3.2 Spinal Cord Injury Syndromes

ABPMR Physical Medicine and Rehabilitation Board Exam Study Guide Exam

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1 Chapter 1: Introduction & Exam Overview

1.1 ABPMR Part I Exam Overview & Format 1.2 Board Review Strategy & Content Blueprint Breakdown

2 Chapter 2: Musculoskeletal Medicine

2.1 Shoulder & Upper Extremity Diagnostics 2.2 Knee, Hip & Lower Extremity Conditions 2.3 Spine Pathology, Radiculopathy & Myelopathy 2.4 Inflammatory Arthritis, Tendinopathies & Concussion 2.5 Bone Health, Osteoporosis & Metabolic Bone Disease 2.6 Thoracic Outlet Syndrome & Peripheral Nerve Entrapment 2.7 Fracture Rehabilitation & Immobilization Complications 2.8 Overuse Tendinopathies & Regenerative Medicine 2.9 Gait Analysis & Abnormal Gait Patterns

3 Chapter 3: Spinal Cord Injury Rehabilitation

3.1 ASIA Examination & Impairment Scale 3.2 Spinal Cord Injury Syndromes 3.3 Autonomic Dysreflexia & Acute Complications 3.4 Neurogenic Bladder, Bowel & Secondary Complications

4 Chapter 4: Stroke & Neuromuscular Rehabilitation

4.1 Stroke Vascular Syndromes & Acute Assessment 4.2 Stroke Motor Recovery & Hemiplegic Complications 4.3 Spasticity Assessment & Multimodal Management 4.4 ALS, GBS, CIDP & Neuromuscular Disease Rehab 4.5 Multiple Sclerosis & Demyelinating Disease Rehabilitation 4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder

5 Chapter 5: Electrodiagnostics (EMG/NCS)

5.1 Nerve Conduction Studies Principles & Physics 5.2 Needle Electromyography & MUAP Analysis 5.3 Mononeuropathies & Radiculopathy Patterns 5.4 Neuromuscular Junction Disorders & Myopathies

6 Chapter 6: Traumatic Brain Injury

6.1 TBI Severity Classification, Glasgow Coma Scale, and Pathophysiology 6.2 Rancho Los Amigos Levels of Cognitive Functioning and Disability Rating Scale 6.3 Neurobehavioral Sequelae and Agitation Management 6.4 Concussion Evaluation, Vestibular-Ocular Dysfunction, and Return-to-Play/Work Protocols

7 Chapter 7: Chronic Pain & Interventional Spine

7.1 Fluoroscopic Spine Interventions 7.2 Opioid Stewardship & Controlled Substance Compliance 7.3 Complex Regional Pain Syndrome, Fibromyalgia & Myofascial Pain 7.4 Spinal Cord Stimulation & Intrathecal Therapy

8 Chapter 8: Amputee Rehabilitation & Prosthetics

8.1 Amputation Surgical Levels & Medicare K-Levels 8.2 Socket Designs & Suspension Systems 8.3 Prosthetic Feet & Microprocessor Knee Mechanisms 8.4 Post-Amputation Care, Residual Limb & Phantom Pain

9 Chapter 9: Pediatric Rehabilitation

9.1 Cerebral Palsy Classification & GMFCS 9.2 Spina Bifida & Myelomeningocele Management 9.3 Muscular Dystrophies & Neuromuscular Disease in Children 9.4 Pediatric Brachial Plexopathy & Congenital Disorders

10 Chapter 10: Prosthetics, Orthotics & Assistive Technology

10.1 Lower Limb Orthoses — AFOs & KAFOs 10.2 Spinal & Upper Extremity Orthoses 10.3 Upper Limb Prosthetics — Body-Powered vs Myoelectric 10.4 Wheelchairs, Seating Systems & Pressure Mapping

11 Chapter 11: Medical Rehabilitation & Outcomes

11.1 Dysphagia Assessment & Management 11.2 Neurogenic Bladder & Bowel Management 11.3 Pressure Injuries & Wound Management 11.4 Outcome Measures & Medical Complications 11.5 Cancer Rehabilitation & Oncologic Rehabilitation 11.6 Burns, Endocrine/Metabolic & Medical Complications Rehabilitation

12 Chapter 12: Cardiopulmonary Rehabilitation

12.1 Cardiac Rehabilitation Phases & Metabolic Equivalents 12.2 Pulmonary Rehabilitation & COPD Management

13 Chapter 13: Foundational Rehabilitation Concepts

13.1 Kinesiology, Biomechanics & Functional Anatomy 13.2 Rehabilitation Pharmacology & Medication Management 13.3 Research Methodology, Biostatistics & Evidence-Based Practice 13.4 Nutrition, Metabolism & Energy Expenditure in Rehabilitation 13.5 Diagnostic Procedures: Imaging, MSK Ultrasound, Urodynamics & Neuropsych Assessment

3.2 Spinal Cord Injury Syndromes

Key Takeaways Explain This Topic AI

Incomplete SCI syndromes present with characteristic neuroanatomical patterns based on the selective vulnerability of spinal tracts.

Central Cord Syndrome is the most common incomplete SCI, typically resulting from cervical hyperextension injuries in elderly individuals with spondylosis, causing upper extremity weakness greater than lower extremity weakness.

Anterior Cord Syndrome involves anterior spinal artery occlusion or anterior compression, causing bilateral motor loss and pain/temperature loss while sparing dorsal column vibration and proprioception.

Brown-Séquard Syndrome results from cord hemisection, producing ipsilateral motor and vibration/proprioception loss with contralateral pain/temperature loss starting 1-2 dermatomes below the lesion.

Cauda Equina Syndrome involves LMN compression of nerve roots below the conus, causing asymmetric flaccid paresis, areflexia, and severe radicular pain, whereas Conus Medullaris Syndrome presents with mixed UMN/LMN signs and early bowel/bladder incontinence.

Last updated: July 2026

3.2 Spinal Cord Injury Syndromes

Incomplete spinal cord injury (SCI) syndromes exhibit distinct clinical features reflecting the anatomical organization of pathways within the spinal cord. Recognizing these clinical syndromes allows physiatrists to localize spinal cord lesions, predict functional recovery, and tailor multidisciplinary rehabilitation programs. On the ABPMR board examination, clinical vignettes frequently present specific combinations of motor, sensory, and autonomic deficits requiring prompt identification of the underlying spinal syndrome.

Central Cord Syndrome

Central Cord Syndrome (CCS) is the most prevalent incomplete SCI syndrome, accounting for approximately 70% of incomplete cervical cord injuries.

Etiology & Mechanism of Injury

Mechanism : Classically occurs following low-energy hyperextension trauma to the cervical spine in elderly individuals with pre-existing cervical spondylosis, canal stenosis, or osteophytosis. It can also occur in younger individuals secondary to high-energy trauma (e.g., motor vehicle accidents, diving injuries).

Pathophysiology : Hyperextension causes pinching of the spinal cord between anterior osteophytes and the posterior ligamentum flavum. Buckling of the ligamentum flavum produces central cord edema, hemorrhage, and axonal disruption primarily affecting the gray matter and medially situated white matter tracts.

Clinical Presentation

Motor Deficits : Upper extremity weakness is significantly greater than lower extremity weakness ("hands worse than feet"). This pattern occurs because the corticospinal tract is somatotopically organized, with cervical fibers located medially and sacral fibers situated laterally.

Sensory Deficits : Variable sensory loss below the level of injury, often with a suspended sensory cape-like distribution of pain and temperature impairment across the shoulders and upper chest.

Sphincter Function : Sacral sparing is characteristic. Urinary retention or neurogenic bladder dysfunction is common acutely but often recovers.

Functional Prognosis

Prognosis for functional recovery is fair to good . Approximately 75-80% of patients regain independent ambulation because lateral corticospinal tract fibers supplying the lower extremities are spared.

Distal upper extremity and fine motor hand function recover last and least completely due to permanent damage to central gray matter motor neurons and medial corticospinal fibers.

Anterior Cord Syndrome

Anterior Cord Syndrome represents the incomplete SCI syndrome with the poorest functional prognosis.

Etiology & Neuroanatomy

Mechanism : Flexion-compression injuries of the cervical spine, burst fractures with retropulsed bone fragments, acute anterior disc herniations, or ischemia/infarction within the territory of the anterior spinal artery (ASA) .

Vascular Anatomy : The single anterior spinal artery supplies the anterior two-thirds of the spinal cord, including the lateral corticospinal tracts, lateral spinothalamic tracts, and anterior horns.

Clinical Presentation

Bilateral Motor Paralysis : Complete motor loss below the level of injury due to bilateral corticospinal tract disruption.

Bilateral Pain & Temperature Loss : Complete loss of pain, temperature, and crude touch sensation below the lesion due to lateral spinothalamic tract disruption.

Preserved Sensation : Dorsal column function (light touch, vibration, and joint position sense/proprioception) is completely preserved because the posterior one-third of the cord is supplied independently by the paired posterior spinal arteries.

Functional Prognosis

Poorest functional recovery among incomplete syndromes; only 10-20% of patients regain functional ambulation. Spontaneous motor recovery below the lesion is minimal.

Brown-Séquard Syndrome (Spinal Hemisection)

Brown-Séquard Syndrome results from true or functional hemisection of the spinal cord.

Etiology

Most commonly caused by penetrating trauma (e.g., stab wounds or gunshot wounds). Less common non-traumatic causes include lateral extramedullary tumors, spinal epidural hematomas, or lateral herniated cervical discs.

Clinical Presentation & Neuroanatomy

Ipsilateral Motor Loss : Flaccid paralysis at the level of lesion (anterior horn cell injury) and spastic paresis below the lesion due to lateral corticospinal tract interruption.

Ipsilateral Vibration & Proprioception Loss : Impaired dorsal column function below the level of injury.

Contralateral Pain & Temperature Loss : Impaired lateral spinothalamic tract function beginning 1 to 2 dermatomes below the level of the lesion . This lag occurs because spinothalamic second-order neurons ascend 1-2 spinal segments in Lissauer's tract before decussating across the anterior white commissure.

Functional Prognosis

Best functional prognosis of all incomplete SCI syndromes. Over 90% of patients regain independent ambulation, bowel/bladder continence, and functional independence in activities of daily living (ADLs).

Conus Medullaris vs. Cauda Equina Syndrome

Differentiating Conus Medullaris Syndrome from Cauda Equina Syndrome is a classic ABPMR board topic. Conus Medullaris Syndrome involves injury to the terminal spinal cord (sacral cord segments and lumbar roots), whereas Cauda Equina Syndrome involves compression of lumbosacral nerve roots within the spinal canal below the termination of the spinal cord (conus medullaris at L1-L2).

Clinical Feature Conus Medullaris Syndrome Cauda Equina Syndrome
Anatomical Site Terminal cord (T12-L2 vertebral level) Lumbosacral nerve roots (below L2 vertebral level)

Neurological Character Mixed Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) Pure Lower Motor Neuron (LMN)

Onset Sudden, bilateral, and symmetric Gradual, unilateral or asymmetric

Motor Deficit Symmetric lower extremity weakness; mild to moderate Asymmetric flaccid lower extremity weakness; marked at lower root levels

Reflexes Hyperreflexic or intact Achilles reflexes; extensor plantar response (Babinski) Areflexic/hyporeflexic patellar and Achilles reflexes; absent Babinski

Sensory Deficit Symmetric perianal "saddle" anesthesia (S3-S5) Asymmetric saddle anesthesia; radicular pain along root distributions

Radicular Pain Uncommon or mild; prominent bilateral symmetrical low back pain Severe, sharp, radiating radicular pain into buttocks and legs

Bowel & Bladder Early, severe urinary retention and fecal incontinence (areflexic/hyperreflexic bladder) Late onset of urinary retention and overflow incontinence

Sexual Function Frequent early erectile dysfunction and loss of ejaculation Impaired erection/ejaculation; variable severity