Motor System

Corticospinal Tract & Motor Localization

Select a lesion level along the motor pathway from cortex to muscle. See UMN vs LMN signs, brainstem crossed findings, and acute vs chronic presentations.

UMN

Clinical Presets

Lesion Level

Clinical vignette

A 68-year-old with sudden right face and arm weakness, sparing the leg. Speech is slurred. Right arm drifts within 2 seconds.

Precentral gyrus (Brodmann area 4)

Motor Cortex

Upper motor neuron cell bodies in layer V. Lesions produce contralateral weakness with a somatotopic pattern (face/arm > leg for MCA territory).

Crossing: Pyramidal decussation (caudal medulla)Distribution: Contralateral, somatotopic (vascular territory)

Contralateral signs

Tone

Spastic (velocity-dependent, clasp-knife)

Loss of descending inhibition on spinal stretch reflex circuits produces velocity-dependent hypertonia.

Reflexes

Hyperreflexic

Disinhibited spinal motoneurons respond excessively to Ia afferent input.

Babinski sign

Upgoing plantar (extensor)

Loss of corticospinal input unmasks the primitive flexion withdrawal reflex.

Atrophy

Minimal (disuse only)

The LMN is intact, so trophic support to muscle is preserved. Only prolonged disuse causes mild wasting.

Fasciculations

Absent

Fasciculations require LMN instability. UMN lesions produce spasticity, not denervation.

Weakness pattern

Contralateral, somatotopic (face/arm > leg in MCA)

Corticospinal fibers are somatotopically organized. Capsular lesions are dense because fibers are packed; cortical lesions follow vascular territory.

Temporal evolution

Acute

Initially flaccid and areflexic (spinal shock if spinal; cortical shock if cerebral). Babinski may be present from the start.

Chronic

Over days to weeks, spasticity, hyperreflexia, and clonus develop as spinal circuits become disinhibited.

Key distinctions

  • UMN: spastic, hyperreflexic, Babinski+, minimal atrophy, no fasciculations
  • LMN: flaccid, areflexic, early atrophy, fasciculations, no Babinski
  • NMJ: fatigable, fluctuating, no sensory, normal reflexes, no atrophy early
  • Myopathy: proximal, symmetric, no sensory, preserved reflexes, elevated CK
  • Mixed (ALS): hyperreflexia + atrophy + fasciculations = the deadly combination

Red flags

Sudden onset suggests vascular; progressive suggests structural or degenerative.

Complete motor pathway

Motor cortex → posterior limb internal capsule → cerebral peduncle → basis pontis → medullary pyramid → pyramidal decussation → lateral corticospinal tract → anterior horn cell → ventral root → peripheral nerve → NMJ → muscle.