3.2 Spinal Cord Injury Syndromes
Key Takeaways
- 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.
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 |
An 72-year-old male with a history of cervical spondylosis trips over a rug and sustains a cervical hyperextension injury. Physical examination reveals 2/5 motor strength in the intrinsic hand muscles and wrist flexors, 4/5 motor strength in the hip flexors and knee extensors, and patchy sensory loss across the upper extremities. Lower extremity sensation, light touch, and proprioception are preserved. What is the most likely diagnosis?
A 34-year-old female presents with acute paraplegia following a flexion-compression fracture of T12. Examination reveals complete loss of motor function and loss of pinprick and temperature sensation bilaterally below the L1 dermatome. However, her joint position sense and vibration perception are completely intact in both lower extremities. Dysfunction of which blood vessel is responsible for this clinical presentation?
A 45-year-old male presents following a large L4-L5 central disc herniation. He reports severe, asymmetrical right leg pain, lower extremity weakness, and numbness around his groin. Physical examination reveals asymmetric flaccid weakness of ankle dorsiflexors and plantarflexors, absent right Achilles reflex, and asymmetric saddle anesthesia. Voluntary anal sphincter tone is diminished. Which feature best distinguishes Cauda Equina Syndrome from Conus Medullaris Syndrome in this scenario?