Motor system
Motor system: motor cortex, corticospinal tract, extrapyramidal tracts, UMN vs LMN
Voluntary movement starts in the precentral gyrus, runs down the corticospinal tract, crosses in the lower medulla and ends on anterior horn cells. Covers the motor homunculus, UMN versus LMN signs, Babinski in infants, spasticity, posture tracts and MND.
Motor areas of the cortex
| Area | Location | Role |
|---|---|---|
| Primary motor cortex (area 4) | Precentral gyrus | Executes voluntary movement; giant Betz cells in layer V; contralateral somatotopic map; lowest threshold for electrically evoked movement |
| Premotor cortex (lateral area 6) | In front of area 4 | Plans movement guided by external cues; posture of proximal muscles |
| Supplementary motor area (medial area 6) | Medial frontal surface | Plans internally generated sequences; active even when movements are only imagined |
| Frontal eye field (area 8) | Middle frontal gyrus | Voluntary saccades to the opposite side; a destructive lesion turns the eyes towards the lesion |
| Broca area (44, 45) | Inferior frontal gyrus, dominant side | Motor speech; lesion gives expressive aphasia |
- Motor homunculus: the hand (especially the thumb) and face (lips, tongue) have the largest representation, matching their fine control; the trunk is small. The leg lies on the medial surface (anterior cerebral artery); the face and arm on the lateral surface (middle cerebral artery).
- Inputs to the motor cortex: the ventrolateral thalamus (relaying cerebellar and basal ganglia output), premotor and supplementary areas, and the somatosensory cortex.
The corticospinal (pyramidal) tract
Precentral gyrus, corona radiata, posterior limb of the internal capsule, middle three-fifths of the cerebral peduncle, basis pontis, medullary pyramids; about 85–90% cross at the pyramidal decussation in the lower medulla and continue as the lateral corticospinal tract, ending on anterior horn cells (often via interneurones). The uncrossed 10–15% form the anterior corticospinal tract for axial muscles.
- Corticobulbar fibres supply cranial motor nuclei, mostly bilaterally. Exceptions: the lower face part of the facial nucleus and the hypoglossal nucleus receive mainly contralateral input, so a stroke weakens the lower face but spares the forehead.
- Axial and respiratory muscles have bilateral descending control (anterior corticospinal and reticulospinal pathways), so a man with dense hemiplegia after a middle cerebral artery stroke can still sit up, breathe deeply and cough.
Alpha motor neurones
Large, myelinated Aα neurones in lamina IX of the anterior horn and in cranial motor nuclei; the final common pathway for all movement. One alpha neurone and all the muscle fibres it supplies form a motor unit.
- Fasciculations are visible, irregular twitches from spontaneous firing of a whole motor unit, a sign of LMN disease (anterior horn cell or root, for example chronic C7 root compression with a wasted triceps). Benign fasciculations without wasting or weakness are common in healthy people. Fibrillations are single fibres firing, seen only on EMG.
Upper versus lower motor neurone lesions
| Feature | Upper motor neurone (cortex to cord) | Lower motor neurone (anterior horn cell to muscle) |
|---|---|---|
| Tone | Increased (spasticity, clasp-knife) | Decreased (flaccid) |
| Power | Pyramidal pattern (arm extensors, leg flexors weakest) | Weakness of muscles supplied |
| Reflexes | Brisk, with clonus | Reduced or absent |
| Plantar | Extensor (Babinski) | Flexor or absent |
| Wasting | Mild, late (disuse) | Marked, early |
| Fasciculation | Absent | Present |
- A unilateral flaccid lower limb with calf wasting and absent ankle reflex is an LMN lesion; with loss of pain on the lateral leg and foot it localises to the L5/S1 roots or sciatic territory.
- Spinal or cerebral shock: immediately after a severe UMN lesion the limb is flaccid and areflexic; spasticity and hyperreflexia develop over days to weeks.
- Why spasticity occurs: a lesion confined to the pyramidal tract mainly causes weakness, loss of fine finger movements and a Babinski sign. Spasticity and clasp-knife tone come from damage to the accompanying cortical fibres to the brainstem reticular formation (part of the extrapyramidal system), which normally inhibit stretch reflexes; the unopposed facilitatory reticulospinal and vestibulospinal drive then raises gamma and alpha activity. Capsular and cord lesions damage both together.
- Babinski sign indicates corticospinal tract damage anywhere from cortex to cord. It is normal in infants (up to about 1–2 years) because the corticospinal tracts are not yet fully myelinated; it disappears as myelination completes.
- Motor neurone disease (ALS): mixed UMN and LMN signs (wasting, fasciculation and brisk reflexes in the same limb) with no sensory loss. Eye movements and bladder control are preserved because the oculomotor nuclei and Onuf nucleus (sacral motor neurones to the sphincters) resist degeneration. Early sphincter or sensory problems point to cord compression instead.
- Multiple sclerosis gives spastic weakness, often in the legs, with intention tremor and urinary urgency.
- Hyperextension injury of the cervical spine in an older person causes central cord syndrome: arm weakness worse than leg weakness, because cervical (arm) fibres lie medially in the lateral corticospinal tract.
The extrapyramidal system and posture
Older term for motor pathways outside the pyramids and their controllers (basal ganglia, cerebellum).
| Tract | Origin | Main role |
|---|---|---|
| Rubrospinal | Red nucleus (crosses) | Facilitates flexors of the upper limb |
| Lateral vestibulospinal | Lateral vestibular (Deiters) nucleus (uncrossed) | Antigravity extensor tone and posture |
| Pontine reticulospinal | Pontine reticular formation | Facilitates extensors and axial posture |
| Medullary reticulospinal | Medullary reticular formation | Inhibits extensor tone |
| Tectospinal | Superior colliculus | Head turning to visual stimuli |
- Basal ganglia disorders cause rigidity (lead-pipe or cogwheel), bradykinesia and involuntary movements without pyramidal weakness or Babinski sign.
- Decorticate posture (lesion above the red nucleus, e.g. internal capsule): arms flexed, legs extended, because rubrospinal flexor drive to the arms survives.
- Decerebrate posture (lesion between the red and vestibular nuclei): all limbs extended from unopposed vestibulospinal and pontine reticulospinal drive. Worse prognosis.
Neuromuscular junction
ACh acts on nicotinic receptors at the end plate. Myasthenia gravis (antibodies to postsynaptic receptors: fatigable ptosis and diplopia, decrement on repetitive stimulation, normal reflexes), Lambert–Eaton (antibodies to presynaptic Ca²⁺ channels: weakness improving with exercise; small cell lung cancer), botulism (blocks ACh release), organophosphates (acetylcholinesterase inhibition: pinpoint pupils, secretions, fasciculations).
Remember Precentral gyrus, posterior limb, pyramids, cross in the lower medulla, lateral tract, anterior horn: above the anterior horn is spastic, below it is flaccid.
Exam trap The corticospinal tract runs in the posterior limb of the internal capsule and crosses in the lower medulla.
Exam trap An upgoing plantar is normal under about 1–2 years (incomplete myelination), abnormal afterwards.
How FCPS asks about this
- Largest representation in area 4: hand and face.
- Decussation of fibres in a UMN lesion with Babinski sign: lower medulla (pyramidal decussation); after crossing they form the lateral corticospinal tract.
- UMN versus LMN: spastic, brisk, Babinski versus flaccid, wasted, fasciculating, areflexic.
- Fasciculations: spontaneous firing of whole motor units.
- Trunk and breathing spared in hemiplegia: bilateral control of axial muscles.
- Normal bladder in MND: Onuf nucleus is resistant.
- Antigravity posture: lateral vestibulospinal tract; decerebrate rigidity follows lesions below the red nucleus.
Test yourself on this topic
5 of the 23 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 58-year-old man has progressive weakness over a year. There is wasting and fasciculation of the hand and tongue muscles, but his knee jerks are brisk and plantars extensor. Sensation is normal. Which structures are affected?
Answer: Anterior horns and pyramidal tracts
Motor neurone disease (amyotrophic lateral sclerosis) causes degeneration of both upper motor neurons (motor cortex and corticospinal tracts) and lower motor neurons (anterior horn cells and cranial motor nuclei). The combination of LMN signs (wasting, fasciculation, weakness of hand and tongue muscles) and UMN signs (brisk reflexes, extensor plantars) in the same patient is characteristic. Sensory pathways, eye movements and sphincters are typically spared, which helps separate it from cervical myelopathy, where sensory signs and sphincter disturbance are common. Riluzole (glutamate release inhibitor) modestly prolongs survival.
UMN vs LMN
- UMN: spastic, brisk, Babinski
- LMN: wasting, fasciculation, flaccid, areflexic
- MND: both, no sensory loss
- Sphincters and eye movements spared
Remember Twitching and brisk together: think MND.
Exam trap Fasciculations mean lower motor neuron disease, even when reflexes are brisk.
Why the other options are wrong
- Dorsal columns and spinothalamics Sensation is normal.
- Peripheral sensory and motor nerves A peripheral neuropathy would not cause brisk reflexes or extensor plantars.
- The neuromuscular junction Junction disorders do not cause fasciculations with UMN signs.
- Cerebellum and basal ganglia Neither causes wasting with fasciculation.
A man with a dense right hemiplegia after a left middle cerebral artery stroke can still sit up, breathe deeply and cough normally. Why are his trunk and respiratory muscles spared?
Answer: Axial muscles have bilateral descending control
About 85–90% of corticospinal fibres cross in the medullary pyramids to form the lateral corticospinal tract, which controls the distal limb muscles of the opposite side. The rest descend uncrossed in the anterior corticospinal tract and end on both sides of the cord, and reticulospinal and vestibulospinal pathways from both hemispheres also drive axial and proximal muscles. Trunk, neck and respiratory muscles therefore receive input from both hemispheres and are largely spared by a one-sided lesion, while the hand, which depends on the crossed lateral tract, is most affected.
Axial versus distal control
- Lateral CST: crossed, distal limbs
- Anterior CST: bilateral, axial muscles
- Trunk and breathing spared by one-sided lesions
- Hand worst affected
Remember One hemisphere can run the trunk; each hand needs its own.
Exam trap Bilateral hemispheric or brainstem lesions can affect breathing and swallowing even though a single stroke rarely does.
Why the other options are wrong
- Trunk muscles are supplied by cranial nerves Trunk muscles are supplied by spinal nerves.
- The infarct spares all corticospinal fibres Dense hemiplegia shows the corticospinal fibres are damaged.
- Spinal reflexes alone drive trunk muscles Voluntary sitting and coughing need descending control, not reflexes alone.
- Trunk muscles lack lower motor neurones All skeletal muscles have lower motor neurones.
A 68-year-old man who has had two strokes, one in each hemisphere, now has slurred speech, choking on liquids, a brisk jaw jerk and bouts of crying without sadness. His tongue is small and stiff but not wasted. Which of the following is damaged?
Answer: Corticobulbar tracts on both sides
Pseudobulbar palsy is an upper motor neurone lesion of the bulbar muscles. Most bulbar motor nuclei receive corticobulbar fibres from both hemispheres, so one stroke causes little lasting bulbar weakness, but lesions on both sides remove cortical control. The result is spastic dysarthria and dysphagia, a brisk jaw jerk, a small stiff tongue without fasciculation, and emotional lability. Lesions of the brainstem nuclei or nerves (bulbar palsy) instead give a wasted, fasciculating tongue and an absent jaw jerk.
Pseudobulbar palsy
- Bilateral corticobulbar lesions
- Brisk jaw jerk, spastic tongue
- Emotional lability
- Bulbar palsy: wasted, fasciculating tongue
Remember A brisk jaw jerk puts the lesion above the pons.
Exam trap Motor neurone disease can cause bulbar and pseudobulbar signs together.
Why the other options are wrong
- Nucleus ambiguus on one side A one-sided lesion would not give a brisk jaw jerk or lability.
- Hypoglossal nuclei in the medulla Nuclear damage gives a wasted, fasciculating tongue.
- Lower cranial nerves at the skull base A peripheral nerve lesion causes lower motor neurone signs.
- Neuromuscular junctions of bulbar muscles Myasthenia causes fatigable weakness without a brisk jaw jerk.
A man with chronic C7 root compression has visible irregular twitches in his wasted triceps at rest. What do these twitches represent?
Answer: Spontaneous firing of whole motor units
Fasciculations are spontaneous discharges of a whole motor unit, that is all the muscle fibres supplied by one lower motor neurone, so they are visible through the skin. They occur with lower motor neurone damage at the anterior horn cell or root and accompany wasting, hypotonia and reduced reflexes. Fibrillations are discharges of single denervated muscle fibres and are seen only on EMG. Upper motor neurone lesions do not cause fasciculation.
Fasciculation
- Spontaneous motor unit discharge
- Visible through the skin
- Sign of LMN damage
- Fibrillation: single fibre, EMG only
Remember Twitches plus wasting: lower motor neurone.
Exam trap Benign fasciculations are common in healthy people; they matter when combined with wasting and weakness.
Why the other options are wrong
- Single fibres firing (fibrillation) Too small to see; detected only on EMG.
- Myoclonic jerks from the cortex Myoclonus causes sudden jerks of a limb or body part.
- Tremor from the basal ganglia Tremor is rhythmic oscillation of a body part.
- Muscle spindle discharge to the cord Spindles are sensory and do not twitch the muscle.
A 58-year-old man with amyotrophic lateral sclerosis has wasting, fasciculation and brisk reflexes in all four limbs. Two years on, his eye movements, bladder control and sensation are still normal. Which of the following explains his normal bladder control?
Answer: Onuf's nucleus motor neurones are resistant
ALS destroys upper motor neurones in the cortex and lower motor neurones in the brainstem and anterior horns. Two groups of lower motor neurones are relatively resistant: those of the oculomotor, trochlear and abducens nuclei, and Onuf's nucleus in the anterior horn at S2, which supplies the external urethral and anal sphincters. Sensory neurones are not affected. Eye movements, continence and sensation are therefore usually preserved until late, which helps separate ALS from cord compression.
What ALS spares
- Eye movements (III, IV, VI)
- Sphincters (Onuf's nucleus)
- Sensation
- Mixed UMN and LMN signs elsewhere
Remember ALS spares the eyes, the bladder and sensation.
Exam trap Early sphincter disturbance or sensory loss in a patient with mixed UMN and LMN signs should prompt imaging for cord compression.
Why the other options are wrong
- The sphincters are supplied only by autonomic nerves The external sphincter is striated muscle with somatic motor neurones.
- The disease spares the sacral cord entirely Other sacral anterior horn cells, to the leg muscles, are affected.
- Sphincters have no lower motor neurones Onuf's nucleus provides somatic motor neurones to the sphincters.
- Sensory input keeps the sphincter closed Sensory input does not maintain voluntary sphincter control.
Where this sits in the CPSP syllabus
- Paper 1: Nervous system, Motor system: cortex, pyramidal and extrapyramidal tracts, UMN vs LMN
- Surgery & Allied, Paper 2: Nervous system, Motor system: cortex, pyramidal and extrapyramidal tracts, UMN vs LMN
- Medicine & Allied, Paper 2: Nervous system, Motor system: cortex, pyramidal and extrapyramidal tracts, UMN vs LMN