Motor System & Reflexes
Physiology · CNS · lean revision notes
Motor System & Reflexes
The motor system converts intention into coordinated movement through a hierarchy: cortex → brainstem → spinal cord → muscle, sculpted continuously by the cerebellum and basal ganglia. This topic is a NEET PG perennial because the bedside neurology examination — tone, power, reflexes, plantars, posturing — maps directly onto these pathways, and a single lesion-localisation question can hinge on one sign.
Organisation of the Motor System
Movement is controlled at four hierarchical levels, each adding refinement:
- Spinal cord — reflex circuits and central pattern generators (rhythmic locomotion).
- Brainstem — postural control via reticular, vestibular, tectal and rubral nuclei.
- Motor cortex — voluntary, fractionated movement (especially of the hand).
- Cerebellum & basal ganglia — not in the direct descending line; they modulate and plan, projecting back via thalamus and brainstem.
The final common pathway is Sherrington's term for the alpha (α) motor neuron in the anterior horn — every motor command, voluntary or reflex, must funnel through it to reach muscle. A motor unit = one α-motor neuron + all muscle fibres it innervates. Small units (extraocular, lumbrical muscles: ~3–10 fibres) allow fine control; large units (gastrocnemius: >1000 fibres) generate gross force.
High-yield: The α-motor neuron is the final common pathway. Any lesion of the anterior horn cell, root, plexus, peripheral nerve, NMJ or muscle produces a lower motor neuron (LMN) picture.
Descending Motor Pathways
Descending tracts are grouped by where they terminate in the spinal grey matter — lateral systems control distal (limb) muscles for skilled movement; medial systems control axial/proximal muscles for posture.
Pyramidal (Corticospinal) Tract
- Origin: ~30% from primary motor cortex (Brodmann area 4), 30% premotor/supplementary, 40% somatosensory cortex (areas 3,1,2). Only ~3% are the giant Betz cells.
- Course: corona radiata → posterior limb of internal capsule → cerebral peduncle (crus cerebri) → pons → medullary pyramids.
- At the lower medulla, ~80–90% fibres decussate (pyramidal decussation) → lateral corticospinal tract (controls distal limb muscles). The uncrossed ~10% form the anterior (ventral) corticospinal tract (axial muscles, decussates at segmental level).
- Corticobulbar fibres supply cranial nerve motor nuclei — mostly bilateral, except the lower face and genioglossus (CN XII), which receive predominantly contralateral supply.
High-yield: Upper-half of face has bilateral corticobulbar supply → in an UMN (supranuclear) facial palsy the forehead is spared; in an LMN/Bell's palsy the whole half of the face is paralysed including forehead.
Extrapyramidal / Brainstem Pathways
| Tract | Origin | Function | Effect on tone |
|---|---|---|---|
| Lateral vestibulospinal | Lateral vestibular (Deiters) nucleus | Antigravity extensor support, balance | ↑ Extensor tone |
| Medial vestibulospinal | Medial vestibular nucleus | Head–neck position (vestibulocollic) | Neck muscles |
| Pontine (medial) reticulospinal | Pontine reticular formation | Facilitates extensors/antigravity | ↑ Extensor tone |
| Medullary (lateral) reticulospinal | Medullary reticular formation | Inhibits extensors (cortex-driven) | ↓ Extensor tone |
| Rubrospinal | Red nucleus (magnocellular) | Flexor tone in upper limb | ↑ Flexor tone |
| Tectospinal | Superior colliculus | Reflex head/eye orientation to visual/auditory stimuli | Axial |
Upper vs Lower Motor Neuron Lesions
This is the single most tested comparison in the topic.
| Feature | UMN lesion | LMN lesion |
|---|---|---|
| Site | Cortex, internal capsule, brainstem, corticospinal tract | Anterior horn cell, root, nerve, NMJ, muscle |
| Bulk | No early wasting (mild disuse atrophy late) | Marked wasting |
| Tone | Increased (spasticity, clasp-knife) | Decreased (flaccid, hypotonia) |
| Power | Weakness ("pyramidal pattern": UL extensors + LL flexors weaker) | Weakness in nerve/root distribution |
| Deep tendon reflexes | Exaggerated (hyper-reflexia), clonus | Lost/diminished |
| Superficial reflexes | Lost (e.g. abdominal) | Variable |
| Plantar response | Extensor (Babinski +) | Flexor or absent |
| Fasciculations | Absent | Present (esp. ALS) |
| Electrophysiology | Normal NCS, no denervation | Denervation, fibrillations, ↓ CMAP |
High-yield: Clasp-knife spasticity (sudden give after initial resistance) = pyramidal/UMN. Cogwheel/lead-pipe rigidity = extrapyramidal (Parkinsonism, basal ganglia). Don't confuse rigidity with spasticity.
High-yield: Amyotrophic lateral sclerosis (ALS) is the classic disease with combined UMN + LMN signs (e.g. brisk reflexes in a wasted, fasciculating limb) with no sensory loss.
A note on acute UMN lesions: immediately after a stroke or acute cord transection there is a phase of spinal shock / flaccidity with areflexia lasting days to weeks before the classic spasticity and hyper-reflexia emerge.
The Stretch (Myotatic) Reflex
The stretch reflex is the body's only monosynaptic reflex and underlies muscle tone and the tendon-jerk examination.
The Muscle Spindle
- Lies in parallel with extrafusal fibres; senses muscle length and rate of change of length.
- Contains intrafusal fibres: nuclear bag (dynamic, rate-sensitive) and nuclear chain (static, length-sensitive).
- Sensory innervation:
- Group Ia (primary/annulospiral) endings — fastest, sense dynamic + static stretch.
- Group II (secondary/flower-spray) endings — static length.
- Motor innervation: gamma (γ) motor neurons set spindle sensitivity by contracting the intrafusal fibre ends, keeping the spindle taut as the whole muscle shortens.
High-yield: Alpha–gamma coactivation — voluntary movement fires α and γ neurons together so the spindle stays responsive across the muscle's working length and is not "unloaded" when the muscle shortens.
Reflex Arc (the classic 5-step flow)
Tap tendon → muscle stretched → spindle Ia afferent fires → synapse on α-motor neuron in cord → α-neuron fires → extrafusal contraction (jerk)
Simultaneously, Ia afferents make inhibitory connections (via Ia inhibitory interneurons) onto antagonist α-motor neurons → reciprocal innervation (Sherrington) so the antagonist relaxes.
| Reflex | Root | Nerve |
|---|---|---|
| Biceps jerk | C5, C6 | Musculocutaneous |
| Supinator (brachioradialis) | C5, C6 | Radial |
| Triceps jerk | C7, C8 | Radial |
| Knee jerk (patellar) | L2, L3, L4 | Femoral |
| Ankle jerk | S1, S2 | Tibial (sciatic) |
High-yield: Knee jerk = L2–L4 (mainly L3,L4); ankle jerk = S1,S2. A loss of ankle jerk localises to S1 — classic in S1 radiculopathy.
Golgi Tendon Organ & Inverse Stretch Reflex
- The Golgi tendon organ (GTO) lies in series with muscle fibres at the musculotendinous junction; it senses tension/force, not length.
- Afferent: Group Ib fibres → spinal inhibitory interneuron → inhibits the homonymous α-motor neuron (disynaptic). This is the inverse stretch reflex / autogenic inhibition / clasp-knife reflex.
- Function: protects against excessive tension; contributes to the clasp-knife phenomenon in spasticity (sudden melt-away of resistance).
| Receptor | Location | Arrangement | Stimulus | Afferent | Effect |
|---|---|---|---|---|---|
| Muscle spindle | Within belly | Parallel | Length / stretch | Ia, II | Excites agonist (stretch reflex) |
| Golgi tendon organ | Musculotendinous junction | Series | Tension / force | Ib | Inhibits agonist (inverse stretch) |
High-yield: Spindle = parallel, length, Ia, excitatory. GTO = series, tension, Ib, inhibitory. Examiners love to swap these.
Polysynaptic Spinal Reflexes
Withdrawal (Flexor) Reflex & Crossed Extensor Reflex
A noxious stimulus to a limb produces:
- Ipsilateral flexion (withdrawal) — protective, polysynaptic, via flexor muscle activation and extensor inhibition.
- Crossed extensor reflex — contralateral limb extends to bear weight and support the body. Demonstrates irradiation and reciprocal innervation across the cord.
Features: shows temporal & spatial summation, afterdischarge (response outlasts the stimulus), and the local sign (response patterned to the stimulus location).
Other testable reflexes
- Babinski sign: stroking the lateral sole → dorsiflexion of great toe + fanning of toes = UMN lesion (normal in infants <1–2 yr due to incomplete myelination of corticospinal tract).
- Clonus: rhythmic involuntary contractions on sustained stretch = exaggerated stretch reflex (UMN).
- Superficial reflexes (abdominal, cremasteric, plantar): polysynaptic, lost in UMN lesions.
Decorticate vs Decerebrate Posturing
These reflect the level of brain injury and the balance between rubrospinal (flexor) drive above the red nucleus and unopposed vestibulospinal/reticulospinal (extensor) drive below it.
| Feature | Decorticate | Decerebrate |
|---|---|---|
| Lesion level | Above red nucleus (cerebral hemispheres / internal capsule / above midbrain) | Below red nucleus (midbrain/pons, between superior & inferior colliculi) |
| Upper limbs | Flexed, adducted to chest | Extended, internally rotated |
| Lower limbs | Extended | Extended |
| Mechanism | Rubrospinal flexor tone preserved (red nucleus intact) | Loss of rubrospinal; unopposed extensor (vestibulospinal) tone |
| GCS motor score | 3 | 2 |
| Prognosis | Less ominous | More ominous (deeper lesion) |
High-yield: deCORticate = arms toward the CORe (flexion); lesion is higher/better prognosis. Decerebrate = extension; lesion lower/worse. Progression from decorticate → decerebrate signals rostro-caudal deterioration (uncal/transtentorial herniation).
High-yield: Classic experimental decerebrate rigidity (intercollicular transection in cat) is an exaggerated extensor (antigravity) hypertonia — a release phenomenon from loss of cortical/rubral inhibition; it is abolished by cutting dorsal roots (it is a "gamma" rigidity dependent on spindle afferents).
Cerebellum & Basal Ganglia (brief, for differentials)
- Cerebellum: ipsilateral signs — ataxia, intention tremor, dysmetria, dysdiadochokinesia, nystagmus, scanning speech, hypotonia, pendular knee jerk. (Mnemonic DANISH: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Scanning speech, Hypotonia.)
- Basal ganglia: rigidity, bradykinesia, resting tremor (Parkinson) or hyperkinetic chorea/hemiballismus. No weakness, normal reflexes, no Babinski — this distinguishes extrapyramidal disease from pyramidal disease.
Key Differentials / Lesion Localisation
- Hemiplegia with face involved → above the level of facial nucleus (capsule/cortex).
- Crossed (alternating) hemiplegia (ipsilateral CN palsy + contralateral limb weakness) → brainstem.
- Quadriparesis / paraparesis with a sensory level → spinal cord.
- Brown-Séquard (hemicord): ipsilateral UMN weakness + dorsal column loss, contralateral spinothalamic (pain/temp) loss.
- Pure LMN, wasting, fasciculation, no sensory loss → anterior horn (e.g. spinal muscular atrophy, poliomyelitis).
- UMN + LMN, no sensory loss → ALS.
Recently asked / exam angle
- Final common pathway = α-motor neuron (Sherrington) — direct one-liner.
- Match the receptor to its afferent: spindle → Ia (and II); GTO → Ib. Very frequently asked.
- Clasp-knife (UMN) vs cogwheel/lead-pipe (extrapyramidal) rigidity differentiation.
- Decorticate vs decerebrate posturing with lesion level and GCS motor score (M3 vs M2).
- Pyramidal decussation at the lower medulla; internal capsule (posterior limb) carries corticospinal fibres — capsular stroke causes dense contralateral hemiplegia.
- Reflex root values — especially ankle jerk S1, knee jerk L3,L4.
- Babinski normal in infants; pathological (UMN) in adults.
- Reciprocal innervation and crossed extensor reflex as examples of polysynaptic spinal integration.
- Alpha–gamma coactivation concept and the role of γ-motor neurons in setting spindle sensitivity.
- ALS as the mixed UMN+LMN, sensory-sparing disease.
Rapid revision
- α-motor neuron = final common pathway; motor unit = neuron + its fibres.
- Lateral corticospinal tract decussates at the lower medulla (pyramids) and controls distal limb muscles.
- Corticospinal fibres run in the posterior limb of the internal capsule.
- UMN: ↑ tone (spastic/clasp-knife), hyper-reflexia, Babinski +, no wasting/fasciculation.
- LMN: ↓ tone (flaccid), areflexia, wasting + fasciculations.
- Stretch reflex is the only monosynaptic reflex; afferent = Ia.
- Muscle spindle = parallel, senses length; GTO = series, senses tension (afferent Ib, inhibitory = inverse stretch reflex).
- γ-motor neurons keep spindle taut; α–γ coactivation during voluntary movement.
- Crossed extensor reflex: ipsilateral flexion + contralateral extension; shows reciprocal innervation, afterdischarge.
- Decorticate = flexion (arms to core), above red nucleus, M3; Decerebrate = extension, below red nucleus, M2, worse prognosis.
- Knee jerk L3,L4; ankle jerk S1,S2; UMN facial palsy spares the forehead (bilateral corticobulbar supply to upper face).
- ALS = mixed UMN + LMN, no sensory loss; basal ganglia/cerebellar disease has no Babinski and normal power.