Motor System
Motor System
What You'll Learn
- Motor hierarchy — cortex → basal ganglia/cerebellum → brainstem → spinal cord → peripheral nerve → NMJ → muscle
- Corticospinal tract anatomy — origin, internal capsule somatotopy, pyramidal decussation, lateral vs. anterior CST
- UMN vs. LMN distinction — tone, reflexes, Babinski, atrophy, fasciculations — the single most tested motor concept
- Motor unit physiology — alpha vs. gamma motor neurons, muscle spindle, Golgi tendon organ, stretch reflex arc
- NMJ transmission — ACh release cycle, safety factor, and how myasthenia gravis, Lambert-Eaton, and botulism each disrupt it
- Descending pathways — lateral system (voluntary distal limb) vs. medial system (postural/axial) and their clinical relevance
- Basal ganglia & cerebellum roles — movement selection vs. coordination/error correction
- Motor neuron disease patterns — ALS (UMN+LMN), PLS (pure UMN), PMA (pure LMN), SMA, Kennedy disease
- Localization — cortex vs. subcortical vs. brainstem vs. spinal cord vs. root vs. nerve vs. NMJ vs. muscle
HighYield Pearls
- UMN vs LMN signs: UMN → spasticity + hyperreflexia + clonus + Babinski + Hoffmann + minimal/late disuse atrophy + NO fasciculations; LMN → flaccidity + hyporeflexia/areflexia + early prominent atrophy + fasciculations + downgoing toes — the single highest-yield distinction in motor neurology
- Pyramidal decussation: 85–90% of corticospinal fibers cross at the cervicomedullary junction → lateral CST (distal limb fine motor); 10–15% stay uncrossed → anterior CST (axial/proximal, crosses segmentally)
- Internal capsule somatotopy: GENU = corticobulbar (face); POSTERIOR LIMB = corticospinal (arm anterior → leg posterior) → lacunar infarct here = pure motor hemiparesis (face = arm = leg)
- Central vs peripheral CN VII: UMN (central) → contralateral LOWER face weakness, FOREHEAD SPARED (bilateral upper-face innervation); LMN (Bell) → entire ipsilateral hemiface including forehead
- Tongue deviation: UMN/cortical CN XII lesion → tongue deviates AWAY from lesion; LMN (hypoglossal nucleus/nerve) → tongue deviates TOWARD lesion + atrophy + fasciculations
- Spinal shock: acute UMN cord lesion initially mimics LMN (flaccid, areflexic, mute Babinski) → spasticity + hyperreflexia + Babinski emerge over days to weeks — do not be fooled on boards
- ALS = mixed UMN + LMN in the same region with progressive spread; sensation, EOMs, and sphincters spared (Onuf nucleus spared); split-hand syndrome (APB + FDI wasting, ADM relatively spared) is highly characteristic
- FEF lesion (Brodmann 8): destructive cortical lesion (MCA stroke) → eyes deviate TOWARD the lesion (away from hemiparesis); irritative/seizure focus → eyes deviate AWAY from focus
- Motor unit = one alpha motor neuron + all muscle fibers it innervates; Henneman size principle → smallest (type I, slow-twitch) recruited first, then larger (type II, fast-twitch); alpha = extrafusal; gamma = intrafusal (spindle sensitivity)
- Stretch reflex is monosynaptic: Ia afferent from muscle spindle → alpha motor neuron same muscle; UMN normally INHIBITS the reflex arc → UMN lesion releases it → hyperreflexia + clonus
- Spasticity (UMN) vs rigidity (BG): spasticity = velocity-dependent + clasp-knife + antigravity muscles + pyramidal; rigidity = velocity-independent + lead-pipe/cogwheel + flexors and extensors equally + extrapyramidal
- Decerebrate vs decorticate: de-COR-ticate (cortex/IC lesion above red nucleus) → arms flexed, legs extended; decerebrate (lesion below red nucleus) → all extremities extended + arms pronated → worse prognosis
🔍 Quick ReferenceAnatomy / pathways · UMN / LMN signs · Lesion / disease
Anatomy / pathways
- Betz cells layer V of M1 (Brodmann 4) → largest pyramidal neurons in CNS; ~3% of corticospinal fibers
- Pyramidal decussation at cervicomedullary junction → 85–90% cross → lateral CST (distal limb fine motor)
- Anterior corticospinal tract (uncrossed in cord) → axial/proximal control; crosses at segmental level via anterior white commissure
- Posterior limb of internal capsule → corticospinal somatotopy: arm anterior → leg posterior; genu = corticobulbar (face)
- Cerebral peduncle (crus cerebri) middle 3/5 → descending corticospinal/corticobulbar fibers; face medial, leg lateral
- Rubrospinal tract (red nucleus → crosses at ventral tegmental decussation of Forel) → upper-limb flexor bias; vestigial in humans
- Lateral vestibulospinal tract (Deiters nucleus, ipsilateral) → extensor facilitation + antigravity posture → drives decerebrate rigidity
- Pontine (medial) reticulospinal vs medullary (lateral) reticulospinal → extensor facilitation vs flexor facilitation → balance sets resting tone
- Tectospinal tract (superior colliculus → dorsal tegmental decussation, cervical cord only) → reflexive head/neck turning to visual/auditory stimuli
- Motor unit (alpha motor neuron + all fibers it innervates) → final common pathway; Henneman size principle (small → large)
- Alpha vs gamma motor neuron → extrafusal force generation vs intrafusal (muscle spindle) sensitivity; alpha-gamma co-activation
- Muscle spindle Ia afferent → monosynaptic alpha motor neuron → stretch (myotatic) reflex — fastest arc in the body
- Golgi tendon organ (Ib afferent, in series with extrafusal fibers) → autogenic inhibition — tension/force limiter (clasp-knife)
- Renshaw cell (glycinergic, recurrent inhibition of alpha motor neuron) → lateral inhibition; lost in tetanus → rigidity/spasms
UMN vs LMN signs
- Spasticity (velocity-dependent, clasp-knife, antigravity preference) → UMN
- Hyperreflexia + clonus (>3 beats) → UMN
- Babinski sign (extensor plantar response — release of primitive flexor-withdrawal) → UMN
- Hoffmann sign (flick middle fingernail → thumb/index flexion) → UMN in upper extremity (“Babinski of the arm”)
- Trömner sign (flick volar fingertip upward → thumb/index flexion) → UMN, same significance as Hoffmann
- Pronator drift (arms outstretched, palms up, eyes closed → arm pronates and drifts down) → subtle UMN weakness
- Finger escape sign (little finger drifts into abduction) → UMN/pyramidal (cervical myelopathy)
- Crossed adductor reflex (pathologic spread to contralateral thigh) → UMN above L2–L4
- Inverted radial reflex (absent BR + paradoxical finger flexion) → UMN — cervical spondylotic myelopathy at C5–C6
- Pyramidal weakness pattern (UE extensors > flexors; LE flexors > extensors) → UMN
- Flaccidity / hypotonia + areflexia → LMN
- Fasciculations (spontaneous motor unit firing from denervation) → LMN
- Early prominent denervation atrophy (weeks) → LMN
- Muscle cramps + tongue fasciculations + flaccid dysarthria → LMN (bulbar palsy)
Lesion / disease association
- UMN + LMN signs in the same region, progressive, sensation/EOM/sphincters spared → ALS
- Split-hand syndrome (APB + FDI wasting, ADM relatively spared) → ALS (highly characteristic, Wilbourn)
- C9orf72 hexanucleotide repeat expansion → most common familial ALS (also FTD)
- Pure UMN, progressive spasticity ≥4 yr without LMN signs → primary lateral sclerosis (PLS)
- Pure LMN, anti-GM1 antibodies + conduction block on NCS → multifocal motor neuropathy (treatable ALS mimic)
- Adult X-linked bulbar weakness + proximal weakness + gynecomastia + sensory neuronopathy + CAG repeat in androgen receptor → Kennedy disease (SBMA)
- Infant floppy baby + tongue fasciculations + areflexia + SMN1 deletion (5q) → SMA type 1 (Werdnig-Hoffmann)
- New weakness ≥15 yr after polio + giant motor units on EMG → post-polio syndrome
- Pure motor hemiparesis affecting face = arm = leg equally → lacunar infarct in posterior limb of internal capsule
- Contralateral lower face weakness with forehead spared → UMN (central) CN VII lesion (cortex/IC/upper pons)
- Entire ipsilateral hemiface weakness including forehead → LMN CN VII lesion (Bell palsy)
- Tongue deviates AWAY from lesion → UMN/cortical CN XII lesion
- Tongue deviates TOWARD lesion + atrophy + fasciculations → LMN CN XII (hypoglossal nucleus/nerve)
- Pseudobulbar palsy (pseudobulbar affect + dysarthria + dysphagia, brisk jaw jerk) → bilateral UMN corticobulbar (PSP, ALS, bilateral strokes, MS)
- Eyes deviate TOWARD lesion (FEF destructive cortical lesion) → MCA cortical stroke (“eyes look at the lesion”)
- Eyes deviate AWAY from focus → irritative seizure focus in FEF (Brodmann 8)
- Acute flaccid areflexic paraparesis evolving to spasticity + hyperreflexia + Babinski weeks later → spinal shock resolving (acute UMN cord lesion)
- Onuf nucleus (S2–S4) selectively SPARED → ALS (bowel/bladder/sexual function preserved until late)
- Onuf nucleus involved early (early urinary incontinence) → MSA (distinguishes from idiopathic PD)
- Decorticate posturing (arms flexed, legs extended) → lesion above red nucleus (cortex/internal capsule)
- Decerebrate posturing (all limbs extended, arms pronated) → lesion below red nucleus (midbrain/pons) — worse prognosis
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