A classic way Q-banks test spinal cord anatomy is by giving you one clean clue (often a unilateral cord lesion) and then seeing whether you can predict a whole constellation of deficits—and avoid seductive distractors like “anterior cord syndrome” or “syringomyelia.” Brown-Séquard syndrome is the perfect setup: it rewards students who can map tract + crossing level + side without panicking.
Tag: Neurology > Peripheral Nerve & Spinal Cord
The Clinical Vignette (Q-bank style)
A 28-year-old man is brought to the ED after a stabbing injury to the right side of his back at the level of the umbilicus. On exam, he has right leg weakness, loss of vibration and proprioception on the right, and loss of pain and temperature on the left beginning a few levels below the injury. Cranial nerves are intact.
Which spinal cord lesion best explains these findings?
A. Right hemisection of the spinal cord at T10
B. Anterior spinal artery infarct at T10
C. Central cord syndrome at T10 (syrinx-like lesion)
D. Dorsal column lesion on the left at T10
E. Cauda equina syndrome
F. Conus medullaris syndrome
The Correct Answer: A. Right hemisection of the spinal cord at T10 (Brown-Séquard syndrome)
Brown-Séquard = hemicord lesion (trauma, tumor, MS) → predictable “split” deficits because key pathways cross at different places.
What gets hit on the RIGHT at T10?
1) Corticospinal tract (motor)
- Fibers already crossed at the pyramidal decussation in the medulla
- So in the spinal cord, corticospinal deficits are ipsilateral to the lesion
Finding: Right UMN weakness below the lesion
- Hyperreflexia, spasticity, Babinski (may be delayed acutely due to spinal shock)
2) Dorsal columns (vibration, proprioception, fine touch)
- Ascend ipsilaterally in the cord
- Cross in the medulla (internal arcuate fibers → medial lemniscus)
Finding: Right loss of vibration/proprioception below the lesion
3) Spinothalamic tract (pain & temperature)
- Primary afferents enter, then ascend/descend 1–2 levels in Lissauer’s tract
- Synapse in dorsal horn; then second-order neurons cross in the anterior white commissure within ~1–2 levels
Finding: Left loss of pain & temperature, typically starting 1–2 levels below the lesion
The “Why it Starts a Few Levels Below” Detail (high-yield)
Spinothalamic fibers don’t cross instantly at the exact dermatome level—they often travel up/down 1–2 segments in Lissauer’s tract before synapsing and crossing.
So a right T10 hemicord lesion classically causes:
- Contralateral pain/temp loss beginning ~1–2 levels below T10
Quick Pattern Table (Burn this in)
| Tract | Modality | Where it crosses | Deficit in Brown-Séquard (right hemicord) |
|---|---|---|---|
| Lateral corticospinal | Motor | Medulla (pyramids) | Ipsilateral UMN weakness below lesion |
| Dorsal columns | Vibration/proprioception | Medulla | Ipsilateral loss below lesion |
| Spinothalamic | Pain/temperature | Spinal cord (anterior white commissure) | Contralateral loss starting 1–2 levels below |
Now Kill the Distractors (Each One Teaches Something)
B. Anterior spinal artery infarct at T10 (Anterior cord syndrome)
Anterior spinal artery supplies:
- Anterior 2/3 of cord: corticospinal + spinothalamic + anterior horn Spared:
- Dorsal columns (posterior spinal arteries)
Expected deficits:
- Bilateral motor weakness below lesion
- Bilateral pain/temp loss below lesion
- Preserved vibration/proprioception
Why it’s wrong here: This vignette has ipsilateral dorsal column loss and a hemicord pattern, not bilateral deficits with dorsal column sparing.
USMLE tip: Think “ASA = motor + pain/temp gone; dorsal columns spared.”
C. Central cord syndrome / syringomyelia-like lesion at T10
Central cord lesions hit the anterior white commissure first → crossing spinothalamic fibers.
Expected deficits:
- Bilateral loss of pain/temp at the level(s) of lesion (“cape-like” in cervical syrinx)
- Dorsal columns often spared early
- Can progress to involve corticospinal if large (weakness often upper extremities > lower in cervical lesions)
Why it’s wrong here: Brown-Séquard causes contralateral pain/temp loss below lesion plus ipsilateral motor + dorsal column loss. A central lesion causes segmental bilateral pain/temp loss.
D. Dorsal column lesion on the left at T10
Would cause:
- Left loss of vibration/proprioception below lesion
- No primary effect on pain/temp
- No corticospinal UMN weakness unless lesion extends laterally
Why it’s wrong here: The vignette has the full triad: ipsilateral motor, ipsilateral dorsal column, contralateral pain/temp—this is not an isolated posterior column lesion.
E. Cauda equina syndrome
Cauda equina = lumbosacral nerve roots (PNS) in the spinal canal below the cord.
Expected deficits:
- LMN signs: flaccid weakness, decreased reflexes, atrophy, fasciculations
- Radicular pain
- Saddle anesthesia, bowel/bladder dysfunction can occur
- Often asymmetric but not a clean tract-based dissociation pattern
Why it’s wrong here: Brown-Séquard is a spinal cord tract lesion (UMN + sensory tract dissociation). Cauda equina is nerve roots → LMN findings and dermatomal/radicular pattern.
High-yield: Cauda equina = asymmetric LMN + severe radicular pain.
F. Conus medullaris syndrome
Conus = terminal cord segments (roughly L1 vertebral level), mixed UMN/LMN features.
Expected deficits:
- Early bowel/bladder dysfunction
- Saddle anesthesia
- Often symmetric
- Variable motor weakness; less severe radicular pain than cauda equina
Why it’s wrong here: The vignette emphasizes hemicord tract findings (ipsilateral UMN + dorsal column with contralateral pain/temp). Conus is not a hemicord syndrome and usually screams sphincters/saddle anesthesia early.
Extra High-Yield Add-ons Q-banks Love
1) Segmental LMN findings at the level of the lesion
A hemicord lesion can also damage:
- Anterior horn at that level → ipsilateral LMN signs (weakness, atrophy) in muscles supplied by that segment
- Dorsal root entry zone → segmental sensory loss
So you might see:
- LMN signs at the level, UMN signs below
2) “Bilateral pain/temp loss at the level” can coexist
If the lesion expands centrally, it may hit the anterior white commissure at that segment, producing bilateral pain/temp loss at the lesion level—on top of the classic Brown-Séquard pattern below.
3) Know your causes
Common etiologies tested:
- Penetrating trauma (knife, gunshot) = classic
- Tumor (extrinsic compression)
- Multiple sclerosis (can mimic partial hemicord syndromes)
Rapid Test-Day Algorithm (10 seconds)
- Unilateral motor weakness below lesion (UMN)? → think corticospinal (ipsilateral in cord)
- Unilateral vibration/proprioception loss? → dorsal columns (ipsilateral in cord)
- Contralateral pain/temp loss starting 1–2 levels below? → spinothalamic crossing in cord
- All three together → Brown-Séquard
One-Line Summary
Brown-Séquard syndrome = ipsilateral UMN weakness + ipsilateral loss of vibration/proprioception + contralateral pain/temp loss (starting a couple levels below), classically from hemicord injury.