Spinal Cord Tracts and Syndromes

Ascending Sensory Tracts

• Dorsal Column-Medial Lemniscus pathway: Transmits fine touch, vibration, and proprioception via first-order neurons that synapse in medulla (fasciculus gracilis for lower body, cuneatus for upper body); ipsilateral deficit below the lesion; decussates in medulla
• Spinothalamic tract: Transmits pain and temperature via first-order neurons synapsing in dorsal horn (substantia gelatinosa), with second-order neurons crossing immediately within 1-2 spinal levels; contralateral deficit with crossed pattern (body on opposite side, face on same side if brainstem involved)
• Spinocerebellar tracts (anterior and posterior): Transmit unconscious proprioception for coordination; ipsilateral deficits affect gait and coordination

Descending Motor Tracts

• Corticospinal tract: Primary motor pathway carrying ~90% of descending motor fibers from motor cortex; crosses in medullary pyramids (90%) or crosses at spinal cord level (10%); contralateral weakness below lesion; upper motor neuron signs (hyperreflexia, spasticity, Babinski sign)
• Rubrospinal tract: Facilitates flexor tone and assists corticospinal function; damage produces relative weakness in extensors
• Vestibulospinal and reticulospinal tracts: Maintain postural tone and balance; ipsilateral effects on axial musculature

Mechanisms of Injury

• Demyelination: Loss of myelin sheath disrupts action potential propagation; reversible if oligodendrocytes survive
• Axonal transection: Permanent loss of axons causes irreversible motor and sensory deficits; partial transection allows some functional recovery via plasticity
• Ischemia: Spinal cord has watershed zones (mid-thoracic region most vulnerable); anterior spinal artery occlusion causes anterior cord syndrome
• Inflammation and edema: Disrupts ion gradients and increases intracranial pressure within dura; early intervention reduces secondary injury

Complete Spinal Cord Transection (Complete SCI)

• Total loss of motor, sensory, and autonomic function below the level of injury
• Spinal shock phase: Initial flaccid paralysis, absent reflexes, loss of sensation (lasts hours to weeks); progresses to spasticity in upper motor neuron distribution
• Autonomic dysfunction: Bowel/bladder incontinence, temperature dysregulation, orthostatic hypotension
• Sensory level clearly demarcates injury (e.g., intact sensation at T4, absent below)

Incomplete Spinal Cord Syndromes

Central Cord Syndrome

• Mechanism: Damage to central gray matter and crossing spinothalamic fibers
• Presentation: Disproportionate weakness in upper extremities (hands affected more than shoulders/legs); cape-like distribution of pain/temperature loss across shoulders and arms with preserved lower extremity sensation
• Classic cause: Hyperextension injury in elderly with cervical spondylosis; diving accident in young patient
• Prognosis: Best of all incomplete syndromes (50% recover ambulation)

Anterior Cord Syndrome

• Mechanism: Anterior spinal artery occlusion or compression of anterior cord (tumor, herniated disc, fracture)
• Presentation: Loss of motor function and spinothalamic sensation (pain/temperature); preserved dorsal column function (vibration, proprioception, fine touch) — dissociated sensory loss
• Lower extremities typically affected worse than upper extremities
• Prognosis: Poorest of incomplete syndromes

Posterior Cord Syndrome (Rare)

• Mechanism: Dorsal column damage from posterior spinal artery occlusion or compression
• Presentation: Loss of vibration and proprioception with preserved motor function and pain/temperature sensation
• Results in sensory ataxia and positive Romberg test despite motor strength intact
• Functional disability often significant despite preserved strength

Brown-Séquard Syndrome (Hemisection)

• Mechanism: Penetrating injury (stab wound), tumor, demyelination affecting half of spinal cord
• Presentation: Ipsilateral weakness and dorsal column loss (same side as injury); contralateral pain/temperature loss (opposite side, starting 1-2 levels below lesion)
• Classic teaching point: Loss of pain sensation on opposite side is delayed relative to weakness
• Prognosis: Best prognosis of all SCI syndromes (60% regain useful walking)

Conus Medullaris Syndrome

• Mechanism: Injury to sacral spinal cord (S1-S5) and lower lumbar segments
• Presentation: Bilateral leg weakness, sacral sensory loss (perianal/saddle anesthesia), early and severe sphincter dysfunction (urinary retention or incontinence), sexual dysfunction
• Reflexes may be preserved (sacral reflexes intact), unlike cauda equina

Cauda Equina Syndrome

• Mechanism: Compression of nerve roots below conus (typically L4-S5)
• Presentation: Asymmetric leg weakness, asymmetric sensory loss, late sphincter involvement, variable reflexes (lower motor neuron pattern)
• Radicular pain prominent; saddle anesthesia may be present
• Distinction from conus: Asymmetric findings, preserved sacral reflexes, later sphincter involvement

Functional Red Flags in Presentation

• Preserved anal tone or perianal sensation suggests incomplete injury and better prognosis
• Very rapid improvement in first 48 hours suggests mild injury with edema; improvement after 48 hours indicates plasticity and regeneration
• Presence of sacral sparing (preserved sensation at S4-S5 or voluntary anal contraction) defines incomplete injury

Clinical Examination - Neurological Localization

• Sensory level determination: Test sensation dermatomally with sharp object to identify exact level of loss; typically 1-2 levels below vertebral injury due to spinal cord anatomy
• Motor testing: Grade strength 0-5 for key muscles; identify myotomal pattern (C5-T1 for upper extremity, L2-S1 for lower extremity)
• Reflex testing: Hyperactive reflexes and Babinski sign indicate upper motor neuron lesion (above conus); absent reflexes indicate lower motor neuron lesion (conus/cauda equina)
• Rectal examination: Check anal tone (normal = external anal sphincter intact), perianal sensation, and voluntary anal contraction (critical for incomplete vs. complete determination)

Imaging - Structural Diagnosis

• Spinal MRI: Gold standard for evaluating spinal cord injury, compression, demyelination, ischemia, and hemorrhage; defines exact lesion level and extent; should be obtained emergently in acute SCI
• T1 and T2 sequences distinguish cord hemorrhage (T1 hyperintense), edema (T2 hyperintense)
• Sagittal imaging shows lesion extent; axial imaging shows hemisection pattern
• CT spine: Initial imaging in trauma to assess vertebral fractures, alignment, and bony compression; better bone detail than MRI
• Plain radiographs: Limited utility; assess gross alignment but miss ligamentous and soft tissue injury

Laboratory and Functional Tests

• Evoked potentials: Motor (MEP) and somatosensory (SSEP) evoked potentials measure tract integrity; preserved potentials indicate some axonal continuity and may correlate with recovery potential
• Urinalysis and post-void residual: Assess bladder dysfunction; >100 mL residual suggests significant dysfunction
• Cerebrospinal fluid analysis: Consider in suspected infection

Tract crossing rules (the single most tested concept)

• Dorsal columns decussate in the medulla, so a cord lesion gives ipsilateral loss of vibration/proprioception below the level; the spinothalamic tract decussates in the anterior white commissure within 1–2 segments, so the same lesion gives contralateral pain/temperature loss beginning a level or two below. This dissociation is the entire basis of Brown-Séquard stems.
• Common distractor: choosing "contralateral vibratory loss" for a cord hemisection. Contralateral dorsal column loss requires a lesion above the medullary decussation, not in the cord.

Named associations examiners reuse

• Subacute combined degeneration (B12, and copper or nitrous oxide abuse): dorsal columns + lateral corticospinal + spinocerebellar tracts, with sensory ataxia, positive Romberg, and paradoxically brisk reflexes with an extensor plantar response; check B12 with methylmalonic acid and homocysteine, which rise before anemia or macrocytosis appear.
• Syringomyelia: expanding central cavity, classically cervical and associated with Chiari I malformation, producing the cape-like loss of pain/temperature with sparing of touch and vibration.
• Tabes dorsalis: tertiary syphilis striking dorsal columns and dorsal roots — lancinating pains, Argyll Robertson pupils, absent reflexes.
• ALS: mixed upper and lower motor neuron signs with no sensory loss — sensory findings essentially exclude it.
• Anterior cord infarction: watershed mid-thoracic cord supplied by the artery of Adamkiewicz; classic after aortic dissection or aortic aneurysm repair.

Best next steps

• Suspected cord compression or cauda equina syndrome (saddle anesthesia, urinary retention, bilateral radicular pain): emergent MRI of the whole spine, then urgent surgical decompression — consistent with AANS/CNS and NASS guidance. Urinary retention with an elevated post-void residual is the more reliable early red flag than incontinence.
• Malignant epidural spinal cord compression: start corticosteroids (dexamethasone) while arranging MRI and neurosurgery/radiation oncology consultation, per NCCN.
• Blunt trauma: immobilize, then CT for bony injury and MRI for cord/ligamentous injury; high-dose methylprednisolone is not recommended routinely in acute traumatic SCI per AANS/CNS guidelines — a frequent trap answer. Focus instead on hemodynamic support and avoiding hypoxia to limit secondary injury.
• Sacral sparing (perianal sensation or voluntary anal contraction) defines an incomplete injury — always document the rectal exam.