extensor-biased tracts (Kingsley 1999) (Fig. 3.33). 54. What are the origins of the arterial supply of the spinal cord? How do the anterior and posterior spinal arteries form and supply the spinal cord? The arterial supply of the spinal cord originates from the vertebral arteries and radicular arteries, which are branches of the thoracic and abdominal aorta. The vertebral artery arises from the subclavian artery, the innominate artery, or directly from the aorta (Williams et al. 2017). Each vertebral artery gives rise to an anterior spinal artery, which merge to form a single midline vessel running along the anterior median fissure of the spinal cord. Vertebral or posterior inferior cerebellar arteries on each side also give rise to poste-

rior spinal arteries that run along the line of attachment of the dorsal rootlets, bilaterally (Vanderah and Gould 2016). The anterior spinal artery, located anteriorly, and the two posterior spinal arteries, located posteriorly, supply the spinal cord directly (Fig.  3.34). Throughout the length of the vertebrae, these vessels receive input from the subclavian artery via the vertebral artery, the thyrocervical trunk, and the costocervical trunk (Thron 2016) (Fig. 3.35). During embryonic development, the anterior spinal artery is derived from 31 bilateral segmental arteries. By the end of the fourth month of gestation, most segmental arteries regress and become obliterated (Fig. 3.36). Only a few of these arteries (2–14, mean 6) persist in adults, with an average of 2–3 at the cervical level, 2–3 at the thoracic level, and 0–1 at the lumbosacral level (Melissano et al. 2015, 2010). 55. What are the radicular and medullary feeder arteries, and how do they feed the

Fig. 3.33  The principal descending motor pathways in the spinal cord. Flexor-biased tracts lie in the lateral funiculus of white columns and extensor-biased tracts lie in the anteromedial funiculus. (Adapted from Kingsley (1999))

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

a

69

b

Fig. 3.34 (a) The spinal cord is covered by a net-like anastomosing vascular system in which the anterior spinal artery and the two posterior spinal arteries. The pial network and intramedullary anastomoses may only be important for slower circulatory adjustments since their calibers are inadequate for a sudden intake of larger volumes of blood. (b) The intrinsic arterial system of the spinal cord

is divided into a central (centrifugal) system and a peripheral (centripetal) system. The central system is represented by the sulcal arteries, which approach from the anterior arterial tract, pass into the anterior median fissures. The peripheral system consists of numerous small arteries “rami perforantes.” (From Melissano et al. (2015) with permission)

spinal nerve roots and traverse the intervertebral foramina with the spinal nerves? What is the significance of the radicular artery of Adamkiewicz, and what is the relationship between the artery of Adamkiewicz and the anterior spinal artery? Radicular branches of segmental arteries approach the spinal column, running along with the ventral nerve roots through the intervertebral foramina (Fig.  3.37). More radicular branches feed the cervical and lumbar enlargements, while fewer supply the thoracic cord due to its reduced metabolic requirement and less gray matter. The anterior spinal artery may be discontinuous in these regions. Medullary feeder arteries arise from the segmental arteries of the vertebral column and traverse the intervertebral foramen with the spinal nerves. Radicular arteries, which feed the spinal nerve roots, develop along with medullary feeder arteries from the seg-

mental arteries and the longitudinal arterial trunks (Windle 1980). Dorsal medullary feeder arteries are more numerous but smaller than ventral feeder arteries, which vary in number and location. Medullary feeder arteries in the thoracic region are smaller and fewer than those at higher and lower levels of the spinal cord. This low arterial supply to the upper and midthoracic levels represents a watershed area susceptible to systemic hypotension or occlusion of a single vessel (Fig. 3.38). The relatively midthoracic region (T4–8) watershed area is between the rostral region, where the anterior spinal artery is more robust, and the caudal region, where blood supply is supplemented by the relatively large radicular artery of Adamkiewicz. From the lower thoracic to upper lumbar regions, the larger radicular artery of Adamkiewicz supplies the anterior spinal artery. It originates in the abdominal aorta at T9, traverses the intervertebral foramen, and finally anastomoses with

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

70 Fig. 3.35  Main source of arterial supply to the anterior spinal artery. (From Thron (2016))

the anterior spinal artery (Nijenhuis et  al. 2006). The Adamkiewicz artery is more often located on the left side than the right and can be found anywhere between the T7 and L4 segments of the spinal cord (Murthy

et al. 2010). It accompanies the left T10 ventral root in 30% of patients, and the rest are accompanied by any root from T9 to L1 (Hughes 1989). The artery of Adamkiewicz is generally oriented cranially.

3  Neuroanatomical Overview to Understand the Complexities of Spinal Cord Function

Fig. 3.36  Embryonic development (GW 16) of the anterior spinal artery from 31 bilateral segmental feeders. In the adult, most of the segmental feeders of anterior spinal

71

artery regress. Only a few (2–4, mean 6) of these feeders are left in the adult.). (From Melissano et al. (2015) with permission)

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Fig. 3.37  Schematic drawing of the great radicular artery or arteria radicularis magna (Adamkiewicz artery). The nervo-medullary artery divides into an anterior and posterior radicular artery. The division of the Adamkiewicz artery has a steep cranially directed course (A), branching takes place lateral to the midline (B), a small ascending branch (C) is issued before reaching the midline, the main artery continues its vertical course, and then bends sharply in a typical hairpin curve (D) into the larger descending branch (E). (From Melissano et  al. (2015) with permission)

The anterior spinal artery supplies most of the ventral two-thirds of the spinal cord, including the nucleus dorsalis (Clarke’s) and the corticospinal tracts. The posterior onethird of the spinal cord, comprising the posterior funiculi and dorsal gray matter, receives blood from pia-penetrating arteriolar branches of the dorsolateral longitudinal arterial trunks (posterior spinal artery). The arteries entering the spinal cord have no anastomoses, except at the conus medullaris, and are considered end arteries. At the level of the conus medullaris, an anastomotic ring containing segmental branches of lumbar and iliolumbar arteries connects the anterior and posterior arterial systems. Within the gray and white matter of the spinal cord, a complex capillary network is formed, with the gray matter being more intricate (Scharrer 1945). Some regions also contain more capillaries than others; for example, the corticospinal tract has about twice as many capillaries as the fasciculus cuneatus (Zeman and Innes 1963).

Fig. 3.38  The sources of arterial blood to the anterior surface of the spinal cord. The shaded upper cervical, upper thoracic, and upper lumbar spinal cord segments are zones located between two regions that draw their blood supply from different major arteries. (Adapted from Strominger et al. (2012))

References Afifi AK, Bergman RA.  Functional neuroanatomy: text and atlas. 2nd ed. New York: Lange Medical Books/ McGraw-Hill; 2005. Altman J, Bayer SA.  Development of the human spinal cord: an interpretation based on experimental studies. 1st ed. New York: Oxford University Press; 2001. Anthoney TR.  Neuroanatomy and the neurologic exam: a thesaurus of synonyms, similar-sounding non-­ synonyms, and terms of variable meaning. Boca Raton: CRC Press; 1994. Armand J.  The origin, course and termination of corticospinal fibers in various mammals. Prog Brain Res. 1982;57:329–60.

References Baehr M, Frotscher M. Duus’ topical diagnosis in neurology. Anatomy, physiology, signs, symptoms. 5th ed. New York: Thieme; 2012. Barson AJ. The vertebral level of termination of the spinal cord during normal and abnormal development. J Anat. 1970;106:489–97. Bayer SA, Altman J. Atlas of human central nervous system development series. The spinal cord from gestational week 4 to the 4th postnatal month. New York: CRC Press; 2002. Bican O, Minagar A, Pruitt AA.  The spinal cord: a review of functional neuroanatomy. Neurol Clin. 2013;31:1–18. Blumenfeld H. Neuroanatomy through clinical cases. 2nd ed. Sunderland: Sinauer Associates; 2010. Bonica JJ, Loeser JD.  Applied anatomy relevant to pain. In: Loeser JD, Butler SH, Chapman CR, Turk DC, editors. Bonica’s management of pain. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001. Breig A, el-Nadi AF. Biomechanics of the cervical spinal cord. Relief of contact pressure on and overstretching of the spinal cord. Acta Radiol Diagn (Stockh). 1966;4:602–24. Breig A, Turnbull I, Hassler O.  Effects of mechanical stresses on the spinal cord in cervical spondylosis. A study on fresh cadaver material. J Neurosurg. 1966;25:45–56. Brown PB, Fuchs JL.  Somatotopic representation of hindlimb skin in cat dorsal horn. J Neurophysiol. 1975;38:1–9. Clifton GL, Coggeshall RE, Vance WH, et al. Receptive fields of unmyelinated ventral root afferent fibres in the cat. J Physiol. 1976;256:573–600. Coggeshall RE, Applebaum ML, Fazen M, et  al. Unmyelinated axons in human ventral roots, a possible explanation for the failure of dorsal rhizotomy to relieve pain. Brain. 1975;98:157–66. Coppola AR. “Cruciate paralysis”: a complication of surgery. South Med J. 1973;66:684. Craw CH.  The distribution of the nerve cells in the ventral columns of the spinal cord. J Comp Neurol. 1928;45:283–99. Critchley E, Eisen A, editors. Spinal cord disease. Basic science, diagnosis and management. London: Springer; 1997. De Vloo P, Monea AG, Sciot R, et  al. The filum terminale: a cadaver study of anatomy, histology, and elastic properties. World Neurosurg. 2016;90:565–73. Dumitru D, Lang JE.  Cruciate paralysis. Case report. J Neurosurg. 1986;65:108–10. Elliott HC. Studies on the motor cells of the spinal cord, I. Distribution in the normal human cord. Am J Anat. 1942;70:95–117. Haymaker W, Woodhall B.  Peripheral nerve injuries: principles of diagnosis. 2nd ed. Philadelphia: W B Saunders Co; 1953. Heimer L. The human brain and spinal cord. Functional neuroanatomy and dissection guide. New  York: Springer; 1983.

73 Holmes A, Han ZH, Dang GT, et al. Changes in cervical canal spinal volume during in vitro flexion-extension. Spine (Phila Pa 1976). 1996;21:1313–9. Hsu JD, Michael JW, Fisk JR. AAOS atlas of orthoses and assistive devices. 4th ed. Philadelphia: Mosby; 2008. Hughes JT. In: Vinken PJ, Bruyn GW, Klawans HL, editors. Vascular diseases, Part III.  London: Elsevier; 1989. Kahle W. Color atlas of human anatomy, Nervous system and sensory organs, vol. 3. 7th ed. New York: Thieme; 2015. Kaiser MG, Haid RW, Shaffrey CI, et  al., editors. Degenerative cervical myelopathy and radiculopathy. Treatment approaches and options. Cham: Springer; 2019. Kameyama T, Hashizume Y, Sobue G.  Morphologic features of the normal human cadaveric spinal cord. Spine (Phila Pa 1976). 1996;21:1285–90. Keegan JJ, Garrett FD.  The segmental distribution of the cutaneous nerves in the limbs of man. Anat Rec. 1948;102:409–37. Kellgren JH. On the distribution of pain arising from deep somatic structures with charts of segmental pain areas. Clin Sci. 1939;4:35–46. Kiernan JA, Rajakumar N. Barr’s the human nervous system. An anatomical viewpoint. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2014. Kingsley RE.  Concise text of neuroscience. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Ko HY, Park JH, Shin YB, et al. Gross quantitative measurements of spinal cord segments in human. Spinal Cord. 2004;42:35–40. Lawrence DG, Kuypers HG. The functional organization of the motor system in the monkey. I. The effects of bilateral pyramidal lesions. Brain. 1968;91:1–14. Lee MW, McPhee RW, Stringer MD.  An evidence-­ based approach to human dermatomes. Clin Anat. 2008;21:363–73. Mai JK, Paxinos G, editors. The human nervous system. 3rd ed. London: Elsevier; 2011. Mancall E, Brock DG, editors. Gray’s clinical neuroanatomy: the anatomic basis for clinical neuroscience. Philadelphia: Elsevier; 2011. Melissano G, Civilini E, Bertoglio L, et  al. Angio-CT imaging of the spinal cord vascularisation: a pictorial essay. Eur J Vasc Endovasc Surg. 2010;39:436–40. Melissano G, Bertoglio L, Rinaldi E, et al. An anatomical review of spinal cord blood supply. J Cardiovasc Surg. 2015;56:699–706. Moore KL, Dalley AF.  Clinically oriented anatomy. 4th ed. Philadelphia: Lippincott Williams and Wilkins; 1999. Murthy NS, Maus TP, Behrns C. Intraforaminal location of the great anterior radiculomedullary artery (artery of Adamkiewicz): a retrospective review. Pain Med. 2010;11:1756–64. Nijenhuis RJ, Mull M, Wilmink JT, et  al. MR angiography of the great anterior radiculomedullary artery (Adamkiewicz artery) validated by digital

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subtraction angiography. AJNR Am J Neuroradiol. 2006;27:1565–72. Nix WA. Muscles, nerves, and pain. A guide to diagnosis, pain concepts and therapy. 2nd ed. Berlin: Springer; 2017. Nolte J, Angevine JB.  The human brain in photography and diagrams. 4th ed. Philadelphia: Elsevier; 2013. Nyberg G, Blomqvist A.  The somatotopic organization of forelimb cutaneous nerves in the brachial dorsal horn: an anatomical study in the cat. J Comp Neurol. 1985;242:28–39. Patestas MA, Gartner LP.  A textbook of neuroanatomy. Oxford: Blackwell Publishing; 2006. Rexed B. The cytoarchitectonic organization of the spinal cord in the cat. J Comp Neurol. 1952;96:414–95. Rexed B. A cytoarchitectonic atlas of the spinal cord in the cat. J Comp Neurol. 1954;100:297–379. Rexed B, Brodal A.  The nucleus cervicalis lateralis: a spinocerebellar relay nucleus. J Neurophysiol. 1951;14:399–407. Scharrer E. Capillaries and mitochondria in neutrophil. J Comp Neurol. 1945;83:237–43. Schuenke M, Schulte E, Schumacher U.  Thieme atlas of anatomy. Head, neck, and neuroanatomy. 2nd ed. New York: Thieme; 2016. Sharrard WJW.  The distribution of the permanent paralysis in the lower limb in poliomyelitis: a clinical and pathological study. J Bone Joint Surg. 1955;37:540–58. Snell RS.  Clinical neuroanatomy. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2010. Standring S, editor. Gray’s anatomy: the anatomical basis of clinical practice. 41st ed. London: Elsevier; 2016. Steinmetz MP, Berven SH, Benzel EC. Benzel’s spine surgery. 5th ed. Philadelphia: Elsevier; 2022.

Strominger NL, Demarest RJ, Laemle LB.  Noback’s human nervous system. Structure and function. 7th ed. New York: Springer; 2012. ten Donkelaar HJ, Lammens M, Wesseling P, et  al. Development and malformations of the human pyramidal tract. J Neurol. 2004;251:1429–42. ten Donkelaar HJ, Yamada S, Shiota K, et al. Overview of the development of the human brain and spinal cord. In: ten Donkelarr HJ, Lammens M, Hori A, editors. Clinical neuroembryology. Development and developmental disorders of the human central nervous system. 2nd ed. Heidelberg: Springer; 2014. Thron AK. Vascular anatomy of the spinal cord. 2nd ed. Cham: Springer; 2016. Toribatake Y, Baba H, Kawahara N, et  al. The epiconus syndrome presenting with radicular-type neurological features. Spinal Cord. 1997;35:163–70. Vanderah TW, Gould DJ.  Nolte’s the human brain. Introduction to its functional anatomy. 7th ed. Philadelphia: Elsevier; 2016. Waxman SG. Clinical neuroanatomy. 26th ed. New York: The McGraw-Hill Companies; 2010. Whitsel BL, Petrucelli LM, Sapiro G, et  al. Fiber sorting in the fasciculus gracilis of squirrel monkeys. Exp Neurol. 1970;29:227–42. Williams KA, Rauschning W, Prasad S. Applied anatomy of the cervical spine. In: Steinmetz MP, Benzel EC, editors. Benzel’s spine surgery. 4th ed. Philadelphia: Elsevier; 2017. Windle WF. The spinal cord and its reaction to traumatic injury. In: Bousquet WF, Palmer RF, editors. Modern pharmacology-toxicology: a series of monographs and textbooks. New York: Marcel Dekker, Inc.; 1980. Zeman W, Innes JRM. Craigie’s neuroanatomy of the rat. New York: Academic; 1963.

4

Assessing and Predicting Function After Spinal Cord Injuries

Abstract

The chapter provides an overview of neurological recovery after spinal cord injury and highlights the various factors that can influence long-term outcomes. The injury’s neurological level and severity are the primary determinants of outcomes, but other factors such as age, gender, pre-injury health status, and coexisting conditions can also impact rehabilitation. The chapter also discusses the four domains of outcomes that are relevant for spinal cord injury rehabilitation: motor recovery, functional independence, social integration, and quality of life. These outcomes are measured using various assessment tools, and the chapter provides an overview of the most commonly used assessments in each domain. The International Classification of Functioning, Disability and Health (ICF) is introduced as a comprehensive framework for discussing functional outcomes after spinal cord injury. The ICF encompasses impairments of body functions, body structures, activity limitations, participation restrictions, and environmental factors, providing a holistic view of the individual’s functioning and the impact of the injury on their life. Overall, the chapter provides a comprehensive overview of assessing and predicting function after spinal cord injuries and highlights the key factors that can influence outcomes. It also introduces useful frameworks and assessment

tools that can help clinicians to provide optimal care for individuals with spinal cord injuries. 1. What is the International Classification of Functioning, Disability and Health (ICF), and how does it serve as a conceptual framework for discussing functional outcomes, functioning, disability, and health in people with spinal cord injuries? How does the ICF differ from the previous classification, ICIDH? Spinal cord injuries often lead to various physical and emotional challenges, such as motor paralysis, which can affect an individual’s ability to carry out vocational, avocational, and self-care activities. This can result in biopsychosocial consequences, including reduced independence, and impaired sexual, bladder, and bowel function. Although the degree of functional loss depends on the neurological level and severity of the spinal cord injury, individual variations in functional recovery exist. There was a need for a comprehensive conceptual framework to better understand the various situations and changes resulting from spinal cord injuries. The World Health Organization (WHO) published the International Classification of Functioning, Disability and Health (ICF) in 2001, providing a standard language and framework for describing health and health-­ related conditions. ICF has become a univer-

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 H.-Y. Ko, A Practical Guide to Care of Spinal Cord Injuries, https://doi.org/10.1007/978-981-99-4542-9_4

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76

sally accepted conceptual framework for discussing functional outcomes and classifying and describing functioning, disability, and health in individuals with spinal cord injuries (Post et  al. 2010). This framework replaced the 1980 classification, ICIDH (International Classification of Impairments, Disabilities, and Handicap), which contained negative connotations. The ICF shifted the focus from disability to health and functioning. It is based on a biopsychosocial model, which considers the interaction between an individual’s health conditions and personal or environmental factors. Although the ICF introduced several improvements, some areas, particularly within the activity domain, still require clarification (Ditunno 2010; Marino 2007). The ICF is a multipurpose classification intended for a wide range of applications across various sectors. It classifies health and health-related domains, helping to describe changes in body function and structure, and the individual’s capacity and performance in a standard and their usual environment, respectively. In the ICF, “functioning” encompasses all body functions, activities, and participation, while “disability” serves as an umbrella term for impairments, activity limitations, and participation restrictions. Additionally, the ICF includes environmental factors that interact with all these components (Fig. 4.1). 2. What are the components and domains of the International Classification of Functioning, Disability and Health (ICF), and how are they classified in terms of functioning and disability, as well as contextual factors? Fig. 4.1 International Classification of Functioning, Disability, and Health Model of Functioning. The bidirectional arrows indicate the interactions between these components. (Adapted from WHO (2001))



The ICF consists of two parts, each with two components as described below. Each component can be expressed in both positive and negative terms and consists of various domains and within each domain categories that represent the classification units. • Part 1. Functioning and disability (a) Body functions and structures (b) Activities and participation • Part 2. Contextual factors (c) Environmental factors (d) Personal factors Body functions are the physiological functions of body system, including psychosocial functions. Body structure refers to the anatomical parts of the body such as organs, limbs and their components. Impairments are problems with body function or structure in the form of significant deviation or loss. Activity and participation refer to a person’s execution of a task or action and involvement in a life situation, respectively. According to the definition of the terms, activity limitations are difficulties a person may have in performing activities and participation restrictions are problems a person may experience in involvement in a life situation. Environmental factors constitute the physical, social, and attitudinal environment in which people live and conduct their lives (WHO 2001). Table 4.1 provides an overview of these concepts.

3. When is the earliest time for reliable neurological assessment and prediction of neurological recovery after a spinal cord injury? What factors can make the initial neurological examination in the emergency department difficult? What factors may Health condion

Part 1

Part 2

Body funcon & structure (impairment)

Environmental factors

Acvies (limitaon)

Parcipaon (restricon)

Personal factors

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4  Assessing and Predicting Function After Spinal Cord Injuries Table 4.1  An overviews of International Classification of Functioning, and Health (ICF) components Components Domains

Constructs

Positive aspect

Negative aspect

Part 1: Functioning and disability Body functions and Activity and participation structures •  Body functions • Life areas (tasks, •  Body structures actions) • Changes in body functions (physiological) • Changes in body structures (anatomical) • Functional and structural integrity Functioning • Impairment

Part 2: Contextual factors Environmental factors Personal factors

• Capacity   Executing tasks in a standard environment • Performance   Executing tasks on the current environment • Activities • Participation

•  Activity limitation •  Participation restriction

External influences on functioning and disability Facilitating or hindering impact of features of the physical, social, and attitudinal world

Internal influences on functioning and disability Impact of attributes of the person

Facilitators

Not applicable

Barriers/hindrances

Not applicable

Disability Adapted from WHO (2001)

influence the neurological status in the first few hours or days after a spinal cord injury? The window from 72 h to 1 week following a spinal cord injury is considered the earliest timeframe for conducting a reliable neurological assessment and making predictions regarding neurological recovery to a certain extent (Alexander et  al. 2009; Herbison et al. 1992). Performing an initial neurological examination in the emergency department can be challenging due to the possibility of the patient having sustained additional injuries or being under the influence of drugs or alcohol. Furthermore, the patient’s neurological status may fluctuate within the first few hours or days and can be affected by various factors, such as unstable vital signs, pain, anxiety, and sedation. 4. What factors other than motor function can affect functional outcomes after spinal cord injuries? While motor function is the primary factor influencing overall functional outcomes after spinal cord injuries, other elements such as age, pain, spasticity, comorbidities, habits, and environmental and psychosocial factors also play significant roles in determining functional outcomes (AlHuthaifi

et  al. 2017; Behrman and Harkema 2007). Motor function recovery can occur up to 2 years or more following a spinal cord injury (Ditunno Jr et  al. 1992; Kirshblum et  al. 2004). However, the recovery rate is fastest during the first 2 months and slows down after 3–6 months. Half to two-thirds of the motor recovery within the first year occurs in the initial 2 months after the injury. 5. What is the recovery rate and prognosis like for patients with incomplete vs. complete injuries? What is the prognosis of individual muscle recovery for muscles with grade 0 strength 1 month after injury compared to those with some strength? Recovery rates and prognosis are better for patients with incomplete injuries compared to those with complete injuries. While 10–20% of patients with complete injury (AIS A) recover to an incomplete injury within 1 year, only 3–6% regain functional muscle strength in their legs (Maynard et  al. 1979). In most patients with complete ­ tetraplegia, muscle strength improves in the 2–3 spinal cord segments below the neurological level of injury in the upper extremity. Muscles with at least grade 1 or 2 muscle strength are more likely to recover than those with no muscle strength. If

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the muscles in the segment just below the injury level have grade 1 or 2 muscle strength, 90% are expected to recover above grade 3 within 1 year after injury. However, if there is no muscle strength in the segment just below the injury level, the probability of recovering to grade 3 or higher within 1 year drops to 45%, and within 2 years, it is 64% (Waters et  al. 1998). Regardless of the neurological level of injury, the prognosis of individual muscle recovery for muscles with grade 0 strength 1 month after injury is poor, with only 5% recovering to grade 3 or greater strength within a year. In contrast, the prognosis for muscles with some strength at 1 month is good, with a 64% chance of achieving functional strength within a year (Waters et  al. 1998). 6. Why is it challenging to distinguish between neurological recovery resulting from spinal nerve root or spinal cord recovery? How can regular assessment of neurological status help in the management of spinal cord injury patients? Distinguishing between neurological recovery resulting from spinal nerve root or spinal cord recovery, or both, can be clinically challenging or impossible. The anatomic propensity for recovery increases in the order of roots, gray matter, and then white matter. This hierarchy likely stems from a combination of increasing vulnerability to injury and decreasing ability of these structures to recover. Additionally, motor roots and descending tracts have higher vulnerability to injury and lower propensity for recovery compared to sensory roots and ascending tracts (Tator 1998). Spinal cord tethering or syringomyelia can also cause neurological deterioration. Therefore, regular assessment of neurological status can help with early detection and appropriate intervention. Moreover, maximum spinal cord compression, spinal cord hemorrhage, and spinal cord swelling in MRI findings of an acute traumatic cervical spinal cord injury are associated with a poor prognosis for neurologic recovery (Miyanji et  al. 2007). The

vertical diameter of the T2 high-intensity area on MRI after spinal cord injury has been reported as a better predictive finding for neurological outcomes (Farhadi et al. 2018; Matsushita et al. 2017). A study has shown that the Brain and Spinal Injury Center (BASIC) Score, based on the extent of axial T2-weighted MR images, is the best predictor of both neurological severity and the conversion of ASIA Impairment Score (AIS) (Farhadi et al. 2018). 7. How does upper extremity function impact a person’s autonomy and quality of life? What are compensatory strategies that can help individuals with spinal cord injuries function in daily life? Upper extremity function plays a crucial role in a person’s autonomy in daily activities and quality of life (Boakye et al. 2012; Rudhe and van Hedel 2009). While the ability to grasp and manipulate objects primarily depends on neurological impairment determined by the injury’s neurological level, compensatory strategies such as learning passive tenodesis grasp during rehabilitation or improving active tenodesis grasp through surgical reconstruction of the hand are essential for an individual’s functioning in everyday life (Mateo et al. 2015). 8. How is autonomy achieved after tetraplegia, and what is the role of tenodesis in spinal cord injuries? How can surgical tendon transfer enhance autonomy in tetraplegia? Autonomy following tetraplegia relies on upper extremity movements, achieved by relearning open-chain movements like grasping and learning new closed-chain movements such as manual wheelchair propulsion or sitting pivot transfer (Koontz et al. 2011). A C5 spinal cord injury maintains innervation of the shoulder and elbow flexors; C6 injuries retain control of elbow flexors and wrist extensors, while C7 injuries also preserve elbow extensors. Consequently, C5 and C6 injuries functionally impair active elbow extension against gravity, and C5 to C7 inju-

4  Assessing and Predicting Function After Spinal Cord Injuries

9. What is a community ambulator? What is the recovery rate for AIS A patients regaining ambulatory ability? What factors influence the recovery of ambulation in patients with spinal cord injuries? How does age affect the prognosis for functional recovery in spinal cord injury patients? A community ambulator refers to an individual who can walk more than 40 m (130 ft), sit unassisted, stand unassisted, and independently put on and take off orthoses. At the initial assessment, 3% of patients with an ASIA Impairment Scale (AIS) A diagnosis regained ambulatory ability within a year of their injury. However, the majority of individuals with incomplete motor injuries at the initial examination recover the ability to walk. In particular, 50% of patients with AIS B regain ambulatory ability, especially if they have a pinprick sensation in the lower sacral segments, making it highly probable that they will recover to AIS C or D (Hussey and Stauffer 1973). If the pinprick sensation in the lower sacral segments is absent, the probability of regaining the ability to walk ranges from 10% to 33%. Additionally, 75% of individuals with AIS C become community ambulators, while 95% of those initially

diagnosed with AIS D regain the ability to walk. Factors such as age and the extent of preserved spinal cord function below the lesion influence the recovery of ambulation. The more function preserved, the better the prognosis for regaining the ability to walk. However, patients aged 50–60 years or older generally have a poor prognosis for functional recovery (Burns et  al. 1997; Daverat et al. 1988; Waters et al. 1994) (Fig. 4.2). 10. What is the gold standard for assessing body functions and structures in people with spinal cord injuries? What are the commonly used tools for assessing the activities of people with spinal cord injuries? What are the key functional assessment measures for upper extremity function in spinal cord injuries? Which tests are considered the most valid and clinically useful primary outcome measures for gait and ambulation in incomplete spinal cord injury? The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) is the gold standard for assessing body functions and structures in people with spinal cord injuries. First published by ASIA in 1982, the eighth edition is now available. The most commonly used elements of ISNCSCI for determining neurological and functional outcomes include 100

95

90

% ambulatory

ries lack active grasping. Fortunately, since wrist extension is preserved in injuries at C6 or below, tenodesis can substitute active grasp with passive whole hand and lateral grips. During wrist extension, tenodesis leads to passive shortening of the flexor digitorum superficialis and profundus tendons, causing passive finger-to-palm flexion, and of the flexor pollicis longus, resulting in thumb-to-index lateral face adduction (passive lateral grasp) (Mateo et  al. 2013; Woolsey 1985). Autonomy in tetraplegia, performed by open-chain or closed-chain movements, can be achieved through rehabilitation and further supplemented or enhanced by surgical tendon transfer, where a tendon is transferred from a spared muscle stronger than grade 4 manual muscle test to a paralyzed muscle (Fridén and Gohritz 2015).

79

80

75

70 60 50

50 40 30 20 10 0

3

AIS A

AIS B*

AIS C**

AIS D

Initial ASIA Impairment Scale

Fig. 4.2  Prognosis for ambulation after traumatic spinal cord injuries. *Prognosis influenced by presence or absence of pinprick sensation. **Prognosis influenced by age. (Modified from Consortium for Spinal Cord Medicine (1999))

4  Assessing and Predicting Function After Spinal Cord Injuries

80

motor scores, sensory scores, and the ASIA Impairment Scale (Marino 2005). Various tools, such as the Spinal Cord Independence Measure (SCIM), Quadriplegia Index of Function (QIF), Functional Independence Measure (FIM), and Modified Barthel Index (MBI), assess the activities of people with spinal cord injuries (Anderson et  al. 2008). The Craig Handicap Assessment and Reporting Technique (CHART) was developed to assess participation. SCIM III, QIF, FIM, and MBI are summarized in Table 4.2. Upper extremity function assessment measures include the Graded Redefined Assessment of Strength, Sensibility, and Prehension (GRASSP) Test, Capabilities of Upper Extremity Questionnaire (CUE-Q), and Capabilities of Upper Extremity Test (CUE-­ T). The Walking Index for Spinal

Cord Injury II (WISCI II), Spinal Cord Injury-Functional Ambulation Inventory (SCI-FAI), 6-Minute Walk Test (6MWT), 10-Meter Walk Test (10MWT), and Timed Up and Go (TUG) measure ambulation function. WISCI II and 10MWT are considered the most valid and clinically useful primary outcome measures for gait and ambulation in incomplete spinal cord injury due to their criterion-oriented validity, reliability, and sensitivity to change (Alexander et al. 2009). 11. What are the main subscales of the SCIM III, and what is the total score range? What are the limitations of the FIM in assessing people with spinal cord injuries? Which functions are not assessed by the Modified Barthel Index in people with spinal cord injuries?

Table 4.2  Measures for functional assessment of individuals with spinal cord injuries Scale Spinal Cord Independence Measure (SCIM-III)

Quadriplegia Index of Function (QIF)

Evaluation contents •  19 items in 3 subscales: self-care (6 items, subscore 0–20), respiration and sphincter management (4 items, subscore 0–40), and mobility (“room and toilet” and “indoors and outdoors,” 9 items, subscore 0–40) •  10 items: 9 ADL tasks and a question for understanding of personal care

Functional Independence Measure (FIM)

•  18 tasks (13 motor, 5 cognitive) in 6 areas (self-care, sphincter management, transfers, locomotion, communication, and social cognition)

Modified Barthel Index (MBI)

•  10 ADL functions in three areas (self-care, continence, locomotion)

Scoring •  All items are weighted in terms of their assumed clinical relevance •  Total score range: 0–100

Remarks •  Developed specifically for people with SCI •  Most commonly used scale in people with SCI

•  The items are weighted according to their assumed clinical relevance •  For the first 7 tasks: 0–4 each •  The last 3 tasks have separate set of scoring criteria •  Total QIF score: 0–100 •  Each task range 1–7 •  1–5 as levels needing helper(s) •  1 total assist, 2 maximum assist, 3 moderate assist, 4 minimal assist, 5 supervision, 6 modified independence using device, 7 complete independence •  Total score range: 18–126 •  Total score range: 0–100 •  Each item is weighted in terms of its assumed clinical relevance

•  Developed specifically for assessment of people with tetraplegia •  No item for locomotion •  Limitation of this scale use for ambulatory tetraplegic •  Not specified for people with SCI •  No respiratory task •  Less applicable cognitive tasks for SCI •  Score ceiling effect

•  Not developed for people with SCI, limited use in SCI •  Not suitable for a detailed function evaluation as limited to the basic ADL functions

References

The SCIM, specifically designed for people with spinal cord injuries, assesses Activities of Daily Living (ADL) performance and makes functional assessments. The latest version, SCIM III, consists of 19 items in three subscales: self-care, respiration and sphincter management, and mobility (Itzkovich et al. 2007, 2018). The total score ranges from 0 to 100, with items weighted according to clinical relevance (Anderson et al. 2008). Reliable variables predicting the SCIM III total score at 6 months after injury include age at injury, three key muscles, and two mobility assessments (Ariji et al. 2020). The QIF was developed to assess people with tetraplegic spinal cord injuries (Anderson et  al. 2008). It measures independence levels in nine ADL tasks and one question on understanding personal care, with a total score ranging from 0 to 100 (Anderson et al. 2008; Gresham et al. 1986). However, QIF has limited use for ambulatory tetraplegics as it does not assess locomotion. The FIM, developed to assess functional ability in daily activities, was not specifically designed for people with spinal cord injuries. It assesses six functional domains based on 18 tasks, with a total score ranging from 18 to 126. However, the FIM has limitations in assessing respiratory and cognitive functions in people with spinal cord injuries. The MBI measures ten ADL functions in the areas of self-care, continence, and locomotion. Despite its total score ranging from 0 to 100, the MBI does not assess critical functions for individuals with spinal cord injuries, such as respiratory function. 12. What factors positively impact quality of life and life satisfaction in people with spinal cord injuries? What is an example of an instrument measuring health-related quality of life? What tool is used to describe overall subjective well-being in people with spinal cord injuries?

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Quality of life (QOL) and life satisfaction in people with spinal cord injuries positively influence social participation, social support, and perceived control over life. However, no consistent or strong association exists between QOL and biomedical factors such as injury completeness or neurological injury level (Boakye et al. 2012). Enhancing QOL is a common objective in spinal cord injury care and rehabilitation, but measuring and defining it with precision or consistency are challenging. Moreover, the applicability of many popular QOL measures in people with spinal cord injuries is limited, for instance, due to unsuitable questions for those with motor impairments related to walking (Gurcay et  al. 2010). Numerous components contribute to QOL, one of which is health-related quality of life (HRQOL). The Short Form (SF)-36 is an example of an instrument measuring HRQOL, with a modified version also available. Another aspect of QOL is subjective well-being and life satisfaction (Cooper and Cooper 2010). The Diener Satisfaction with Life Scale (SWLS) is a tool used to describe overall subjective well-being, allowing for normative data from the Spinal Cord Injury Model Systems and other sources (Boakye et al. 2012).

References Alexander MS, Anderson KD, Biering-Sorensen F, et al. Outcome measures in spinal cord injury: recent assessments and recommendations for future directions. Spinal Cord. 2009;47:582–91. AlHuthaifi F, Krzak J, Hanke T, et al. Predictors of functional outcomes in adults with traumatic spinal cord injury following inpatient rehabilitation: a systematic review. J Spinal Cord Med. 2017;40:282–94. Anderson K, Aito S, Atkins M, et al. Functional recovery outcome measures work group. Functional recovery measures for spinal cord injury: an evidence-based review for clinical practice and research. J Spinal Cord Med. 2008;31:133–44. Ariji Y, Hayashi T, Ideta R, et al. A prediction model of functional outcome at 6 months using clinical ­findings of a person with traumatic spinal cord injury at 1 month after injury. Spinal Cord. 2020;58:1158–65.

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Behrman AL, Harkema SJ.  Physical rehabilitation as an agent for recovery after spinal cord injury. Phys Med Rehabil Clin N Am. 2007;18:183–202, v. Boakye M, Leigh BC, Skelly AC.  Quality of life in persons with spinal cord injury: comparisons with other populations. J Neurosurg Spine. 2012;17:29–37. Burns SP, Golding DG, Rolle WA Jr, et al. Recovery of ambulation in motor-incomplete tetraplegia. Arch Phys Med Rehabil. 1997;78:1169–72. Consortium for Spinal Cord Medicine. Outcomes following traumatic spinal cord injury. Clinical practice guidelines for health care professionals. Washington, DC: Paralyzed Veterans of America; 1999. Cooper RA, Cooper R.  Quality-of-life technology for people with spinal cord injuries. Phys Med Rehabil Clin N Am. 2010;21:1–13. Daverat P, Sibrac MC, Dartigues JF, et al. Early prognostic factors for walking in spinal cord injuries. Paraplegia. 1988;26:255–61. Ditunno JF. Outcome measures: evolution in clinical trials of neurological/functional recovery in spinal cord injury. Spinal Cord. 2010;48:674–84. Ditunno JF Jr, Stover SL, Freed MM, et al. Motor recovery of the upper extremities in traumatic quadriplegia: a multicenter study. Arch Phys Med Rehabil. 1992;73:431–6. Farhadi HF, Kukreja S, Minnema A, et  al. Impact of admission imaging findings on neurological outcomes in acute cervical traumatic spinal cord injury. J Neurotrauma. 2018;35:1398–406. Fridén J, Gohritz A.  Tetraplegia management update. J Hand Surg Am. 2015;40:2489–500. Gresham GE, Labi ML, Dittmar SS, et  al. The Quadriplegia Index of Function (QIF): sensitivity and reliability demonstrated in a study of thirty quadriplegic patients. Paraplegia. 1986;24:38–44. Gurcay E, Bal A, Eksioglu E, et  al. Quality of life in patients with spinal cord injury. Int J Rehabil Res. 2010;33:356–8. Herbison GJ, Zerby SA, Cohen ME, et al. Motor power differences within the first two weeks post-SCI in cervical spinal cord-injured quadriplegic subjects. J Neurotrauma. 1992;9:373–80. Hussey RW, Stauffer ES.  Spinal cord injury: requirements for ambulation. Arch Phys Med Rehabil. 1973;54:544–7. Itzkovich M, Gelernter I, Biering-Sorensen F, et  al. The Spinal Cord Independence Measure (SCIM) version III: reliability and validity in a multi-center international study. Disabil Rehabil. 2007;29:1926–33. Itzkovich M, Shefler H, Front L, et al. SCIM III (Spinal Cord Independence Measure version III): reliability of assessment by interview and comparison with assessment by observation. Spinal Cord. 2018; 56:46–51.

Kirshblum S, Millis S, McKinley W, et al. Late neurologic recovery after traumatic spinal cord injury. Arch Phys Med Rehabil. 2004;85:1811–7. Koontz AM, Kankipati P, Lin YS, et  al. Upper limb kinetic analysis of three sitting pivot wheelchair transfer techniques. Clin Biomech (Bristol, Avon). 2011;26:923–9. Marino RJ. Neurological and functional outcomes in spinal cord injury: review and recommendations. Top Spinal Cord Inj Rehabil. 2005;10:51–64. Marino RJ.  Domains of outcomes in spinal cord injury for clinical trials to improve neurological function. J Rehabil Res Dev. 2007;44:113–22. Mateo S, Revol P, Fourtassi M, et al. Kinematic characteristics of tenodesis grasp in C6 quadriplegia. Spinal Cord. 2013;51:144–9. Mateo S, Roby-Brami A, Reilly KT, et  al. Upper limb kinematics after cervical spinal cord injury: a review. J Neuroeng Rehabil. 2015;12:9. Matsushita A, Maeda T, Mori E, et al. Can the acute magnetic resonance imaging features reflect neurologic prognosis in patients with cervical spinal cord injury? Spine J. 2017;17:1319–24. Maynard FM, Reynolds GG, Fountain S, et al. Neurological prognosis after traumatic quadriplegia. Three-year experience of California Regional Spinal Cord Injury Care System. J Neurosurg. 1979;50:611–6. Miyanji F, Furlan JC, Aarabi B, et  al. Acute cervical traumatic spinal cord injury: MR imaging findings correlated with neurologic outcome–prospective study with 100 consecutive patients. Radiology. 2007;243:820–7. Post MW, Kirchberger I, Scheuringer M, et al. Outcome parameters in spinal cord injury research: a systematic review using the International Classification of Functioning, Disability and Health (ICF) as a reference. Spinal Cord. 2010;48:522–8. Rudhe C, van Hedel HJA. Upper extremity function in persons with tetraplegia: relationships between strength, capacity, and the spinal cord independence measure. Neurorehabil Neural Repair. 2009;23:413–21. Tator CH. Biology of neurological recovery and functional restoration after spinal cord injury. Neurosurgery. 1998;42:696–707; discussion 707–8. Waters RL, Adkins RH, Yakura JS, et al. Motor and sensory recovery following incomplete paraplegia. Arch Phys Med Rehabil. 1994;75:67–72. Waters RL, Adkins R, Yakura J, et al. Donal Munro lecture: functional and neurologic recovery following acute SCI. J Spinal Cord Med. 1998;21:195–9. WHO.  International Classification of Functioning, Disability and Health (ICF). 2001. https://www.who. int/docs/default-­source/classification/icf/icfchecklist. pdf?sfvrsn=b7ff99e9_4. Woolsey RM.  Rehabilitation outcome following spinal cord injury. Arch Neurol. 1985;42:116–9.

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Abstract

This chapter investigates the complex interaction between the biomechanics of the spine and spinal cord and the pathophysiology of spinal cord injuries. The chapter begins by discussing the unique anatomical and biomechanical features of the spinal cord, emphasizing the need for a thorough understanding of the kinematics of the spine to comprehend the underlying mechanisms of traumatic spinal cord injuries. The biomechanical properties of the spinal cord and its supporting structures vary across different regions of the spine, leading to varying degrees of resilience and susceptibility to external forces. The chapter provides a detailed overview of the essential anatomy of the spine, including the vertebrae, intervertebral discs, ligaments, and muscles, which play a critical role in stabilizing and protecting the spinal cord. In addition to the structural features of the spine, the chapter also delves into the mechanics of the spinal cord itself, including its compliance, elasticity, and viscoelastic properties. The author provides a comprehensive overview of the biomechanical factors that contribute to spinal cord injuries, including the magnitude, duration, and direction of the applied forces. To provide a comprehensive understanding of spinal cord injuries, the chapter also examines the underlying pathophysiology of these injuries. The author dis-

cusses the complex cascade of events that occur following a traumatic spinal cord injury, including primary and secondary injury mechanisms, inflammation, and cell death. The chapter also discusses the importance of early intervention and the potential benefits of neuroprotective and regenerative therapies. 1. What are the components of the fundamental spinal unit, and what are the three primary functions of the spine from a biomechanical perspective? How do typical biomechanical studies examine the motion unit, and what limitations might this approach have? The basic spinal unit, also known as the motion unit or motion segment, is composed of two neighboring vertebral bodies and the intervening ligamentous soft tissue (Fig. 5.1). This includes two intact vertebrae joined by an intervertebral disc, two posterior articulations, and several ligaments (Benzel 2015). The motion unit is the smallest anatomical spinal segment that demonstrates the biomechanical properties of the entire spine (Loughenbury et al. 2016; White and Panjabi 1990). By comprehending the natural biomechanics of the spinal motion unit, we can better understand the system’s limitations and the circumstances that may lead to tissue damage and subsequent pain. From a biomechanical

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 H.-Y. Ko, A Practical Guide to Care of Spinal Cord Injuries, https://doi.org/10.1007/978-981-99-4542-9_5

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standpoint, the spine serves three primary functions: transmitting loads through the body, allowing multidimensional movement, and protecting the spinal cord (Bernhardt et al. 2006). However, typical biomechanical studies examine the load and deformation of a motion unit using a cadaver, which may not accurately represent in vivo spine movement due to the influence of muscles. Consequently,

Fig. 5.1  A single spinal unit (motion unit) Fig. 5.2 Key components of a typical vertebra. The vertebral body provides support, while the pedicles and laminae protect the spinal cord in the cervical and thoracic regions, as well as the cauda equina below the L1 vertebra level. The spinous process, transverse processes, articular processes, and especially the articular facets function to control movement. (Adapted from Cramer and Darby (2014)

there may be significant differences compared to laboratory-obtained information. 2. What are the roles of the various regions in a spinal motion unit? Each region of a spinal motion unit (Fig.  5.2) is associated with one or more functions of the vertebral column. The vertebral bodies and intervertebral discs primarily manage the axial load-bearing responsibilities of the spine. The pedicles and laminae protect the spinal cord, with the pedicles connecting the anterior and posterior elements of each spinal segment. The laminae create a protective covering for the spinal canal, and the facet joints restrict rotation, flexion, extension, lateral bending, and translation to varying degrees depending on the region (Benzel 2015). The superior and inferior articular processes contribute to spinal motion through the orientation of their facets. Lastly, the transverse and spinous processes facilitate movement by serving as lever arms for the spinal muscles to act upon.

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3. What are the two main elements of the spinal motion unit? What is the biomechanical purpose of the posterior elements, and what are the roles of the pedicles and laminae in the spinal motion unit? The spinal motion unit, or functional spinal unit, consists of two main elements: the anterior element, which includes the vertebral bodies and the anterior and posterior longitudinal ligaments, and the posterior element, which is composed of the laminae, pedicles, transverse processes, spinous process, ligamentum flavum, facet joints, and interspinous and intraspinous ligaments. The biomechanical purpose of the posterior elements is to regulate the position of the vertebral bodies. These elements serve as attachment points for muscles, allowing them to control the vertebrae’s position and provide leverage for mechanical advantage, motion control, and the prevention of excessive vertebral body movement. The pedicles offer a sturdy support structure, facilia

b

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tating force transmission between the posterior elements and the anterior element. Each lamina extends from the pedicles and meets at the body’s midline, forming a neural arch. 4. How do the zygapophyseal (facet) joints change in inclination throughout the spine? There are two sets of articulation surfaces within the posterior elements. A bony extension called the superior articular process projects from each of the upper lateral corners of the lamina. The superior articular process of the lower vertebra interacts with the inferior articular process of the vertebra above, creating a synovial joint known as the zygapophyseal joint, or facet joint. The facet joint’s inclination changes as it moves from the cervical spine through the thoracic spine and into the lumbar spine. In the lumbar region, the facet joint’s angle relative to the sagittal plane increases from L1–L2 to L5– S1 (Fig.  5.3). The varying orientations of c

d

Fig. 5.3  Facet joint orientation. (a) Coronal plane orientation in the cervical spine. (b) Intermediate orientation in the thoracic spine. (c) Sagittal orientation in the lumbar

spine. (d) Substantial changes in facet orientation in the lumbar spine. (Adapted from Steinmetz and Benzel (2017), with permission)

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these facet joints restrict movement in different planes of motion, permitting certain movements while limiting others in the spine (Steinmetz and Benzel 2017). 5. What is the order of the ligamentous structures comprising the spinal motion unit from anterior to posterior, and what is the primary function of spinal ligaments? Beginning at the front and progressing toward the back, the spinal ligaments include the anterior longitudinal ligament, posterior longitudinal ligament, capsular ligaments, intertransverse process ligaments, ligamentum flavum, interspinous ligament, and supraspinous ligament (Ozapinar et al. 2022) (Fig. 5.4). These ligaments play a crucial role in stabilizing the subaxial spine within its physiological range of motion. While allowing normal spinal movement, the ligaments and facet joint capsules restrict excessive motion to safeguard the spinal cord (Steinmetz and Benzel 2017). 6. Describe the anterior and posterior longitudinal ligaments and their roles in spinal stability. The anterior longitudinal ligament extends the full length of the vertebral column, starting at the occiput, the front edge Fig. 5.4  Spinal motion unit ligaments. (Adapted from Ozapinar et al. (2022), with permission)

of the foramen magnum (basion), as the anterior occipitoatlantal membrane and continuing to the sacrum. It covers one-fourth to one-third of the ventral circumference of the vertebral bodies and intervertebral discs. The ligament’s width decreases at the disc level and is narrower and thicker in the thoracic region. The deepest layer connects adjacent vertebrae and the edges of the intervertebral discs, while the middle layer binds the vertebral bodies and intervertebral discs across three levels, and the superficial layers span approximately four to five levels (Steinmetz and Benzel 2017). The anterior longitudinal ligament is relatively strong and resists extension due to its ventral position relative to the instantaneous axis of rotation. The posterior longitudinal ligament also covers the entire length of the spinal column, starting at C2 as the tectorial membrane and continuing to the sacrum. Its fibers widen at the disc level and narrow in the middle of the vertebral body, in contrast to the anterior ­longitudinal ligament. The ligament adheres closely to the disc annulus but attaches only marginally to the vertebral body (Fig.  5.5). This ligament is thinner over the vertebral body and intervertebral disc and is thickest in the thoracic region. The posterior longitudi-

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7. What are the characteristics of the ligamentum flavum and its role in spinal stability? The ligamentum flavum consists of broad paired ligaments connecting the spinal laminae. They originate from the ventral surface of the lower lamina and attach to the dorsal margin of the adjacent upper lamina. These ligaments are discontinuous at midvertebral levels and in the midline. The fibers are longer and more relaxed in the cervical region than in the thoracic and lumbar regions (Steinmetz and Benzel 2017). They extend laterally to the joint capsules and become confluent. The ligamentum flavum, a segmentally discontinuous ligament, stretches from C1–2 to L5–S1. As one of the most elastic tissues in the human body, it is not slack except when hyperextended, minimizing buckling during extension (Yoganandan et al. 2022). The ligamentum flavum is a strong ligament but offers less resistance to flexion due to its more ventral attachment site and shorter moment arm compared to the interspinous ligaments. Generally, ligaments farther from the instantaneous axis of rotation have greater strength because of their relatively longer lever arm length. A very strong ligament with a relatively short moment arm may contribute less to stability than a weaker ligament with a longer moment arm due to the latter’s mechanical advantage (Fig. 5.6).

Fig. 5.5  The posterior longitudinal ligament: This ligament features fibers that widen at the level of the intervertebral disc and become narrower in the middle of the vertebral body, contrasting with the anterior longitudinal ligament. The posterior longitudinal ligament connects only to the margins of the vertebral body in the area of the intervertebral disc space. (Adapted from Steinmetz and Benzel (2017))

nal ligament is not as strong as the anterior longitudinal ligament and weakly resists flexion due to its dorsal position relative to the instantaneous axis of rotation combined with a short moment arm.

8. What is the instantaneous axis of rotation, and how is it related to the bending moment experienced by a lever? What factors can influence the position of the instantaneous axis of rotation? The bending moment experienced by a lever (moment arm) results from a force vector that induces a rotational motion around an axis. This axis, known as the instantaneous axis of rotation, is the point at which two hypothetical lines extending from a constant point within a vertebra intersect as the vertebra transitions between two positions (Marras et al. 2018). As a spinal segment moves, an

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axis that passes through or near the vertebral body remains stationary. The location of this axis is influenced by factors such as the spine’s intrinsic curvature, degenerative disease, fractures, or instrumentation, which can alter the position of the instantaneous axis of rotation (Benzel 2015) (Fig. 5.7).

Fig. 5.6  The relative lever arm lengths of ligaments during flexion. These lengths are dependent on the position of the instantaneous axis of rotation (IAR, represented by the dot). The ligaments include the anterior longitudinal ligament (ALL), posterior longitudinal ligament (PLL), ligamentum flavum (LF), capsular ligament (CL), and interspinous ligament (ISL). (Adapted from Ozapinar et al. (2022), with permission)

a

9. What is the coordinate system used to describe the motion and force transmission through tissue? How are flexion, extension, lateral bending, and rotation movements described in the coordinate system? To accurately depict motion and force transmission through tissue, it is essential to precisely define both the direction of movement and the direction and magnitude of the force acting on the tissue. The coordinate system used is a traditional three-­dimensional Cartesian coordinate system with three mutually perpendicular axes: the x, y, and z axes.

b

Fig. 5.7  When a bending moment is applied, the location of the instantaneous axis of rotation (IAR) shifts from its position during the preload state (a) to a new position in the postload state (b)

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The x-axis follows the posterior-to-­anterior direction, the y-axis aligns with the right-toleft direction, and the z-axis extends from the caudal-to-rostral direction. In the righthanded system, positive moments correspond to flexion (negative for extension), left-toright lateral bending (negative for right-toleft lateral bending), and right axial rotation (negative for left axial rotation) (Yoganandan et  al. 2017). All spine movements are described relative to the central coordinate system’s origin. Flexion and extension typically occur in the sagittal plane, lateral bending in the coronal plane, and rotation along the horizontal or transverse plane. Most activities involve combinations of movements in these planes. Figure 5.8 illustrates the coordinate system, including the instantaneous axis of rotation (Marras et al. 2018). 10. What is spinal coupling in the context of spinal movement and why is it clinically important?

a

Fig. 5.8  The coordinate system featuring the instantaneous axis of rotation as the center of motion. (a) Traditional three-dimensional Cartesian coordinate system illustrating planes and directions of motion for the spinal motion segment. (b) Biomechanical coordinate

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Movements in the spine are considered coupled when motion in one plane is accompanied by motion in another plane. Coupling is a phenomenon where spinal movement around one axis forces movement around a different axis (Benzel 2015). Primary motion refers to motion in the primary or intended plane, while coupled motions are the accompanying movements. Coupling depends on the geometric characteristics of specific vertebrae, limitations of the tissue properties of the intervertebral disc and ligaments, and spine curvature (Marras et al. 2018). Coupling is clinically significant for understanding the impact of various pathologies, such as scoliosis and different spine traumas. Coupling mostly occurs in the cervical and lumbar spine but can also happen in the thoracic spine. In the cervical and lumbar spine, axial rotation is coupled with lateral bending (White and Panjabi 1990). 11. How does the cervical spine display coupling? How do coupling patterns in the

b

system depicting the direction of forces and moments; Translation and rotation can occur in their respective directions along each axis. (Adapted from Marras et  al. (2018), with permission)

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lumbar spine differ from those in the cervical and thoracic spine? The cervical spine displays noticeable coupling, as lateral neck flexion is accompanied by cervical rotation. This is evident when observing the position of the spinous processes during lateral flexion. With left lateral flexion, the spinous processes point to the right, away from the concave side of the curvature. When right lateral flexion occurs, the spinous processes move to the left. The angle of inclination of the facet joints in the sagittal plane generally increases from the head toward the lower spine, as does the presence of uncovertebral joints (Benzel 2015; White and Panjabi 1990). Coupling patterns in the lumbar spine differ from those in the cervical and thoracic spine. The lumbar spine’s most dominant coupling pattern appears to be lateral flexion coupled with axial rotation. In this case, the spinous process moves in the same direction as the concave side of the lateral flexion direction, the opposite of the pattern found in the cervical and upper thoracic spine (Marras et al. 2018). Lumbar spine coupling motions vary with the spine level (White and Panjabi 1990). In vitro studies have reported that lateral flexion motions are coupled with flexion motions between L1 and L3, while in vivo studies have reported that lateral motions are coupled with extension movements in these vertebrae (Cholewicki et al. 1996). 12. What determines spinal column motion and its limitations? How does the orientation of facet joints affect spine motion? Spinal column motion is influenced by bony structures such as vertebral bodies, intervertebral discs, and facet joints, as well as the bony and ligamentous structures of the spinal motion segment (Cramer and Darby (2014); White and Panjabi 1990; Standring 2016) (Table 5.1). The intervertebral disc and facet joint anatomical features that determine spine motion include the size of the intervertebral discs influences the potential moments in the spine, while the orientation of the facet joints determines the direction of movement. Facet joint orientation varies across regions, and the

Table 5.1 Structures or situations restricting spine motion Spine motion Flexion

Extension

Lateral flexion

Rotation

Structures or situations limiting motion Posterior longitudinal ligament Ligamentum flavum Articular capsule Posterior fibers of intervertebral disc Interspinous ligament Supraspinous ligament Tension of back extensor muscles Anterior surface of inferior articular facet against posterior surface of superior articular facet Anterior longitudinal ligament Anterior aspect of intervertebral disc Approximation of spinous processes, articular processes, and laminae Contralateral side of intertransverse ligament and intervertebral disc Approximation of articular processes Approximation of uncinate processes (cervical region) Approximation of costovertebral joints (thoracic region) Antagonist muscles Tightening of lamellar fibers of annulus fibrosus Orientation and architecture of articular processes

Adapted from Cramer and Darby (2014), White and Panjabi (1990), and Standring (2016)

primary motion in each area depends on the plane of facet orientation. The spine’s ability to resist load-­imposed stiffness is determined by the facet joint design (White and Panjabi 1990). The spine’s stiffness increases gradually from T7 to L4, peaking between T12 and L1. At this level, facet joints hinder rotation, leading to high stress concentration and potential mechanical failure, as evidenced by the frequent occurrence of spinal injuries at the thoracolumbar junction (Breig 1970). 13. What are the characteristic movements in the cervical, thoracic, and lumbar regions of the spine? Maximum flexion and extension movements occur between C4 and C6 (White and Panjabi 1990). The thoracic region is less flexible and more stable than the cervical spine due to rib limitations and unique anatomical features of the spinous processes and

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joint capsules in this area. All directional movements are possible but are limited by changes in facet orientation from the upper to lower thoracic region. Flexion and extension are restricted in the upper thoracic region but increase in the lower thoracic spine. Rotation is not limited in the upper thoracic spine but is more restricted in the lower thoracic spine. Lumbar facets favor flexion and extension while limiting lateral flexion and rotation. In the lumbar spine, flexion is more restricted than extension. 14. What are the three mechanisms that maintain spinal stability? Spinal stability, a fundamental concept for characterizing and evaluating the spinal column, is maintained by three mechanisms: (1) the active subsystem (musculoskeletal system), (2) the passive subsystem (spinal column), and (3) the neural system (neurological control of the active system) (Miele et  al. 2012). Although criteria for defining and quantifying spinal stability and instability are not well established, under normal conditions, these three subsystems maintain mechanical stability while the spinal column translates and rotates about the three cardinal anatomical axes (Breig 1970; Vinken and Bruyn 1976). 15. What is the difference between acute and chronic instability? How is spinal instability quantified using a point system approach? According to White and Panjabi, clinical spinal instability is the loss of the spine’s ability to maintain its pattern of displacement under physiologic loads without causing initial or additional neurological deficits, major deformities, or disabling pain (White and Panjabi 1990). Instability can be classified as acute or chronic. Acute instability, often resulting from trauma, can be further divided into overt (or gross) or limited. Overt instability involves the inability of the spine to support the torso during normal activity, while limited instability refers to the loss of either anterior or posterior spinal integrity

while preserving the other. Chronic instability can be divided into glacial instability, with slow deformation progression, and dysfunctional segment motion, which involves a pain syndrome generated by dysfunctional motion (Miele et al. 2012). Several authors have attempted to quantify the degree or extent of acute instability through a point system approach. White and Panjabi developed a region-specific scoring system to emphasize the difference between cervical, thoracic, and lumbar anatomy. Benzel later modified this scoring system for the subaxial spine, making it non-region specific (Benzel 2015). A score of 5 points or more indicates overt instability, and a score of 2–4 points implies limited instability (Table 5.2). Table 5.2  Quantitation point system for assessing acute instability in subaxial cervical, thoracic, and lumbar injuries Condition Loss of integrity of anterior (and middle) columna Loss of integrity of posterior column(s)a Acute resting translational deformityb Acute resting angulation deformityb Acute dynamic translation deformity exaggerationc Acute dynamic angulation deformity exaggerationc Neural element injuryd Acute disc narrowing at level of suspected pathology Dangerous loading anticipated

Point assigned 2 2 2 2 2 2 3 1 1

Adapted from Benzel (2015) 5 ≥ overt instability; 2–4 limited instability a  By clinical examination, MRI, CT, or radiography. A single point may be allotted if incomplete evidence exists—for example, only MRI evidence of dorsal ligamentous injury (i.e., evidence of only interspinous ligament injury on T2-weighted images) b  From static resting anteroposterior and lateral spine radiographs. Must be the result of an acute clinical process c  From dynamic (flexion and extension) spine radiographs. Recommended only after other mechanisms of instability assessment have been exhausted and then only by an experienced clinician. Usually indicated only in the cervical region. Must be the result of an acute clinical process d  Score of 3 points for cauda equina, 2 points for spinal cord, or 1 point for isolated nerve root neurologic deficit

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16. What are the main components of Holdsworth’s two-column concept? The spine structure can be classified using the two-column concept, Louis’s three-­column concept, and Denis’s three-column concept, which are essential for defining spinal instability (Fig.  5.9). Holdsworth proposed the twocolumn concept by considering both the failure mode and resultant fracture patterns in spinal failure. This concept consists of an anterior column, which includes the vertebral bodies, intervertebral discs, anterior longitudinal ligament (ALL), posterior longitudinal ligament (PLL), and a posterior column containing the facet joints, neural arch, and posterior ligamentous complex. During physiological loading, the anterior column supports compressive loads, while the posterior column resists tension. Holdsworth suggested that disruption of the posterior column indicates instability (Holdsworth 1963, 1970). 17. How does Louis’s three-column concept differ from Holdsworth’s two-column concept? Louis’s three-column concept focuses on the spine’s primary load-bearing components, which include the vertebral body, intervertebral disc, and two facet joint com-

a

plexes at each spinal level. This concept is particularly helpful in assessing instability under predominantly axial loads and is more effective in evaluating bony component failure rather than soft tissue damage (Loughenbury et al. 2016; Louis 1985). 18. What does Denis’s three-column concept introduce, and when does instability occur according to this concept? Denis’s three-column concept is suitable for assessing segmental instability, bony collapse associated with axial load-bearing, and the distraction, flexion, and extension components of spinal column injury. This concept expands on Holdsworth’s two-column theory by introducing a middle column, which comprises the posterior longitudinal ligament, dorsal annulus fibrosus, and dorsal wall of the vertebral body. The anterior and posterior columns remain the same as in Holdsworth’s approach (Denis 1983, 1984; Loughenbury et al. 2016). Instability occurs when the posterior longitudinal ligament and the dorsal part of the intervertebral disc are also involved (Steinmetz and Benzel 2017). 19. How does the spinal cord adapt to changes in body positioning?

b

Fig. 5.9  Column concepts of spinal instability. (a) Holdsworth’s two-column concept and Louis’s three-column concept. (b) Denis’s three-column concept. (Adapted from Steinmetz and Benzel (2017))

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The spinal cord is a dynamic and adaptable structure that experiences significant geometric changes during normal physiological movements without any negative consequences (Mattucci et  al. 2019; Miele et  al. 2012). The biomechanical outcomes within the spinal cord are primarily determined by the movement of the spinal column and its impact on the spine, as well as the intrinsic physical properties of the spinal cord and related structures, such as the nerve roots, pia and dura mater, and dentate ligament. The spinal cord undergoes configuration changes in tandem with the spinal column in response to changes in body positioning. During sagittal plane motion, the dural sheath shifts in a rostral direction and stretches as the spinal canal lengthens (Adams and Logue 1971). Physiological motion of the spinal canal also leads to notable changes in the size of the ventral and dorsal subarachnoid spaces. Studies have shown that the ventral subarachnoid space diameter can decrease by up to 43%, and the dorsal subarachnoid space diameter can increase by up to 89% with flexion, while extension can lead to a 9% increase in the ventral subarachnoid space and a 17% decrease in the dorsal subarachnoid space (Muhle et al. 1998). The spinal cord exhibits elastic flexibility, as evidenced by large initial displacements occurring with small force levels, followed by stiffening as additional stretching or distraction requires higher load levels (Cusick 1991; Cusick and Yoganandan 2002; Yoganandan et  al. 2022). The folding and unfolding zone of the spinal cord accounts for 70–75% of the length changes between flexion and extension, with the remaining length changes taking place in the elastic deformation zone (Breig 1960; White and Panjabi 1990) (Fig. 5.10). 20. What are the consequences of spinal cord flexion and extension? During flexion, the spinal cord elongates within the spinal canal and its anterior-­ posterior diameter decreases, causing

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Fig. 5.10  Effect of spinal canal length changes on spinal cord unfolding, folding, and elastic deformation during physiological movements. In the neutral position, the spinal cord is folded like an accordion with a slight tension. As the spine moves into flexion, the spinal cord first unfolds with a minimal increase in tension, followed by an elastic deformation near full flexion. Conversely, during extension, the spinal cord first folds with minimal decrease of tension, followed by some elastic compression. (Adapted from White and Panjabi (1990))

increased axial tension in the axonal cylinders of the white matter tracts and lesions of the spinal canal that affect the cross-sectional area. When the spinal cord is in a neutral position, tensile forces applied to it produce a relatively even load distribution across the structure; however, bending results in increased compressive forces on the concave side and increasing distractive forces on the convex side. Shear forces, which act in a perpendicular plane to the tensile forces, are maximal toward the center of the cord. The interaction of these force vectors applied to different regions of the spinal cord during flexion suggests the potential for complex injury patterns (Fig.  5.11). In extension, the spinal cord shortens, and its anterior-­posterior diameter increases, leading to relative relaxation of the axonal cylinders. Poisson’s effect occurs when a material is stretched in one direction and tends to contract (or sometimes expand) in the other two directions perpendicular to the direction of the stretch, resulting in an increase in cross-­sectional area with a decrease in length or vice versa, while the total volume remains the same (Miele et  al. 2012; White and Panjabi 1990). Extension can lead to a pincer-­like effect on the spinal cord due to the reduced cross-sectional area

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Increased local axial stress

Flexion

Fig. 5.11  Effect of flexion and ventrally placed osteophyte on tensile and compressive stresses in the spinal cord. The figure illustrates increased tensile stresses in the dorsal half of the spinal cord during flexion, along with an increased compressive stress caused by a ventrally placed osteophyte. (Adapted from Steinmetz and Benzel (2017))

of the spinal canal caused by the dorsal protrusion of the annulus and the infolding of the ligament flavum and scaffolding of the lamina (Yoganandan et al. 2022). 21. Could you concisely explain the key distinctions between adult and pediatric spinal biomechanics, and how do children’s lower cervical spine movements differ from those in adults? What age range typically sees the development of adult-like motion characteristics in the spine? How does axial loading impact an infant’s immature spine? The biomechanics of the spine in children vary significantly from adults due to several factors. These include ligamentous laxity, incomplete ossification, shallow angulation of the facet joints, wedge-shaped and incompletely ossified vertebral bodies, and underdeveloped neck musculature, all of which contribute to an increased physiological mobility in the pediatric spine (Roaf 1960). In terms of movement, while the most substantial flexion and extension in adults occur at the C5-C6 level, in children, it’s more pro-

Fig. 5.12  Types of physical damage mechanisms to the spinal cord. The figure illustrates different mechanisms that can cause physical damage to the spinal cord, including concussion, contusion or compression, dislocation, distraction, and laceration

nounced at the C2-C3 level. However, the fulcrum of motion gradually descends with age. By the time a child is between 8 and 10 years old, the motion characteristics of the spine have typically developed to resemble those of an adult (Penning 1978). Another crucial factor is the cartilaginous nature of infantile vertebral bodies, which allows the immature spine to easily lengthen under axial loading. This elongation can reach up to 2 inches, necessitating adaptive changes in the spinal cord to avoid irreversible injury. With flexion and extension, individual spinal cord segments can adjust by up to 25% to prevent serious traction injuries to the nervous tissue (Hohl 1964). Overall, these anatomical features of the immature spine make it exceptionally mobile. This is why children with significant spinal cord injuries might not show

5  Biomechanics of the Spine and Spinal Cord and Pathophysiology of Spinal Cord Injuries

any radiological evidence of bony abnormalities, despite the severity of their condition (Cusick and Yoganandan 2002). 22. When does spinal cord damage become irreversible? Spinal cord damage may become irreversible when compression surpasses approximately 30% of the initial spinal cord diameter. Spinal cord injury primarily results from direct harm to the spinal cord neural and supportive glial tissue but can also stem from changes in vascular physiology and metabolic dysfunction (Carlson et  al. 2003; Harrison et al. 1999). When the spinal cord is deformed, the axonal membrane is subjected to varying degrees of local stretch damage. 23. What types of mechanical pathomechanisms can cause spinal cord damage? How do distraction, contusion, and dislocation injuries differ in terms of their effects on the spinal cord? Different types of mechanical pathomechanisms can cause spinal cord damage, such as concussion, contusion or compression, dislocation, distraction, and laceration (Fig. 5.12). Among these injury mechanisms, contusion, distraction, and dislocation are the most commonly encountered. These injury patterns can occur in combination. Distraction injuries are more evenly distributed throughout the spinal cord compared to 25. contusion and dislocation. Distraction injury has been associated with increased caudal-­ cranial injury severity compared to contusion and often results in the greatest strains in the dorsal column, while the ventral column experiences the least strain. In contrast to contusion, dislocation is associated with compressive lateral strains and increased strains in the lateral columns (Choo et  al. 2007; Miele et al. 2012). 24. How does the spinal cord respond to slowly progressive chronic compression? What are the differences in mechanical stiffness between gray matter and white matter in the spinal cord, and how does

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the sensitivity of cervical gray matter relate to central spinal cord injury? The spinal cord is highly susceptible to damage from acute compression. Despite this vulnerability, it demonstrates remarkable tolerance to slowly progressive chronic compression, as seen in degenerative cervical myelopathy, where function is often preserved even in cases of spinal cord deformation or atrophy (Baba et  al. 1996; Ichihara et al. 2003). Research on the mechanical stiffness differences between gray matter and white matter in the spinal cord has yielded varied results (Baba et  al. 1996, 1997; Ichihara et  al. 2001; Levine 1997; Ozawa et al. 2001). One study found that gray matter is more rigid than white matter, but it fails at lower strains, indicating that gray matter may be more fragile in comparison to white matter (Ichihara et  al. 2001, 2003). This finding seems to explain the expansion of damage from the gray matter at the center of the cervical cord to the surrounding white matter as compression increases in traumatic spinal cord injury. It has been hypothesized that this correlates with the sensitivity of the cervical gray matter (i.e., central cord syndrome) after mechanical stress is applied to the spinal cord, explaining why central spinal cord injury occurs first following mechanical stress on the spinal cord (Ichihara et al. 2001). What are the three phases of pathophysiological changes in the spinal cord after injury, and why is understanding the pathophysiological processes important after spinal cord injury? What strategies can be employed to minimize or reverse secondary spinal cord damage during the acute phase? The pathophysiological changes of the spinal cord can be categorized into three phases: the early acute phase, which lasts from 2 to 48  h after injury; the subacute phase, extending from 2 days to 2 weeks; and the intermediate phase, which ranges from 2 weeks to 6 months (Rowland et al. 2008). Understanding the pathophysiological processes that occur following a spinal cord

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injury is crucial for developing effective therapies to minimize or reverse the damage. In addition to local pathophysiological processes causing secondary injury at the injury site, systemic factors also play a role. Strategies for addressing these issues include immediate resuscitation, minimizing prolonged hypoxia, and preventing and treating neurogenic shock and hypotension in the acute phase after spinal cord injury, as well as limiting secondary spinal cord damage (Cadotte and Fehlings 2011). 26. What is the difference between primary and secondary spinal cord injuries? What are some of the processes that contribute to secondary injury after spinal cord injury, and how do hemorrhages progress after a spinal cord injury? Traumatic spinal cord injuries lead to mechanical destruction of neural tissue and hemorrhage at the epicenter within the spinal cord. Primary injury results from direct physical trauma to the spinal cord due to various mechanisms, including penetrating or blunt injuries (Hachem et  al. 2017). The initial loss of axons exhibits a centrifugal pattern, which can be explained by the longitudinal displacement of the central content of the spinal cord (Onose et al. 2009). Primary injury triggers a cascade of pathochemical events, leading to significant further axonal loss, representing secondary injury (Anderson and Hall 1993). Secondary injury processes occur within days to weeks after the injury (Kwon et  al. 2004, 2011b) and include vascular perfusion abnormalities, edema, inflammation, free radical generation, lipid peroxidation, excitotoxicity with changes in  local ionic concentrations and calcium influx, and cell death (Borgens and Liu-Snyder 2012; Hachem et al. 2013; Rowland et al. 2008) (Fig. 5.13). Hemorrhages occur almost immediately in the gray matter and spread within minutes to the white matter, affecting microcirculation. Small hemorrhages coalesce to form a central hemorrhagic necrosis and progress to a centrifugal pattern involving the surrounding

white matter. The summarized temporal mechanisms of the primary and secondary injuries of spinal cord injury are shown in Fig. 5.14. 27. What are the key factors responsible for delayed injuries after spinal cord injury? What are the stages and characteristics of pathologic events after a severe impact injury to the spinal cord? Detailed animal studies have shown that for a few minutes after a severe impact injury to the spinal cord, the spinal cord may appear grossly and histologically normal. However, the sequence of pathologic events converts this normal appearance to complete focal necrosis and inflammation within 24–48  h post-injury (Okazaki et al. 2018) (Table 5.3). Subarachnoid and subpial hemorrhages occur on the spinal cord’s surface just under the injury site. Hemorrhages in the corticospinal tracts are first observed at about 4  h. Eight hours after injury, white matter tracts are characterized by a nonhemorrhagic necrosis associated with edema (Okazaki et al. 2018). Ischemia, edema, and hemorrhages are responsible for most delayed injuries that can occur after spinal cord injury (Lammertse 2004). Ischemia is due to the release of vasoactive substances causing local vasoconstriction and microvascular injury sustained at the time of injury. Inflammatory responses with wounds cause edema, leading to compression of neurological structures, additional damage to the spinal cord’s microvasculature, and promoting neurological deficits. 28. What does the term “discomplete” mean, and what is the significance of the “discomplete” concept in spinal cord injury cases? The term “discomplete” was first introduced by Dimitrijevic et  al. (1983) to describe their discovery of electrophysiological signal transmission across the lesion in patients who have lost all sensation and voluntary motor function below the injury level, despite being clinically complete. These patients have a varying number of intact

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Secondary injury Vasospasm/ischemia Excitotoxicity Mitochondrial dysfuncon Oxidave damage/lipid peroxidaon Neuroinflammaon Axonal degeneraon Ca2+, Na+ influx

Primary injury such as contusion, shear, compression, laceraon, stretch

Barriers to regenera on and recovery Cell necrosis and apoptosis Oliogodendrocyte/myelin loss Axonal degeneraon Glial scar Cyst formaon Myelin/extracellular matrix inhibion Fig. 5.13  Pathophysiology of spinal cord injuries: primary and secondary injury. Spinal cord injuries result from an initial primary injury caused by various mechanisms, such as contusion, shear, compression, laceration, and stretch. Secondary injury then follows, which involves

Primary injury

Early acute Vasogenic edema Vasospasm Thrombosis Release of neurotoxic opioids Inflammaon Cytotoxic edema Ion imbalance Loss of sodium gradient Formaon of free radicals

Days

Hours

Mechanism

Immediate Hemorrhage Increased ATP Decreased lactate (acidosis)

Secondary injury

Minutes

Seconds

Injury

Timeline

Primary injury Compression Laceraon Shearing Distracon

progressive tissue destruction over weeks and months after the primary injury due to additional systemic and cellular insults. (Adapted from Hachem et al. 2013, with permission)

Subacute Apoptosis Macrophage acvaon Microglial smulaon

Fig. 5.14  Primary and secondary injury mechanisms of spinal cord injury. (Adapted from Wilson et al. (2013))

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Table 5.3  Pathophysiologic responses to spinal cord injury Time Immediate 1 min

Anatomical change •  Cord deformation

5 min 15 min

•  Axonal swelling

30 min 1 h 4 h

•  Central hemorrhages

8 h 24 h

•  •  •  • 

Physiological change

Biochemical change

•  Loss of evoked potentials

•  Lipid peroxidation •  Free-radical formation

• Vasoconstriction •  Decreased gray and white matter blood flow • Ischemia

•  Increased thromboxane levels •  Increased tissue norepinephrine levels •  Profound tissue hypoxia

Blood vessel necrosis White matter edema Central hematoma formation White matter necrosis

From Wilberger (1986), with permission

nerve fibers crossing the lesion level and can be considered “anatomically discomplete.” The observation that a significant proportion of these cases display some anatomical continuity of spinal cord white matter across the lesion in clinically incomplete and “discomplete” patients highlights the relative preservation of tracts, even in the most severe spinal cord injury cases (Kakulas 1999). 29. What were the findings of the NASCIS II and III studies? Why has methylprednisolone been the subject of controversy and disagreement? What is the current stance of AANS/ CNS and NICE guidelines on methylprednisolone for spinal cord injury treatment? Despite the exponential growth in research, there has not been an FDA accepted or approved treatment to improve neurological function after spinal cord injury (Kwon et al. 2011a; Lammertse et al. 2007). High-­ dose methylprednisolone administered intravenously within 8  h of injury was the only drug widely used clinically for a period of time after the publication of positive results after spinal cord injury in the 1990s (Cadotte and Fehlings 2011; Kwon et al. 2011a). The American National Acute Spinal Cord Injury Study (NASCIS) phases I–III evaluated the use of methylprednisolone sodium succinate

in various protocols regarding dose and timing of administration after acute spinal cord injuries. Post-hoc analysis of the NASCIS II data showed that patients who received methylprednisolone within 8 h of injury had significant improvement in sensory and motor function at 1 year (Bracken et al. 1990, 1992). Post-hoc analysis of the NASCIS III data showed that there is no need to extend treatment beyond 24 h if the treatment starts within 3 h from injury, while motor recovery is better if treatment extended to 48  h if it starts after 3  h (Bracken et  al. 1997). However, the study has been the subject of much controversy and lack of consensus (Cadotte and Fehlings 2011; Curt 2012). Patients treated with methylprednisolone have an increased incidence of wound infections, pneumonia, sepsis, and death from respiratory complications. For this reason, the American Association of Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS) guidelines for the management of acute cervical spine and spinal cord injury, updated in 2013, now explicitly recommend not administering methylprednisolone for the treatment of spinal cord injuries. The National Institute of Clinical Excellence (NICE) guidelines do not recommend the standard use of methylprednisolone following the acute stage after traumatic spinal cord injuries (NICE 2016).

References

30. Which diet has shown potential effectiveness for neuroprotection in acute spinal cord injury? It should be noted that there are numerous studies indicating that the ketogenic diet is effective for neuroprotection, including acute spinal cord injury (Demirel et al. 2020; Koh et  al. 2020; Sayadi et  al. 2021; Tan et  al. 2020; Veyrat-Durebex et al. 2018).

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99 Cadotte DW, Fehlings MG. Spinal cord injury: a systematic review of current treatment options. Clin Orthop Relat Res. 2011;469:732–41. Carlson GD, Gorden CD, Nakazawa S, et  al. Sustained spinal cord compression: Part II: Effect of methylprednisolone on regional blood flow and recovery of somatosensory evoked potentials. J Bone Joint Surg Am. 2003;85-A:95–101. Cholewicki J, Crisco JJ III, Oxland TR, et al. Effects of posture and structure on three-dimensional coupled rotations in the lumbar spine. A biomechanical analysis. Spine (Phila Pa 1976). 1996;21:2421–8. Choo AM, Liu J, Lam CK, et al. Contusion, dislocation, and distraction: primary hemorrhage and membrane permeability in distinct mechanisms of spinal cord injury. J Neurosurg Spine. 2007;6:255–66. Cramer GD, Darby SA.  Clinical anatomy of the spine, spinal cord, and ANS. St. Louis: Elsevier; 2014. Curt A.  The translational dialogue in spinal cord injury research. Spinal Cord. 2012;50:352–7. Cusick JF.  Pathophysiology and treatment of cervical spondylotic myelopathy. Clin Neurosurg. 1991;37:661–81. Cusick JF, Yoganandan N. Biomechanics of the cervical spine 4: major injuries. Clin Biomech. 2002;17:1–20. Demirel A, Li J, Morrow C, et al. Evaluation of a ketogenic diet for improvement of neurological recovery in individuals with acute spinal cord injury: study protocol for a randomized controlled trial. Trials. 2020;21:372. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine. 1983;8:817–31. Denis F. Spinal instability as defined by the three-column spine concept in acute spinal trauma. Clin Orthop Relat Res. 1984;189:65–76. Dimitrijevic MR, Faganel J, Lehmkuhl D, et  al. Motor control in man after partial or complete spinal cord injury. Adv Neurol. 1983;39:915–26. Hachem LD, Schneider L, Hawryluk GWJ, et  al. Pathophysiology and treatment of spinal cord injury. In: Neurological surgery. 8th ed. Philadelphia: Elsevier; 2013. Hachem LD, Ahuja CS, Fehlings MG.  Assessment and management of acute spinal cord injury: from point of injury to rehabilitation. J Spinal Cord Med. 2017;40:665–75. Harrison DE, Cailliet R, Harrison DD, et al. A review of biomechanics of the central nervous system-Part II: Spinal cord strains from postural loads. J Manipulative Physiol Ther. 1999;22:322–32. Holdsworth FW.  Fractures, dislocations, and fracture-­ dislocations of the spine. J Bone Joint Surg Br. 1963;45:6–20. Holdsworth F.  Fractures, dislocations, and fracture-­ dislocations of the spine. J Bone Joint Surg Am. 1970;52:1534–51. Hohl M. Normal motions in the upper portion of the cervical spine. J Bone Joint Surg Am. 1964;46:1777–9. Ichihara K, Taguchi T, Shimada Y, et al. Gray matter of the bovine cervical spinal cord is mechanically more

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rigid and fragile than the white matter. J Neurotrauma. 2001;18:351–67. Ichihara K, Taguchi T, Sakuramoto I, et  al. Mechanism of the spinal cord injury and the cervical spondylotic myelopathy: new approach based on the mechanical features of the spinal cord white and gray matter. J Neurosurg. 2003;99(3 Suppl):278–85. Kakulas BA.  A review of the neuropathology of human spinal cord injury with emphasis on special features. J Spinal Cord Med. 1999;22:119–24. Koh S, Dupuis N, Auvin S. Ketogenic diet and neuroinflammation. Epilepsy Res. 2020;167:106454. Kwon BK, Tetzlaff W, Grauer JN, et al. Pathophysiology and pharmacologic treatment of acute spinal cord injury. Spine J. 2004;4:451–64. Kwon BK, Okon E, Hillyer J, et al. A systematic review of non-invasive pharmacologic neuroprotective treatments for acute spinal cord injury. J Neurotrauma. 2011a;28:1545–88. Kwon BK, Okon EB, Plunet W, et al. A systematic review of directly applied biologic therapies for acute spinal cord injury. J Neurotrauma. 2011b;28:1589–610. Lammertse DP.  Update on pharmaceutical trials in acute spinal cord injury. J Spinal Cord Med. 2004;27:319–25. Lammertse D, Tuszynski MH, Steeves JD, et  al. Guidelines for the conduct of clinical trials for spinal cord injury as developed by the ICCP panel: clinical trial design. Spinal Cord. 2007;45:232–42. Levine DN. Pathogenesis of cervical spondylotic myelopathy. J Neurol Neurosurg Psychiatry. 1997;62:334–40. Loughenbury PR, Tsirikos AI, Gummerson NW.  Spinal biomechanics-biomechanical considerations of spinal stability in the context of spinal injury. Orthop Trauma. 2016;30:369–77. Louis R. Spinal stability as defined by the three-column spine concept. Anat Clin. 1985;7:33–42. Marras WS, Mageswaran P, Khan SN, et al. Biomechanics of the spine motion segment. In: Garfin SR, Eismont FJ, Bell GR, et  al., editors. Rothman-Simeone and Herkowitz’s the spine. 7th ed. Philadelphia: Elsevier; 2018. Mattucci S, Speidel J, Liu J, et al. Basic biomechanics of spinal cord injury–how injuries happen in people and how animal models have informed our understanding. Clin Biomech (Bristol, Avon). 2019;64:58–68. Miele VJ, Panjabi MM, Benzel EC.  Anatomy and biomechanics of the spinal column and cord. Handb Clin Neurol. 2012;109:31–43. Muhle C, Wiskirchen J, Weinert D, et al. Biomechanical aspects of the subarachnoid space and cervical cord in healthy individuals examined with kinematic magnetic resonance imaging. Spine (Phila Pa 1976). 1998;23:556–67. NICE. Spinal injury: assessment and initial management, NICE guidelines [NG41]. 2016. https://www.nice.org. uk/guidance/ng41.

Okazaki T, Kanchiku T, Nishida N, et  al. Age-related changes of the spinal cord: a biomechanical study. Exp Ther Med. 2018;15:2824–9. Onose G, Anghelescu A, Muresanu DF, et  al. A review of published reports on neuroprotection in spinal cord injury. Spinal Cord. 2009;47:716–26. Ozapinar A, Joseph JR, Kanter AS.  Functional anatomy of the spine. In: Steimetz MP, editor. Benzel’s spine surgery. 5th ed. Philadelphia: Elsevier; 2022. Ozawa H, Matsumoto T, Ohashi T, et  al. Comparison of spinal cord gray matter and white matter softness: measurement by pipette aspiration method. J Neurosurg. 2001;95(2 Suppl):221–4. Penning L. Normal movements of the cervical spine. AJR Am J Roentgenol. 1978;130:317–26. Roaf R. A study of the mechanics of spinal injury. J Bone Joint Surg. 1960;42(B):810–23. Rowland JW, Hawryluk GW, Kwon B, et  al. Current status of acute spinal cord injury pathophysiology and emerging therapies: promise on the horizon. Neurosurg Focus. 2008;25:E2. Sayadi JJ, Sayadi L, Satteson E, et al. Nerve injury and repair in a ketogenic milieu: a systematic review of traumatic injuries to the spinal cord and peripheral nervous tissue. PLoS One. 2021;16:e0244244. Standring S, editor. Gray’s anatomy. 41st ed. London: Elsevier; 2016. Steinmetz MP, Benzel EC.  Benzel’s spine surgery. Techniques, complication avoidance, and management. 4th ed. Philadelphia: Elsevier; 2017. Tan BT, Jiang H, Moulson AJ, et  al. Neuroprotective effects of a ketogenic diet in combination with exogenous ketone salts following acute spinal cord injury. Neural Regen Res. 2020;15:1912–9. Veyrat-Durebex C, Reynier P, Procaccio V, et al. How can a ketogenic diet improve motor function? Front Mol Neurosci. 2018;11:15. Vinken PJ, Bruyn GW, editors. Injuries of the spine and spinal cord. Part I. Handbook of clinical neurology, vol. 25. Oxford: North-Holland Publishing Company; 1976. White AA, Panjabi MM.  Clinical biomechanics of the spine. 2nd ed. Philadelphia: Lippincott; 1990. Wilberger JE, editor. Spinal cord injuries in children. New York: Futura Publishing Company; 1986. Wilson JR, Forgione N, Fehlings MG.  Emerging therapies for acute traumatic spinal cord injury. CMAJ. 2013;185:485–92. Yoganandan N, Arun MWJ, Dickman CA, et al. Practical anatomy and fundamental biomechanics. In: Steimetz MP, Benzel EC, editors. Benzel’s spine surgery. 4th ed. Philadelphia: Elsevier; 2017. Yoganandan N, Arun MWJ, Dickman CA, et al. Practical anatomy and fundamental biomechanics. In: Steimetz MP, editor. Benzel’s spine surgery. 5th ed. Philadelphia: Elsevier; 2022.

6

Kinematics-Related Understanding for Enhancing Extremity Muscle Functionality After Spinal Cord Injuries

Abstract

In the chapter, the author explores the critical role that functional anatomy and kinesiology play in the rehabilitation process following a spinal cord injury. The chapter highlights the significance of addressing the unique challenges faced by individuals with spinal cord injuries and emphasizing the need to restore upper limb function as a top priority. The chapter begins by providing an overview of the physiological implications of spinal cord injuries, which can lead to a wide range of disabilities. It then discusses how the neurological level of injury and its severity determine the extent to which functional rehabilitation can restore lost functions. This section also outlines the importance of considering individual differences when developing rehabilitation plans, as even those with similar injury levels and impairments may exhibit varying responses to treatment. Next, the authors discuss the importance of functional training for muscles that remain in the unaffected spinal cord segments. This includes understanding the origin, insertion, and joint fixation of each muscle to develop targeted and efficient training programs. By focusing on these fundamental aspects of muscle function, rehabilitation professionals can design interventions that optimize the use of remaining muscle strength. Furthermore, the chapter elaborates on the significance of integrating kinematic principles into rehabilitation programs. By focusing

on the biomechanics of movement and the interaction between different muscle groups, clinicians can develop more effective strategies for restoring lost functions. This may involve compensatory techniques or the use of assistive devices to enable individuals with spinal cord injuries to regain independence and improve their quality of life. Overall, this chapter underscores the critical role of understanding functional anatomy and kinesiology in spinal cord injury rehabilitation. 1. What is the relationship between the neurological level of injury, its severity, and the potential for functional training and recovery after a spinal cord injury? Which factors can lead to variations in functional outcomes among individuals with the same neurological injury level and similar ASIA Impairment Scales? The extent of functional training and recovery after a spinal cord injury is significantly influenced by the neurological level and the severity of the injury. Moreover, effective functional rehabilitation necessitates using the muscle strength of the remaining muscles or those within the zone of partial preservation beneath the neurological level of injury. It is noteworthy that even with the same neurological injury level and similar ASIA Impairment Scale, individuals may exhibit considerable functional differences in sitting, transferring, standing,

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 H.-Y. Ko, A Practical Guide to Care of Spinal Cord Injuries, https://doi.org/10.1007/978-981-99-4542-9_6

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and personal care activities. These disparities are comparable to the variations seen in the general population regarding abilities such as swimming and cycling. 2. How are expected outcomes for daily living activities estimated, and what other factors can impact these outcomes? Outcomes for daily living activities, including personal care and mobility, can be predicted based on the neurological level of injury (Consortium for Spinal Cord Medicine 1999) (Table  6.1). However, the outcome for each activity varies significantly among individuals. Although voluntary motor function greatly influences a person’s functional capacity, it is not the sole determining factor. The expected outcome is roughly established by the neurological injury level, with additional factors such as body build (e.g., short arms), individual motivation, psychological state, and environmental conditions playing a role. Consequently, it is unnecessary to rely solely on generally expected outcomes for goal-setting. 3. What is kinematics, and how does kinetics differ from kinematics? What is kinesiology and what components does it study? Kinematics, as a branch of mechanics, focuses on the study of motion for points, bodies, and systems without taking into account the physical properties and forces that influence them. This area of study is commonly referred to as the geometry of motion. In contrast, kinetics delves into the physical properties, such as mass, stiffness, and tensile or compressive strength, as well as the forces that drive the motion of these bodies or systems. Kinesiology encompasses the analysis of human movement dynamics and their various components, including anatomical, physiological, biochemical, biomechanical, neurological, neuromotor, and psychological aspects, all while interacting with the environment. To put it simply, kinesiology can be considered as the scientific investigation of human kinetics or human movement. 4. What is biomechanics? How is biomechanics related to kinesiology?

Biomechanics explores the relationship between biological systems and the mechanical forces they experience, emphasizing the connection between structure and function. To fully comprehend the workings of the musculoskeletal system, it is essential to have a thorough understanding of both biomechanics and anatomy. This knowledge can also prove beneficial in evaluating and treating patients. Familiarity with basic biomechanics is crucial for understanding certain terminologies associated with kinesiology, such as torque, moment, and moment arms (Oatis 2009). 5. What were the top priorities for tetraplegics and paraplegics in the US study, and how did the Dutch and UK study participants view the importance of hand function improvement for tetraplegics? What were the major functional recovery goals for people with spinal cord injuries in South Korea, and how did the South Korean study differ from previous studies in terms of the importance of sexual function? A study conducted in the United States using various methods, such as email, postal mail, internet, interviews, and word of mouth, found that regaining arm and hand function was the top priority for tetraplegics, while paraplegics prioritized regaining sexual function. Improvement in bladder and bowel function was a shared concern for both injury groups (Anderson 2004). Research with Dutch and UK participants revealed that 77% of tetraplegics anticipated a significant improvement in their quality of life if their hand function improved, especially among the C4, C5, C6, and C7 UK groups. This improvement was considered as important as the improvement in bladder and bowel function (Snoek et al. 2004). A South Korean survey on recovery goals for people with spinal cord injuries identified the primary objectives as regaining upper extremity function for tetraplegics and bladder and bowel function for paraplegics (Huh and Ko 2020). Previous studies have consistently

Bed Total assist

Total assist

Some assist

Some assist

Independent

Independent

Independent

Independent

NLI C1–C4

C4

C5

C6

C7–C8

T1–T9

T10–L1

L2–S5

Independent

Independent

Independent

Independent

Some assist to independent

Some to total assist

Total assist

Transfers Total assist

Table 6.1  Outcome expectations for mobility

Independent

Independent

Independent

Wheelchair (W/C) use •  Independent in power recline and/or tilt W/C with head, chin, or breath control •  Total assist in manual W/C •  Independent in power recline and/or tilt W/C with head, chin, or breath control •  Total assist in manual W/C •  Independent in power recline and/or tilt W/C with arm drive control •  Total assist to independent in manual W/C •  Independent in power W/C •  Total assist to independent depending on terrain Independent

Total assist Standing in tilt table •  Some assist to independent in standing using HKAFOs or KAFOs •  Not typical of walking using HKAFOs or KAFOs and bilateral Lofstrands or walker •  Independent in standing using KAFOs •  Some assist to independent in walking using KAFOs and bilateral Lofstrands or walker •  Functional ambulation with KAFOs or AFOs and Lofstrand(s) or cane(s)

Total assist Standing in tilt table

Total assist Standing in tilt table

Total assist Standing in tilt table

Standing/walking Total assist Standing in tilt table

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6  Kinematics-Related Understanding for Enhancing Extremity Muscle Functionality After Spinal Cord…

highlighted the importance of restoring upper extremity function, sexual function, and bladder and bowel function (Anderson 2004; Estores 2003; Hanson and Franklin 1976; Simpson et  al. 2012). However, the South Korean study indicated that sexual function was considered less important. 6. What are the two basic types of motion, and how does translation differ from rotation? What are degrees of freedom, and how many can a joint have? How is the axis of rotation related to a joint? Two fundamental types of motion exist: translation and rotation. Translation results in linear movement within the body. In contrast, rotation involves motion around an axis, causing points on the rotating body to travel varying distances depending on their proximity to the point of rotation. Degrees of freedom represent the number of possible angular motions at a joint. A joint can possess up to three degrees of freedom, corresponding to the three cardinal planes (sagittal, frontal or coronal, and horizontal or transverse planes). Each rotational motion in these cardinal planes comprises six degrees of freedom (Fig.  6.1). The movement of a

joints or body parts along the degrees of freedom is centered at the fulcrum of the angular motion, known as the axis of rotation. This axis of rotation is either within or very close to the joint (Oatis 2017). 7. What are open and closed kinetic chains in the context of physical rehabilitation, and how do they differ in terms of the movement of the distal and proximal segments of a kinetic chain? The concepts of open and closed kinetic chains are frequently used in physical rehabilitation to describe relative segment kinetics. The terms “open” and “closed” indicate whether the distal end of an extremity is attached to the ground or another stationary object. An open kinetic (or kinematic) chain refers to a situation where the distal segment of a kinetic chain is not fixed to the ground or another stationary object, allowing the distal segment to move freely (Fig.  6.2a). In contrast, a closed kinetic chain occurs when the distal segment of the kinetic chain is fixed to the ground or another stationary object, ­leaving the proximal segment free to move (Neumann 2010) (Fig. 6.2b). b

y

y

x

y

x

z

y

x

z

Fig. 6.1  Degrees of freedom of movement. (a) An object moving in two-dimensional space has up to three degrees of freedom, including translation along the x and y axes and rotation in the plane of the two axes about the z axis.

z

x

z

(b) An object moving in three-dimensional space has up to six degrees of freedom, including translation along the x, y, and z axes and rotation about the three axes. (Adapted from Oatis (2017))

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105

b

a

Fig. 6.2  Sagittal plane motion at the knee demonstrates the kinematics of (a) distal-on-proximal segment kinematics and (b) proximal-on-distal segment. (Adapted from Neumann (2010))

8. How do open and closed kinetic chains related to upper extremity movements in tetraplegic individuals? In what ways can closed kinetic chain kinematics benefit individuals with C5 or C6 spinal cord injuries? What is the primary barrier to achieving independence in daily activities for high tetraplegics? Typically, upper extremity movements involve distal-on-proximal segment kinetics. For instance, when standing upright with an arm at your side and a free hand, you can flex your elbow without moving adjacent joints. However, during a push-up, elbow flexion requires simultaneous wrist and shoulder movements. In the first case, the elbow moving in isolation is part of an open chain, while during a push-up, it functions as part of a closed kinetic chain. This is considered a closed kinetic chain condition because the moving joints of the upper extremity are positioned between the relatively immovable loads of the body and the ground. Movement at any joint in the closed kinetic chain impacts movement at adjacent joints. During pinching, the thumb and fingers operate in a

closed kinetic chain, with each digit’s distal end fixed. Joints and muscles adapt in various ways to maintain thumb-finger contact and support the object (Neumann 2010; Oatis 2017). Extending the elbows during transfer activities in C5 or C6 tetraplegics exemplifies closed kinetic motion of proximal-­ on-distal segment kinetics. Applying closed kinetic chain kinematics to individuals with spinal cord injuries can aid in pressure relief, transfers, and wheelchair propulsion for those with injuries as high as C5 or C6. The primary barrier to achieving independence in daily activities for high tetraplegics is the lack of active antigravity muscle strength for elbow extension. The anterior deltoid, biceps, and brachialis muscles, all innervated by the C5 and/or C6 segments, are employed in a closed kinetic chain to convert elbow and shoulder flexion motion into elbow extension motion when the hand is fixed to the wheelchair’s handrim by friction or to the floor (Little et  al. 2000; Karandikar and Vargas 2011). This motion mechanism does not involve active triceps extension but rather a substitution of muscles

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with intact innervation capable of elbow extension in a closed chain system (Fig. 6.3). 9. What are the different classes of levers in the human body, and how do they function? How do rigid lever systems and their classification as first, second, and third-­ class levers explain joint motion in the human body, and how do the mechanical advantage and the ratio of the muscle and resistive moment arms of each lever class affect the function of the musculoskeletal system? Joint motion can be described through rigid lever systems. Bony levers in the body experience torques produced by internal and external forces (Neumann 2010). The fulcrum, or the pivot point around which movement occurs, is usually the center of a joint between two articulating bones. The lever system also includes two arms or distances from the fulcrum that work against each other during movement (Sliwinski and Druin 2008). Fulcra are typically located at the joints, and the load can be body weight or

Fig. 6.3  Substitution for elbow extension utilizing closed kinetic chain kinematics. Adduction of the humerus and supination of the forearm result in extension of the elbow joint. (Adapted from Somers (2010))

external resistance, with the force often generated by muscular effort (Palastanga et  al. 2002). Levers are categorized as first, second, or third class based on the arrangements of the fulcrum, load, and force arms. 10. What are examples of first-, second-, and third-class levers in the human body? First-class levers have the fulcrum between the load and force arms, with its axis of rotation between the opposing forces. An example of a first-class lever in the body is the head-and-neck extensors, which manage the head’s posture in the sagittal plane. Second-class levers have the fulcrum at one end and the force applied at the other, with the load between them. The calf muscles employ a second-class lever to generate the torque needed to stand on tiptoes, with the fulcrum in the metatarsophalangeal joints. Second-class levers are rare in the musculoskeletal system. Third-class levers have the fulcrum at one end of a bone, the load at the other, and the force applied between them. Elbow flexor muscles utilize a third-class lever to produce the flexion torque required to support the forearm and hand. This type of lever is the most common in the musculoskeletal system (Neumann 2010; Palastanga et al. 2002) (Fig. 6.4). All human body movements rely on the interplay of these three lever classes. Analyzing the human body’s structure involves understanding the relationship between joints, muscle attachments, and the load to be moved, leading to a grasp of functional anatomy and human movement (Palastanga et al. 2002). 11. How does the mechanical advantage of the lever system relate to the musculoskeletal system, and how can it be utilized in patients with spinal cord injuries? The mechanical advantage of a lever is the ratio of the muscle (internal moment arm) and resistive moment arms (external moment arm). Depending on the fulcrum’s location, the mechanical advantage is always greater than one for a second-class lever and less than one for a third-class lever. A first-­

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a

b

c

Fig. 6.4  Illustration of classes of levers. (a) First-class lever showing the forces on both sides of the fulcrum. (b) Second-class lever showing the muscle or internal force having greater leverage than the external force because it is

further from the pivot, but both forces are on the same side of the fulcrum. (c) Third-class lever showing the muscle or internal force closer to the axis of rotation than the external force. (Adapted from Standring (2016), with permission)

class lever can have a mechanical advantage equal to, less than, or greater than one. Most muscles in the musculoskeletal system function with a mechanical advantage much less than one, which may be a mechanical disadvantage. For instance, the biceps at the elbow, the quadriceps at the knee, and the supraspi-

natus and deltoids at the shoulder are attached to bone relatively close to the joint’s axis of rotation (Neumann 2010; Oatis 2017). The human body’s musculoskeletal system mainly comprises a third-class lever mechanism, so the mechanical advantage provided by effect muscles is less than one. Therefore,

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6  Kinematics-Related Understanding for Enhancing Extremity Muscle Functionality After Spinal Cord…

strengthening effect muscles should be emphasized as an internal force to perform effective activities using muscles proximal to the neurological level of injury in patients with spinal cord injuries. The first-class lever system is rare in the musculoskeletal system, but standing or forward-leaning transfer activities can be effectively performed with the first-class lever of the head-and-neck and trunk. 12. What are the three types of muscle contractions, and how do they differ from each other? How does the internal and external torque relate to each type of muscle contraction? What is an example of an eccentric contraction in everyday life? Muscle contractions can take place in three distinct ways: isometric, concentric,

and eccentric. During isometric contractions, muscles generate force while maintaining a constant length (Fig.  6.5). In this case, the internal torque at the joint equals the external torque, resulting in no muscle shortening or joint rotation. Concentric contractions involve the muscle generating force as it shortens. Here, the internal torque surpasses the external torque, leading to muscle contraction and joint rotation in the direction of the activated muscle. Lastly, eccentric contractions occur when a muscle generates active force while lengthening. In this situation, the external torque around the joint is greater than the internal torque. An example of this is slowly lowering a cup of water onto a table, where the activated biceps muscle elongates to control the descent. The triceps muscle, typically considered an elbow exten-

Fig. 6.5  Different types of muscle actions. Isometric muscle action occurs when the muscle tension generates no change in joint position. Concentric muscle action

occurs when the tension shortens the muscle. Eccentric muscle action occurs when the muscle lengthens under an external force. (Adapted from Hamill et al. (2015))

6  Kinematics-Related Understanding for Enhancing Extremity Muscle Functionality After Spinal Cord…

sor, is likely inactive during this motion (Hamill et al. 2015; Neumann 2010). 13. How are the origin and insertion points of a muscle defined? In the study of anatomy, a muscle’s origin and insertion points are defined by their relative mobility. The origin site is typically less mobile than the insertion site, while the insertion site is generally more mobile than the origin. The muscle’s movement and function can vary the joint movement between its origin and insertion, depending on which site is being stabilized. A muscle can either move a segment on one end of its attachment or two segments on both ends of its attachment. Most muscles only cross one joint, so their primary action occurs at that specific joint. For instance, the soleus muscle is a plantar flexor of the ankle and can also force the knee into extension, even though it does not cross the knee joint. When the soleus contracts, it creates plantar flexion of the ankle. If the foot is on the ground, plantar flexion movement necessitates extension of the knee joint as the soleus pulls backward on the proximal tibia.

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joint muscle is influenced by the body’s position and the muscle’s interaction with external objects, such as the ground. For example, the rectus femoris mainly ­contributes to knee extension due to the position of the hip joint, limiting its action and effectiveness in producing hip flexion (Hamill et al. 2015; Rasch and Burke 1971). In another case, the biceps brachii generates little force when sufficiently shortened during simultaneous elbow and shoulder flexion, while shoulder extension increases the biceps contraction strength during elbow flexion (Oatis 2017). 15. What are passive and active insufficiency in the context of two-joint muscles? A two-joint muscle’s function can be restricted at specific joint positions. Passive insufficiency refers to the restriction of a two-joint muscle’s elongation, occurring when the antagonistic muscle can no longer be elongated, and the full range of motion cannot be achieved. Tight hamstrings preventing a full range of motion in knee extension is an example of passive insufficiency. Active insufficiency, on the other hand, inhibits a two-joint muscle’s contraction when it becomes slackened to the point of losing its ability to generate maximum tension. For instance, finger flexors cannot produce maximum force in a grip when they are shortened by a concurrent flexion movement of the wrist (Hamill et al. 2015).

14. What is a two-joint muscle, and what are some examples? How does the position of the body and interaction with external objects affect the action of a two-joint muscle? A two-joint muscle is unique in that it crosses two joints and generates multiple movements, often in opposing sequences. Examples of two-joint muscles in the lower 16. extremity include the gastrocnemius, rectus femoris, two-joint hamstrings, gracilis, and sartorius. In the upper extremity, the biceps brachii and long head of the triceps brachii are two-joint muscles. Several distal muscles in the human leg and arm cross more than one joint and are considered multi-joint muscles. They span not only the knee or ankle and the elbow and wrist joints but also the metatarsophalangeal or metacarpophalangeal joints and interphalangeal joints through long distal tendons and ligaments (Zatsiorsky and Prilutsky 2012). The action of a two-­

What is muscle substitution, and when does it occur? What are some methods of muscle substitution? Muscle substitution is a common occurrence in individuals with spinal cord injuries. When a muscle involved in a specific joint movement is weak or absent, other muscles that are not involved or have relatively greater strength can be utilized to substitute the motion. Various methods of substitution include tensioning other structures, such as the tenodesis grip (Fig.  6.6), using gravity (e.g., forearm pronation/supination by shoulder motion), or employing closed kinetic

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a

b

Fig. 6.6  Tenodesis grasp demonstrated with wrist extension and flexion. (a) When the wrist is extended, tension increases in the extrinsic flexor muscles that facilitate finger flexion. (b) When the wrist is flexed, tension increases in the extrinsic extensor muscles, leading to finger extension. (Adapted from https://www.physiopedia.com/ images/6/6a/Tenodesis_grasp.jpeg)

chain kinematics (e.g., locking the elbow extension for a weak triceps). Additionally, when the prime movers of joint motion are weak or absent, the secondary mover muscles can substitute the motion, such as the tensor fascia lata for a weak gluteus medius in hip abduction or anconeus and extensor carpi radialis longus for an absent triceps. 17. What is the tenodesis grip, and how does it function? What precautions should be taken for individuals with C6 spinal cord injury to maintain an effective tenodesis grip, and how should the interphalangeal joints be positioned during weight-­bearing activities? The tenodesis grip is an example of substitution using tension on nonfunctioning muscles or tendons. This reciprocal motion occurs when finger extension takes place as

Fig. 6.7  A hand in tetraplegia position, where the fingers are flexed to avoid stretching of the finger flexor muscles during weight-bearing. (Adapted from Harvey (1996))

the wrist is flexed due to increased tension on the extrinsic extensor muscles. Conversely, when the wrist extends by activating the extensor carpi radialis longus and brevis, tension increases in the extrinsic flexor muscles that flex the fingers (Lippert 2011) (Fig. 6.6). The tenodesis grip can lead to a more forceful motion than substitution using gravity (Harvey 1996). For individuals with C6 spinal cord injury, overstretching the extrinsic finger flexors should be avoided to maintain an effective tenodesis grip (Little et al. 2000). Range of motion exercises should include finger extension to neutral with the wrist fully flexed and full finger flexion with the wrist fully extended. When bearing weight on the palms in a closed kinetic chain, the interphalangeal joints should remain flexed (Fig. 6.7).

6  Kinematics-Related Understanding for Enhancing Extremity Muscle Functionality After Spinal Cord…

18. How can gravity be utilized in muscle substitution? Functional muscles of the rostral segment in spinal cord injuries can cause position changes in the distal part using gravity, such as pronation of the forearm by shoulder abduction and/or internal rotation. However, the force generated by muscle substitution through gravity is limited and can be restricted by any resistance (Somers 2010). 19. How can stabilizing the distal segment establish motion at an intermediate joint? What are the benefits of using closed kinetic chain kinematics for individuals with tetraplegia? How can the gastrocnemius and hamstring muscles assist in extending the knee when the foot is fixed to the ground? By stabilizing the distal segment, motion can be established at an intermediate joint using proximal muscles. For example, if the hands are fixed on a mat or surface, ­activating the anterior deltoid and clavicular fibers of the pectoralis major can lead to elbow extension (Gagnon et al. 2003; Mulroy et al. 2004). Individuals with tetraplegia who have triceps brachii paralysis can lift themselves by generating active shoulder flexor and adductor moments during weight-relief maneuvers and transfers (Harvey and Crosbie 2000). Using closed kinetic chain kinematics, the elbow can lock in extension while performing weight-bearing activities like push-ups and transfers when the palms are placed on a mat surface or wheelchair wheel handrim. This movement is more effective when the shoulder is externally rotated, and the forearm is supinated (Harvey and Crosbie 1999, 2000; Marciello et al. 1995; Somers 2010). In tetraplegic patients, the anterior deltoid and serratus anterior in the sagittal plane, the pectoralis major in the transverse plane, and the latissimus dorsi in the coronal plane can cause passive extension of the elbow by pulling the proximal humerus forward and adducting the proximal humerus while the distal limb is fixed (Feeko and Mallow 2015). It is crucial to avoid simultaneous extension

111

of the wrist and hand when bearing weight on the palm in a closed kinetic chain to prevent overstretching the long finger flexors. Maintain flexion of the DIP and PIP joints of the fingers when extending the elbow with the palm on the floor (Somers 2010). In the lower extremity, when the foot is fixed to the ground, the gastrocnemius and hamstring muscles can assist in extending the knee by pulling back on the distal femur and proximal tibia, respectively. 20. What are the consequences of spinal cord injury at different neurological levels? Functional mobility activities, such as transfers, wheelchair use, ambulation, and bed activity, are largely determined by the level of voluntary motor function based on the neurological level of injury. Table  6.2 summarizes the function, innervation, and consequences of spinal cord injury at different neurological levels (Mateo et al. 2015). 21. What are the motor functions of people with C4 spinal cord injuries, and what assistive devices can they use to propel a wheelchair? At the C4 level of injury, people do not have helpful voluntary motor function for transfers, and therefore, are completely dependent on others. Fully innervated trapezius (CN XI) and partially innervated rhomboids (C4, C5) and levator scapulae (C3, C4, C5) offer limited function in postural control. Individuals with C4 spinal cord injuries may use an electric power wheelchair with movements of the head, chin, tongue, or breath to propel the wheelchair in very limited cases. 22. What level of assistance is required by individuals with C5, C6, and C7 spinal cord injuries for transfers and wheelchair mobility? What are the motor functions of the muscles innervated by C5, C6, and C7, and how do they assist with pressure relief, transfers, and wheelchair skills? At the C5 level of injury, individuals are dependent on others for all transfers. However, some individuals can be indepen-

Wrist

Elbow

Shoulder glenohumeral

Joint Shoulder scapulothoracic

Flexion Flexion Extension Extension Extension Flexion Flexion

Brachialis Brachioradialis Triceps brachii Extensor carpi radialis longus and brevis Extensor carpi ulnaris Flexor carpi radialis Flexor carpi ulnaris

Subscapularis Supraspinatus Infraspinatus Teres minor Biceps brachii

Teres major

Function Protraction and upward rotation Elevation Retraction Downward rotation Depression and anterior tipping Flexion Abduction Extension Flexion/adduction/medial rotation Flexion/adduction/medial rotation Extension/adduction/medial rotation Extension/adduction/medial rotation Medial rotation Abduction Lateral rotation Lateral rotation Flexion

Muscles Serratus anterior Trapezius upper part Trapezius middle part Trapezius lower part Pectoralis minor Deltoid anterior part and coracobrachialis Deltoid medial part Deltoid posterior part Pectoralis major upper part Pectoralis major middle and lower parts Latissimus dorsi

Table 6.2  Upper limb muscles function and innervation according to neurological level of spinal cord injury

Median Ulnar

Radial Radial

Axillary Musculo-­ cutaneous

C7 C6 C7 C6 C7

C5 C5

C5

C5 C8 C6

Lateral pectoral Medial pectoral Thoracodorsal Subscapularis

C8 C5

Medial pectoral Axillary

C8 C7 C8 C7 C8

C6 C6

C6

C6 T1 C7

T1 C6

Roots C5 C6 XI

Innervation Nerve Long thoracic Accessory spinal

T1 C8

C7

C8

C7

C7

± ± ± ± ± ± ± − − − − −

− − − − − − − − − − − −

± ± − ± − ± −

± ± ± ± ±

+ + ± ± ± ± ±

± ± ± + +

±

±

−

±

C7 ± + + + − + + + ± − ±

SCI level C4 C5 C6 − ± ± + + + + + + + + + − − − − ± ± − ± ± − ± ± − ± ± − − − − − ±

+ + ± ± ± + ±

+ + + + +

+

C8 + + + + ± + + + + ± ±

+ + ± + + + +

+ + + + +

+

T1 + + + + ± + + + + ± +

112 6  Kinematics-Related Understanding for Enhancing Extremity Muscle Functionality After Spinal Cord…

From Mateo et al. (2015)

Fingers and thumb

Flexor digitorum superficialis Flexor digitorum profundus Extensor digitorum Flexor pollicis longus and brevis Extensor pollicis longus and brevis Abductor pollicis longus Abductor pollicis brevis Opponens pollicis Adductor pollicis and intrinsic Abductor digitorum minimi

Flexion Flexion Extension Flexion Extension Abduction Abduction Opposition Adduction Abduction

C7 C8 C6 C8 C7 C8 C8 T1

Median Median and ulnar Radial Median Radial Median Ulnar Ulnar

T1

T1

C8 T1 C7 T1 C8 C8

T1

− − − − − − − − − −

− − − − − − − − − −

− − ± − − − − − − − ± − ± − ± ± − − − −

± ± ± ± ± ± ± ± ± −

± ± + ± + + ± ± ± ±

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dent or require some assistance using a transfer board, overhead loops, or trapezes. They can be independent or require some assistance in propelling a manual wheelchair indoors on non-carpeted floors. They can use high-­friction or pegged handrims (handrim projection bars). However, propelling a manual wheelchair in the community may be inadequate. A pressure relief activity in the manual wheelchair using the lateral lean method is independent or may require some assistance. The muscles that enable elbow flexion include the biceps brachii (C5, C6), brachialis (C5, C6), and brachioradialis (C5, C6), which are partially innervated by C5. The deltoids (C5, C6), which are also partially innervated by C5, contribute to elbow extension through muscle substitution. The infraspinatus (C5, C6) and teres minor (C5, C6) muscles have additional functions that help lock the extended elbow in a closed kinetic chain. On the other hand, the serratus anterior (C5, C6, C7) has minimal innervation from C5 and provides only minimal function in stabilizing the scapulae against the thorax. At the C6 level of injury, individuals can be independent or require some assistance in transfers with or without a transfer board, including transfers between the wheelchair and the mat or bed. Propelling a manual wheelchair indoors on a non-carpeted level is independent. However, wheelchair mobility in the community may be insufficient. Pressure relief in the manual wheelchair by depression, forward lean, or lateral lean method is independent or requires some assistance. The fully innervated biceps brachii (C5, C6) enables stronger elbow flexion, while the deltoids (C5, C6), infraspinatus (C5, C6), teres minor (C5, C6), and clavicular part of the pectoralis major (C5, C6) provide a stronger elbow extension and lock the extended elbow by muscle substitution in NLI C6. The partially innervated serratus anterior (C5, C6, C7) stabilizes the scapulae

against the thorax, improving wheelchair propulsion and self-positioning. The minimally innervated latissimus dorsi (C6, C7, C8) and triceps brachii (C6, C7, C8) assist in shoulder girdle depression, allowing the buttocks to lift for pressure relief and to contribute to transfers and wheelchair skills. At the C7 level of injury, individuals are independent in transfers without a transfer board and between the wheelchair and the bed. Limited individuals are independent in transfers between the wheelchair and the floor using a side-approach transfer. They are independent indoors and outdoors on level terrain for long distances using a manual wheelchair. They can negotiate 1:12 ramps independently or with some assistance. Pressure relief is independent. The triceps brachii (C6, C7, C8) are partially innervated and allow for stronger elbow extension. The latissimus dorsi (C6, C7, C8) and sternocostal part of the pectoralis major (C7, C8, T1) increase the depression of the shoulder girdle, enabling stronger lifting of the buttocks for pressure relief. The serratus anterior (C5, C6, C7), fully innervated at this level of injury, provides more stability to the scapulae against the thorax and stronger protraction of the shoulders. At the C8 level of injury, most individuals can be independent in transfers between the wheelchair and the floor. They are independent in negotiating 1:12 ramps. The triceps brachii (C6, C7, C8) are fully innervated, allowing for normal strength in elbow extension. The latissimus dorsi (C6, C7, C8) and the sternocostal part of the pectoralis major (C7, C8, T1) are more innervated than in NLI C7, which provides a stronger shoulder girdle depression. The muscles, including the flexor digitorum superficialis, flexor digitorum profundus, flexor pollicis longus, and brevis, are partially or almost fully innervated by C7, C8, and T1. This allows for grasping without muscle substitution and easier handling of the legs.

References

References Anderson KD.  Targeting recovery: priorities of the spinal cord-injured population. J Neurotrauma. 2004;21:1371–83. Consortium for Spinal Cord Medicine. Outcomes following traumatic spinal cord injury: clinical practice guidelines for health-care professionals. Washington, DC: Paralyzed Veterans America; 1999. Estores IM.  The consumer’s perspective and the professional literature: what do persons with spinal cord injury want? J Rehabil Res Dev. 2003;40(4 Suppl 1):93–8. Feeko KJ, Mallow M. Kinesiology. In: Maitin IB, editor. Current diagnosis & treatment. Physical medicine & rehabilitation. New  York: McGraw-Hill Education; 2015. Gagnon D, Nadeau S, Gravel D, et  al. Biomechanical analysis of a posterior transfer maneuver on a level surface in individuals with high and low-level spinal cord injuries. Clin Biomech. 2003;18:319–31. Hamill J, Knutzen KM, Derrick TR. Biomechanical basis of human movement. 4th ed. Philadelphia: Wolters Kluwer; 2015. Hanson RW, Franklin MR. Sexual loss in relation to other functional losses for spinal cord injured males. Arch Phys Med Rehabil. 1976;57:291–3. Harvey L.  Principles of conservative management for a non-orthotic tenodesis grip in tetraplegics. J Hand Ther. 1996;9(3):238–42. Harvey LA, Crosbie J.  Weight bearing through fixed upper limbs in quadriplegics with paralyzed triceps brachia muscles. Spinal Cord. 1999;37:780–5. Harvey LA, Crosbie J.  Biomechanical analysis of a weight-bearing maneuver in C5 and C6 quadriplegia. Arch Phys Med Rehabil. 2000;81:500–5. Huh S, Ko HY. Recovery target priorities of people with spinal cord injuries in Korea compared with other countries: a survey. Spinal Cord. 2020;58:998–1003. Karandikar N, Vargas OO.  Kinetic chains: a review of the concept and its clinical applications. PM R. 2011;3:739–45. Lippert LS.  Clinical kinesiology and anatomy. 5th ed. Philadelphia: D. A. Davis; 2011. Little JW, Goldstein B, Hammond MC.  Spinal cord injury rehabilitation. In: Belandres PV, Dillingham

115 TR, editors. Rehabilitation of the injured combatant. Washington, DC: Department of the Army; 2000. Marciello MA, Herbison GJ, Cohen ME, et  al. Elbow extension using anterior deltoids and upper pectorals in spinal cord-injured subjects. Arch Phys Med Rehabil. 1995;70:426–32. Mateo S, Roby-Brami A, Reilly KT, et  al. Upper limb kinematics after cervical spinal cord injury: a review. J Neuroeng Rehabil. 2015;12:9. Mulroy SJ, Farrokhi S, Newsam CJ, et al. Effects of spinal cord injury level on the activity of shoulder muscle during wheelchair propulsion: an electromyographic study. Arch Phys Med Rehabil. 2004;85:925–34. Neumann DA, editor. Kinesiology of the musculoskeletal system: foundations for rehabilitation. 2nd ed. St. Louis: Mosby; 2010. Oatis CA. Kinesiology. The mechanics and pathomechanics of human movement. 3rd ed. Philadelphia: Wolter Kluwer; 2017. Oatis CA. Kinesiology: the mechanics and pathomechanics of human movement, 3rd ed. Philadelphia: Wolters Kluwer; 2009. Palastanga N, Field D, Soames R.  Anatomy and human movement. Structure and function. 4th ed. Oxford: Butterworth-Heinemann; 2002. Rasch PJ, Burke RK. Kinesiology and applied anatomy. The science of human movement. 4th ed. Philadelphia: Lea & Febiger; 1971. Simpson LA, Eng JJ, Hsieh JT, et al. The health and life priorities of individuals with spinal cord injury: a systematic review. J Neurotrauma. 2012;29:1548–55. Sliwinski MM, Druin E. Intervention principles and position changes. In: Sisto SA, Druin E, Sliwinski MM, editors. Spinal cord injuries: management and rehabilitation. 1st ed. St. Louis: Mosby; 2008. Snoek GJ, IJzerman MJ, Hermens HJ, et al. Survey of the needs of patients with spinal cord injury: impact and priority for improvement in hand function in tetraplegics. Spinal Cord. 2004;42:526–32. Somers MF. Spinal cord injury: functional rehabilitation. 3rd ed. New York: Pearson; 2010. Standring S, editor. Gray’s anatomy. 41st ed. Philadelphia: Elsevier; 2016. Zatsiorsky VM, Prilutsky BI.  Biomechanics of skeletal muscles. Champaign: Human Kinetics; 2012.

7

Essential Laboratory Tests for Managing Spinal Cord Injuries

Abstract

This chapter aims to emphasize the importance of laboratory testing in the management of spinal cord injuries and related disorders. Laboratory tests are essential diagnostic tools that can confirm diagnoses, assess the progression of the disease, and guide the treatment plan. Physicians who manage spinal cord injuries need to be aware of the various laboratory tests required for general medical management, as well as specific complications related to spinal cord injuries, such as bladder and bowel dysfunction, electrolyte imbalances, endocrine changes, wound care, autonomic dysfunction, sexual dysfunction, and metabolic disorders. The chapter provides a comprehensive review of the essential laboratory tests used in the diagnosis and management of spinal cord injuries and disorders. It discusses the clinical implications of basic laboratory tests and their applications in the diagnosis of various medical complications and assessment of pathological processes in spinal cord injuries and disorders. By understanding the role of laboratory tests, physicians can provide better management and care for patients with spinal cord injuries. 1. Why is the utilization of laboratory tests important in the management of patients with spinal cord injuries, and what medical issues associated with spinal cord injuries require a thorough diagnostic process,

including laboratory tests? Why is it imperative for physicians to be knowledgeable about relevant diagnostic tests for metabolic disorders in individuals with spinal cord injuries? The diagnosis and management of spinal cord injuries require the use of laboratory tests in addition to a comprehensive medical history and physical examination. Laboratory tests provide important supplementary information about the patient’s condition and response to therapy that may not be evident through the medical history and physical examination alone. Physicians must be familiar with the diagnostic tools and tests required for general medical management, as well as special diagnostic tools and tests relevant to spinal cord injuries and disorders. These conditions often include bladder and bowel dysfunction, sexual problems, autonomic dysfunction, electrolyte changes, endocrinologic changes, and wound care or pressure injury management, which require a thorough diagnostic process including laboratory tests to prevent delays in rehabilitation. Additionally, due to the increased life expectancy and higher prevalence of metabolic disorders in individuals with spinal cord injuries, physicians must be knowledgeable about relevant diagnostic tests for conditions such as obesity, hypertension, and diabetes.

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 H.-Y. Ko, A Practical Guide to Care of Spinal Cord Injuries, https://doi.org/10.1007/978-981-99-4542-9_7

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2. How does posture affect plasma volume measurement and laboratory values, and what are the other factors that can affect derived laboratory values? Proper patient posture is crucial for accurate plasma volume measurement, as it can significantly affect test results. Prolonged supine positioning can lead to a 12–15% increase in plasma volume, while changes in posture, such as transitioning from supine to upright position, can alter laboratory values, including an increase in hemoglobin, red blood cell count, hematocrit, calcium, potassium, phosphorus, aspartate aminotransferase (AST), phosphatases, total protein, albumin, cholesterol, and triglycerides. Conversely, moving from an upright position to a supine one can result in an increase in hematocrit, calcium, total protein, and cholesterol. Additionally, applying a tourniquet for more than 1 min can lead to changes in laboratory values, including an increase in protein (5%), iron (6.7%), AST (9.3%), and cholesterol (5%), and a decrease in potassium (6%) and creatinine (2–3%). Other factors that may impact test results include age, gender, race, environment, diurnal variations, food and beverage intake, fasting or postprandial state, drug use, and exercise. Physicians should be aware of these variables when interpreting laboratory results for patients with spinal cord injuries (Fischbach and Dunning III 2015). 3. What is the primary difference between traditional U.S. units and the International System of Units (SI)? In which domains are SI units increasingly becoming the standard? The primary difference between traditional U.S. units and the International System of Units (SI) is the measurement units employed for various quantities. In the U.S. system, length is measured using inches, feet, yards, and miles, whereas the SI system employs meters. Likewise, the U.S. system measures mass in ounces, pounds, and tons, while the SI system uses grams and kilograms. The SI system is increasingly becom-

ing the standard for scientific and technical applications, while the traditional U.S. units continue to be prevalent in everyday life and certain industries. 4. How are SI concentrations expressed differently than traditional units? How can one convert between SI units and traditional U.S. units? Numerous professional organizations are shifting clinical laboratory data from traditional units to SI units. Consequently, much data is now available in both systems. For example, SI concentrations are expressed as amount per volume (moles or millimoles per liter) instead of mass per volume (grams, milligrams, milliequivalents per deciliter, milliliters, or liters). The numerical values between the two systems may be the same or different. For instance, the value for chloride remains constant at 95–105  mEq/L (traditional unit) and 95–105  mmol/L (SI unit). Clinical laboratory data may be reported using traditional units, SI units, or both, with conversion tables presented in Table 7.1. To convert from SI units to traditional U.S. units, divide by the conversion factor; conversely, to convert from traditional U.S. units to SI units, multiply by the factor. For instance, to convert a digoxin level of 0.6  nmol/L (SI unit), divide by 1.281 to obtain 0.5 ng/dL in traditional units. To convert a Ca2+ value of 8.6  mg/dL (traditional unit), multiply by 0.2495 to achieve 2.15  mmol/L in SI units (Fischbach and Dunning III 2015). 5. What information does the Complete Blood Cell Count (CBC) provide? Which parameters are included in the RBC, WBC, and platelet evaluations of the CBC test? The Complete Blood Cell Count (CBC) is a frequently requested laboratory test that offers vital information about the composition and concentration of various cell types in the blood, such as red blood cells (RBCs), white blood cells (WBCs), and platelets. The CBC test consists of a thorough evaluation of

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7  Essential Laboratory Tests for Managing Spinal Cord Injuries Table 7.1  Examples of conversion between conventional units and SI units Present reference System intervals Serum 5–40

Present unit U/L

Conversion factor 1.00

SI reference intervals 5–40

SI unit symbol U/L

Serum Serum Serum

3.9–5.0 35–110 5–40

g/dL U/L U/L

10 0.01667 0.01667

39–50 0.6–1.8 0.08–0.67

g/L μkat/L μkat/L

0–0.2 0.1–1.2 8.6–10.3 22–30 98–108

mg/dL mg/dL mg/dL mEq/L mEq/L

17.10 17.10 0.2495 1.00 1.00

0–4 2–20 2.15–2.57 22–30 98–108

μmol/L μmol/L mmol/L mmol/L mmol/L