STEPTRACKERNERVOUS SYSTEM | ANATOMY + PATHOLOGY | HIGH-YIELD REVIEW

Spinal Cord Lesions

Read each cross-section first, then predict the deficits — the lesion's position in the cord tells you everything.

FOCUS ON
Three tracts decide the side: dorsal columns and lateral corticospinal give ipsilateral loss; the spinothalamic tract crosses within 1–2 levels and gives contralateral loss. Anterior horn = LMN. Then match the pattern: LMN only (polio, SMA), UMN + LMN (ALS), dorsal columns (tabes, B12), cape-like (syrinx), half-cord (Brown-Séquard).
LESION
DISEASE · AREA HIT
DEFICITS
CAUSE · CLASSIC CLUES
Poliomyelitis
Anterior horns — asymmetric
LMN only: asymmetric flaccid weakness (legs > arms), ↓ reflexes, atrophy, fasciculations. Viral meningitis picture (fever, headache, neck stiffness). Resp. muscles → respiratory failure.
Unvaccinated child; poliovirus (+ssRNA), fecal–oral → oropharynx/gut lymphoid tissue → blood → CNS. CSF: lymphocytes, slight ↑ protein, normal glucose. Virus from stool/throat.
Spinal muscular atrophy
Anterior horns — symmetric (type 1 = Werdnig-Hoffmann)
LMN only, symmetric: "floppy baby" with marked hypotonia, tongue fasciculations, areflexia. Death within months (type 1).
Congenital, autosomal recessive SMN1 mutation → defective snRNP assembly → LMN apoptosis.
Amyotrophic lateral sclerosis
Anterior horns + lateral CST (+ brainstem motor nuclei)
UMN + LMN together: spasticity, hyperreflexia, Babinski and atrophy, fasciculations, flaccid weakness. Bulbar palsy (dysarthria, dysphagia). No sensory, no bowel/bladder deficits.
Age 40–60. Familial: SOD1 (Cu/Zn superoxide dismutase) → free-radical injury. Rx: riluzole (↓ glutamate release), edaravone. Fatal — respiratory failure / aspiration.
Anterior spinal artery occlusion
Anterior 2/3 — spares dorsal columns & dorsal horns
Acute, bilateral. Spinal shock (flaccid) → later UMN below, LMN at level. Bilateral pain/temp loss below. Bowel/bladder dysfunction (urinary retention). Vibration & proprioception intact.
Watershed: mid-thoracic (supplied by artery of Adamkiewicz). Aortic surgery/dissection, burst vertebral fracture.
Tabes dorsalis
Dorsal columns + dorsal roots
Sensory ataxia, wide-based "stomping" gait, ⊕ Romberg. Lightning (shooting) pains. ↓/absent DTRs (root damage). Argyll Robertson pupils. Charcot joints. Strength 5/5.
Tertiary syphilis (T pallidum) — often a patient with other STIs. Rx: IV penicillin.
Subacute combined degeneration
S-C-D: Spinocerebellar + lateral Corticospinal + Dorsal columns
Symmetric, legs > arms, slowly progressive: paresthesias, ↓ vibration/position, ataxic gait, ⊕ Romberg plus UMN signs (spastic paresis, hyperreflexia, Babinski). ± memory loss.
Vitamin B12 deficiency (demyelination). Labs: B12, ↑ methylmalonic acid (more sensitive). Macrocytosis may be absent.
Syringomyelia
Central syrinx → anterior white commissure (crossing STT)
Bilateral "cape-like" pain/temp loss at level only (usually C8–T1: hands, arms, shoulders, back) → unnoticed burns/cuts. Vibration/position preserved; legs normal. Expands → anterior horn (LMN hand weakness/atrophy), lateral horn (Horner), kyphoscoliosis.
Chiari (Arnold-Chiari) malformation, or post-traumatic — months–years after a spinal cord injury (classically cervical, whiplash).
Central cord syndrome
Central gray + medial (arm) CST fibers
Arms > legs weakness — arm fibers lie most medial in the lateral CST. Variable pain/temp loss in upper limbs (crossing STT fibers). Legs may be spared.
Elderly + cervical spondylosis + hyperextension injury (fall, face hits airbag). Syringomyelia is the slow-onset cause of the same picture.
Brown-Séquard syndrome
Hemisection of the cord
Ipsilateral below: UMN weakness (spastic, Babinski) + loss of vibration/proprioception. Contralateral below: pain/temp loss (starts 1–2 segments below). At level, ipsilateral: all sensation lost + LMN signs. Lesion above T1 → ipsilateral Horner.
Penetrating trauma (knife, gunshot) or tumor. Weak side = side of lesion.
Posterior cord syndrome
Dorsal columns, bilateral
Bilateral loss of vibration & proprioception → sensory ataxia, ⊕ Romberg. ± weakness, paresthesias, urinary incontinence/retention. Pain/temp spared.
Multiple sclerosis and vascular disruption (eg, vertebral artery dissection) are most common.
Multiple sclerosis
Random, asymmetric white-matter plaques (mostly cervical)
Mixed UMN + sensory deficits that relapse and remit. Spastic bladder (urge/overflow). Look for optic neuritis, INO (MLF), fatigue.
Women 20s–30s. Autoimmune CNS demyelination (T cells vs myelin, type IV). MRI = gold standard; CSF ↑ protein, oligoclonal bands.

Where each tract crosses → which side you lose

Dorsal columnsLat. CSTSpinothalamicSpino-cerebellarAnt. hornLat. horn
TRACT
CROSSES
CORD LESION
Dorsal columns (vibration, proprioception, fine touch)
Medulla
Ipsilateral loss
Spinothalamic (pain, temperature, crude touch)
Anterior white commissure, 1–2 levels up
Contralateral loss
Lateral corticospinal (motor)
Pyramidal decussation (caudal medulla)
Ipsilateral UMN signs below
Anterior / lateral horn
—
LMN at level · Horner if above T1

UMN vs LMN — the first branch point

SIGN
UMN LESION
LMN LESION
Tone
↑ Spastic (after spinal shock)
↓ Flaccid
Reflexes
↑ Hyperreflexia, clonus
↓ / absent
Babinski
⊕ Upgoing
⊖ Normal
Bulk
Mild disuse atrophy
Marked atrophy
Fasciculations
Absent
Present

Acute cord injury starts as spinal shock — flaccid and areflexic — and becomes spastic over weeks. The cord ends at ~L1–L2; below that, only roots (cauda equina).

Conus medullaris
Bilateral saddle anesthesia, early bowel/bladder dysfunction, impotence; mixed UMN/LMN signs (it is cord tissue).
Cauda equina
Severe low back pain, saddle anesthesia, lost anocutaneous reflex, bladder dysfunction, LMN leg signs, normal Babinski · massive disc, tumor, trauma.

How it's tested

COMMON CONFUSIONSyringomyelia and central cord syndrome both hit the center of the cervical cord. Syrinx: slow, cape-like pain/temperature loss. Central cord: sudden, after hyperextension, arms weaker than legs.
THE TRAPTabes dorsalis and B12 deficiency both give a positive Romberg. Tabes has absent reflexes and lightning pains; subacute combined degeneration adds UMN signs (Babinski, spasticity).
YOUR APPROACHUMN, LMN or both → which sensations lost, on which side → at level or below → acute or slow → cause (vascular, viral, nutritional, genetic, trauma, demyelinating).

If you see… think…

Painless burns on both hands, legs normal → syringomyelia
Everything lost below the lesion except vibration/position, after aortic surgery → ASA occlusion
⊕ Romberg + lightning pains + Argyll Robertson pupils → tabes dorsalis
⊕ Romberg + UMN signs + ↑ methylmalonic acid → SCD (B12)
UMN + LMN signs, sensation completely normal → ALS
Elderly, hyperextension injury, arms weaker than legs → central cord syndrome
Stab wound: weak and no vibration on one side, no pain/temp on the other → Brown-Séquard
Floppy newborn + tongue fasciculations → SMA (SMN1)
Cancer history, back pain worse lying down, sensory level → cord compression — urgent
Distal stocking sensory loss improving up the leg → peripheral neuropathy, not cord