Physiology chapters
Motor cortex, corticospinal tract and motor neurons
How the motor cortex plans and sends commands, the route of the corticospinal tract, the motor unit, and how to tell an upper motor neuron lesion from a lower motor neuron lesion.
- The primary motor cortex (area 4) controls voluntary movement of the opposite side; the premotor and supplementary areas plan it.
- The corticospinal tract runs through the internal capsule and pyramids; most fibres cross at the pyramidal decussation.
- UMN lesions give spasticity, brisk reflexes and a Babinski sign; LMN lesions give wasting, flaccidity, absent reflexes and fasciculations.
On this page
Overview
Voluntary movement starts in the motor areas of the frontal lobe. Commands travel down the corticospinal tract to lower motor neurons in the brainstem and spinal cord, which make muscles contract.
Damage at different levels gives different patterns of weakness. Telling upper from lower motor neuron lesions is one of the most tested ideas in neurophysiology.
Motor areas of the cortex
| Area | Location | Role |
|---|---|---|
| Primary motor cortex (area 4) | Precentral gyrus | Sends commands for voluntary movement of the opposite side; fine control of hand and face |
| Premotor area (area 6, lateral) | In front of area 4 | Plans movement, especially in response to outside cues; sets posture for the movement |
| Supplementary motor area (area 6, medial) | Medial surface, above the cingulate | Plans complex sequences and two-handed movements; active when you rehearse a movement mentally |
| Broca's area | Inferior frontal gyrus (dominant side) | Motor planning of speech |
| Frontal eye field | Area 8 | Voluntary eye movements to the opposite side |
The primary motor cortex is arranged as a motor homunculus, with the leg on the medial surface and the face lowest on the lateral surface. The hand, lips and tongue have huge areas because of their fine control.
The large Betz (giant pyramidal) cells of layer V are found in area 4. They give rise to some of the fast corticospinal fibres, but most corticospinal fibres come from smaller cells.
The corticospinal (pyramidal) tract
About 30% of its fibres come from the primary motor cortex, 30% from the premotor and supplementary motor areas, and about 40% from the somatosensory areas behind the central sulcus.
Route: motor cortex → posterior limb of the internal capsule → crus cerebri of the midbrain → pons → pyramids of the medulla.
- At the lower medulla, most fibres (about 80–90%) cross at the pyramidal decussation and descend as the lateral corticospinal tract.
- The rest descend uncrossed as the anterior corticospinal tract and mostly cross at the level where they end.
- Fibres end on interneurons and on anterior horn cells.
The corticobulbar fibres do the same job for the cranial nerve motor nuclei.
The lateral corticospinal tract is essential for fine, skilled movements of the fingers and hands.
Lower motor neurons and the motor unit
Lower motor neurons are the anterior horn cells (and cranial nerve motor nuclei) whose axons go straight to muscle.
- Alpha motor neurons: supply ordinary (extrafusal) muscle fibres and cause contraction.
- Gamma motor neurons: supply the muscle spindle (intrafusal) fibres and set its sensitivity.
A motor unit is one motor neuron and all the muscle fibres it supplies.
- Small motor units (a few fibres per neuron) allow fine control: eye muscles, small hand muscles.
- Large motor units (hundreds or thousands of fibres) give power: back and thigh muscles.
How force is graded
- Recruitment: more motor units are switched on.
- Size principle: small motor neurons are recruited first, then larger ones, so force increases smoothly.
- Rate coding: each unit fires faster, and contractions sum.
By the size principle, the smallest motor units are recruited first; the largest last.
Upper vs lower motor neuron lesions
| Sign | Upper motor neuron (UMN) | Lower motor neuron (LMN) |
|---|---|---|
| Site | Cortex, internal capsule, brainstem or cord tracts | Anterior horn, root, peripheral nerve |
| Weakness | In a pattern (e.g. arm extensors, leg flexors) | In muscles supplied by the damaged neurons |
| Tone | Increased (spastic, clasp-knife) | Reduced (flaccid) |
| Reflexes | Brisk, clonus may be present | Reduced or absent |
| Plantar response | Extensor (Babinski sign) | Flexor or absent |
| Wasting | Little, late (disuse) | Marked, early |
| Fasciculations | Absent | Present |
The Babinski sign (upgoing big toe when the sole is stroked) indicates a lesion of the corticospinal tract. It is normal in infants under about one year.
A pure lesion of the corticospinal tract causes weakness and a Babinski sign with less spasticity. Spasticity comes mainly from damage to the accompanying extrapyramidal (reticulospinal and vestibulospinal) pathways, which usually happens together in strokes.
Spinal shock
How it happens: sudden transection of the spinal cord removes all descending input to the cord below the injury.
What you see: at first, everything below the level is flaccid, with no reflexes, low blood pressure and loss of bladder function. Over days to weeks, the cord neurons recover their excitability and UMN signs (spasticity, brisk reflexes, Babinski) appear.
Decorticate and decerebrate posture
- Decorticate (lesion above the red nucleus): arms flexed, legs extended.
- Decerebrate (lesion between the red nucleus and vestibular nuclei, in the brainstem): arms and legs extended. The extensor-driving vestibulospinal and reticulospinal pathways act without the brain's control.
Decerebrate rigidity (all limbs extended) has a worse outlook than decorticate posture, because the lesion is lower, in the brainstem.
Clinical relevance
Stroke in the internal capsule
How it happens: bleeding or blockage of small arteries supplying the posterior limb.
What you see: sudden weakness of the opposite face, arm and leg; flaccid at first, then spastic with brisk reflexes and a Babinski sign.
Motor neuron disease
How it happens: degeneration of both upper and lower motor neurons.
What you see: mixed UMN and LMN signs (wasting and fasciculations with brisk reflexes), with no sensory loss.
Poliomyelitis
How it happens: a virus destroys anterior horn cells.
What you see: pure LMN weakness, flaccid and wasted muscles, no sensory loss.
Expect: the role of each motor area, the route and crossing of the corticospinal tract, the definition of a motor unit and the size principle, the full UMN vs LMN table, the Babinski sign, spinal shock, and decorticate vs decerebrate posture.
Quick revision
- Area 4: primary motor; area 6: premotor and supplementary (planning).
- Corticospinal tract: internal capsule → pyramids → decussation → lateral tract.
- Motor unit: one motor neuron and its muscle fibres; small units for fine control.
- Size principle: small units first.
- UMN: spastic, brisk reflexes, Babinski. LMN: flaccid, wasting, fasciculations.
- Spinal shock: flaccid and areflexic first, then spastic.
- Decorticate: arms flexed. Decerebrate: all limbs extended.
Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).
FAQ
What is a motor unit?
One motor neuron and all the muscle fibres it supplies.
What are the signs of an upper motor neuron lesion?
Weakness, increased tone (spasticity), brisk reflexes, clonus and an extensor plantar response (Babinski sign), with little wasting.
What is the size principle?
As force increases, small motor neurons are recruited first, then progressively larger ones.
What is spinal shock?
The temporary loss of all reflexes and tone below a sudden spinal cord injury, before UMN signs develop.