Neuroanatomy • lesion lab

Which side fails?

Tap a syndrome. Change side + cord level. Watch the tracts light up.

POSTERIOR ↑
patient's L ↔ R
patient's LEFTpatient's RIGHT
DCDCCSTCSTSTST LEFT HEMICORD
Dorsal columnsLat. spinothalamicLat. corticospinal
Tap any colored tract to isolate its crossing rule.
1

Lateral corticospinal

Voluntary motor • UMN
Crosses at pyramidal decussation
caudal medulla→In spinal cord: controls the ipsilateral body

Cord lesion → ipsilateral UMN weakness below. At the exact segment, anterior horn/root damage may add ipsilateral LMN signs.

2

Dorsal column–ML

Vibration • proprioception • fine touch
Ascends uncrossed in cord→Crosses as internal arcuate fibers in medulla

Cord lesion → ipsilateral loss below, sensory ataxia and positive Romberg. Legs are medial (gracilis), arms lateral (cuneatus, ≥T6).

3

Lateral spinothalamic

Pain • temperature
Enters, may travel 1–2 segments in Lissauer tract→Crosses in anterior white commissure

Cord hemisection → contralateral loss beginning ~1–2 segments below. Sacral fibers lie lateral; cervical fibers more medial.

The cord-side rule: CST + dorsal column = same side below. Spinothalamic = opposite side, delayed by ~1–2 levels.
Why is pain loss not exactly at the Brown-Séquard level?
First-order fibers may ascend/descend in Lissauer tract before synapsing and crossing. Expect contralateral loss roughly 1–2 segments below.
ASA syndrome: what survives?
Dorsal columns, supplied mainly by posterior spinal arteries. Motor and pain/temperature are lost; vibration/proprioception remain.
Central cord: is “cape loss” the whole syndrome?
No. Crossing spinothalamic fibers can cause suspended/cape-like loss, but traumatic cervical central cord classically gives arms weaker than legs, variable sacral sparing, and possible bladder dysfunction.
Acute complete transection: UMN signs immediately?
Initially spinal shock: flaccidity and areflexia below. Later, UMN signs emerge—spasticity, hyperreflexia, Babinski.
“At level” versus “below level”?
At level: segmental LMN weakness + dermatomal sensory loss. Below: long-tract UMN and ascending sensory deficits.
Autonomic clue?
Lesions above T6 can predispose to autonomic dysreflexia after spinal shock resolves; acute high cervical lesions may impair respiration and cause neurogenic shock.
Cord level
Fast localization anchor
C5
Arm + leg long-tract findings; possible diaphragmatic risk if higher (C3–5).
T10
Trunk sensory level near umbilical region; legs affected, arms spared.
L1
Leg findings; beware conus/cauda distinction. Cord usually ends at L1–L2 vertebral level.