Orientation
Rapid review
What you should already have
About 65 minutes
Plus the time it takes to redraw this lesson’s figures from memory, which is the fastest way to find out what you have not understood.
Where this shows up
The motor unit concept explains neuromuscular monitoring, critical-illness weakness and the recruitment order you exploit every time you interpret a train-of-four. The upper-against-lower-motor-neuron distinction is the single most useful piece of clinical neurology you will carry.
Learning outcomes
By the end of this lesson you should be able to:
- Describe the three levels of motor hierarchy and state what each contributes.
- Define the motor unit, relate innervation ratio to the precision of the muscle, and explain graded force by recruitment and rate coding.
- State the size principle and predict the order of motor unit recruitment.
- Trace the corticospinal tract from cortex to anterior horn cell, stating where it decussates and what proportion does so.
- Name the extrapyramidal tracts, their origin and their function.
- Describe the roles of the cerebellum and basal ganglia in motor control, and the deficit produced by disease of each.
- Distinguish upper from lower motor neuron lesions by tone, reflexes, wasting and plantar response.
Together these settle one syllabus objective: Motor control: cortex, basal ganglia and cerebellum. Tick it on the Physiology objective list once you can do all of the above without notes.
The minimum high-yield framework
- Three levels in series — cortex plans, brainstem sets tone and posture, spinal cord executes.
- Two side loops — basal ganglia and cerebellum. Neither reaches the cord; both act back on cortex through the thalamus.
- The α motor neuron is the final common pathway. Every influence on movement must act through it.
- Motor unit = one α motor neuron and all the muscle fibres it supplies. Innervation ratio is low where control is fine (extraocular muscle, of the order of 1:10) and high where it is coarse (gastrocnemius, of the order of 1:2000).
- Force is graded two ways — recruitment of more units, and rate coding, increasing the firing frequency of active units.
- The size principle. Small motor neurons are recruited first — slow, fatigue-resistant type I units — and large ones last.
- Pyramidal = corticospinal and corticobulbar, for fine voluntary movement; about 85-90% decussate in the medullary pyramids. Extrapyramidal = rubrospinal, vestibulospinal, reticulospinal, tectospinal, for tone and posture.
- Upper motor neuron lesion: spastic, hyperreflexic, extensor plantar, no wasting. Lower: flaccid, areflexic, wasted, fasciculating.
The architecture
The motor hierarchy
The motor hierarchy, and the two loops that are not in it
Three levels in series: the cortex plans and initiates, the brainstem sets tone and posture, and the spinal cord executes through the α motor neuron — the final common pathway, since every influence on movement, whatever its origin, must act through it.
The basal ganglia and the cerebellum are drawn as side loops because that is what they are: neither projects to the spinal cord. Both receive from the cortex and return to it through the thalamus. That single anatomical fact predicts the clinical picture — disease of either produces disordered movement rather than weakness, because the corticospinal pathway itself is intact. The basal ganglia loop selects and initiates the intended movement while suppressing unwanted ones, so its disorders are hypokinetic or hyperkinetic; the cerebellar loop compares intention with performance and corrects in flight, so its disorders are of coordination, timing and accuracy, and are ipsilateral. A separate spinocerebellar pathway carries unconscious proprioception from muscle back to the cerebellum, which is what it compares against.
| Level | Structures | What it contributes | Failure produces |
|---|---|---|---|
| Highest — planning | Prefrontal, premotor and supplementary motor cortex | Intention, strategy and the sequence of a movement. The premotor cortex builds a plan from parietal sensory and spatial input; the supplementary motor area coordinates complex, learned and bimanual movements | Apraxia — the movement can be made, but not on demand or in the right order |
| Middle — execution | Primary motor cortex (Brodmann area 4, precentral gyrus) and brainstem nuclei | Translating the plan into commands. The primary motor cortex is somatotopically organised as the motor homunculus, with face and hand lateral and leg medial | Weakness of voluntary movement, contralateral to a cortical lesion |
| Lowest — the final common pathway | α and γ motor neurons in the anterior horn, and the spinal reflex circuits | The only route to muscle. Also the seat of the reflexes and of the central pattern generators for locomotion | Flaccid paralysis, wasting and areflexia in the affected myotome |
The output element
The motor unit
The innervation ratio — fibres per motor neuron — determines how finely a muscle can be graded. It is low in muscles requiring precision and high in those producing bulk force:
| Muscle | Approximate innervation ratio | Consequence |
|---|---|---|
| Extraocular muscles | Of the order of 1:10 | Extremely fine gradation, for precise conjugate gaze |
| Intrinsic muscles of the hand, laryngeal muscles | Of the order of 1:100 | Fine manipulation and phonation |
| Gastrocnemius, quadriceps | Of the order of 1:1000-2000 | Coarse gradation, large forces, postural work |
All the fibres of one motor unit are of the same type, because the motor neuron determines their phenotype — a fact demonstrated by cross-innervation experiments, in which a muscle switches type when supplied by the other kind of nerve.
| Type | Motor neuron | Muscle fibres | Properties | Recruited |
|---|---|---|---|---|
| Slow (S), type I | Small cell body, small-diameter axon, low threshold | Type I — red, high myoglobin, many mitochondria, oxidative | Slow, low force, highly fatigue-resistant | First, and active during posture and sustained low-level activity |
| Fast fatigue-resistant (FR), type IIa | Intermediate | Type IIa — oxidative-glycolytic | Faster, more force, moderately fatigue-resistant | Second |
| Fast fatigable (FF), type IIb/x | Large cell body, large axon, high threshold | Type IIb/x — white, glycolytic, few mitochondria | Fastest, greatest force, fatigues quickly | Last, and only for maximal or rapid effort |
Producing the right force
Recruitment, rate coding and the size principle
- Recruitment. More motor units are brought into action. This is the dominant mechanism at low and moderate force.
- Rate coding. Already-active units fire faster. Because a muscle twitch outlasts the muscle action potential, successive twitches summate, and at sufficient frequency fuse into a smooth tetanus producing several times the force of a single twitch. This dominates at high force, once most units are recruited.
Note that muscle tetanus is mechanical fusion, not electrical. The muscle action potentials remain discrete and all-or-none; it is the contractile responses that summate, because the twitch is long relative to the electrical event. Nerve cannot be tetanised for the opposite reason, as set out in lesson 2.
Voluntary movement
The pyramidal system
The corticospinal tract arises from pyramidal cells in layers III and V of the premotor, precentral and postcentral cortex. It descends through the posterior limb of the internal capsule, then the cerebral peduncle, pons and medulla. In the ventral medulla the great majority — about 85-90% — decussate in the pyramids to become the lateral corticospinal tract; the remaining 10-15% continue uncrossed as the anterior corticospinal tract and supply axial and proximal muscles, including the thoracic respiratory muscles.
Its function is precise, fractionated movement — the ability to move one finger independently of the others — together with control of the laryngeal muscles. The corticobulbar tract is its cranial equivalent, terminating on lower motor neurons in the brainstem cranial nerve nuclei and controlling facial and bulbar musculature.
Tone and posture
The extrapyramidal tracts
| Tract | Origin | Decussation | Function |
|---|---|---|---|
| Rubrospinal | Red nucleus, midbrain | Crosses immediately, in the midbrain | Facilitates flexor tone, particularly in the upper limb. Receives cortical input |
| Lateral vestibulospinal | Lateral vestibular (Deiters) nucleus | Uncrossed | Extensor (antigravity) tone and balance |
| Medial vestibulospinal | Medial vestibular nucleus | Largely bilateral | Head and neck position, and stabilisation of gaze |
| Reticulospinal (pontine and medullary) | Reticular formation of pons and medulla | Largely uncrossed | Muscle tone, posture, locomotor pattern generation, and descending modulation of pain |
| Tectospinal | Superior colliculus | Crosses in the midbrain | Reflex turning of head and neck toward a visual or auditory stimulus |
The two loops
Cerebellum and basal ganglia
| Cerebellum | Basal ganglia | |
|---|---|---|
| Components | Cerebellar cortex, deep nuclei, three peduncles | Caudate, putamen, globus pallidus, subthalamic nucleus, substantia nigra |
| Loop | Cortex → pons → cerebellum → dentate → thalamus → cortex | Cortex → striatum → pallidum → thalamus → cortex |
| Role | Compares intended with actual movement using proprioceptive feedback, and corrects in flight. Timing, coordination, and motor learning | Selects and initiates the intended movement while suppressing competing ones. Scales amplitude and speed |
| Laterality of signs | Ipsilateral — its output crosses twice | Contralateral |
| Disorder produces | Ataxia, intention tremor, dysdiadochokinesis, dysmetria, nystagmus, scanning speech — with normal power | Hypokinetic (Parkinsonism: bradykinesia, rigidity, resting tremor) or hyperkinetic (chorea, hemiballismus, dystonia) — with normal power |
The reason both produce disorder rather than weakness is anatomical: neither projects to the spinal cord. The corticospinal tract remains intact, so force generation is preserved; what is lost is the selection, scaling and correction of movement.
The clinical distinction
Upper against lower motor neuron
| Feature | Upper motor neuron | Lower motor neuron |
|---|---|---|
| Site of lesion | Anywhere from motor cortex to the anterior horn cell (exclusive) | Anterior horn cell, root, plexus, peripheral nerve, or the neuromuscular junction and muscle |
| Tone | Increased — spasticity, clasp-knife | Decreased — flaccid |
| Reflexes | Exaggerated (hyperreflexia); clonus may be present | Reduced or absent |
| Plantar response | Extensor (Babinski) | Flexor or absent |
| Wasting | Absent or minimal, and late (disuse only) | Marked and early |
| Fasciculation | Absent | Present — a hallmark of anterior horn cell disease |
| Distribution of weakness | Pyramidal pattern — extensors weak in the arm, flexors weak in the leg | Follows the root, plexus or nerve involved; myopathies are proximal |
| Timing | Spasticity develops over days to weeks; initially flaccid (spinal shock) | Immediate |
The pattern is derivable rather than memorisable. An upper motor neuron lesion removes descending inhibition from a reflex arc that is still intact, so tone and reflexes are released — spasticity and hyperreflexia. The muscle is still innervated, so it does not waste or fasciculate. A lower motor neuron lesion destroys the arc itself, so tone and reflexes are lost and the muscle is denervated, wasting and fasciculating.
Previously examinedOctober 2024 · April 2023 — the neural pathway from receptor to effector muscle in a withdrawal response, and the motor unit concept in critical-illness-acquired weakness. Worked answers in the library
Anaesthetic and clinical application
Motor physiology in practice
Neuromuscular monitoring and the motor unit
A twitch response is the summed contraction of all the motor units the supramaximal stimulus recruits. That is why the stimulus must be supramaximal: only then does a change in the response reflect a change at the junction rather than a change in how many axons were stimulated. Fade on train-of-four reflects presynaptic receptor blockade reducing acetylcholine mobilisation with successive stimuli, and post-tetanic facilitation reflects the mobilisation that tetanus produces.
Critical illness and the motor unit
Intensive-care-acquired weakness involves both a critical illness polyneuropathy, an axonal neuropathy giving lower motor neuron signs, and a critical illness myopathy affecting the muscle fibres themselves. Because the motor unit is one neuron and its fibres, damage at either end reduces the force the unit can produce, and the two commonly coexist. Immobility, hyperglycaemia, sepsis, corticosteroids and prolonged neuromuscular blockade are the recognised contributors, and the resulting weakness is proximal, symmetrical and a major determinant of ventilator weaning.
Motor evoked potentials
Because the corticospinal tract runs in the anterior two-thirds of the cord — the anterior spinal artery territory — motor evoked potentials monitor the territory at risk during thoracoabdominal aortic surgery, whereas somatosensory evoked potentials travel in the posterior columns and can remain normal while that territory infarcts. Motor evoked potentials are also exquisitely sensitive to volatile agents and to neuromuscular blockade, which is why they are usually recorded under total intravenous anaesthesia without paralysis.
Consolidation
The lesson in one paragraph
Motor control is hierarchical: prefrontal, premotor and supplementary areas plan; primary motor cortex and brainstem nuclei execute; and α and γ motor neurons in the anterior horn form the final common pathway, through which every influence on movement must act. The basal ganglia and cerebellum are side loops that receive from cortex and return to it through the thalamus without projecting to the cord, which is why disease of either produces disordered movement rather than weakness — hypokinetic or hyperkinetic disorders for the basal ganglia, and ipsilateral ataxia, intention tremor and dysdiadochokinesis for the cerebellum. The motor unit is one α motor neuron and all the fibres it supplies, all of one type; the innervation ratio is low where control is fine and high where force is required. Force is graded by recruitment and by rate coding, and recruitment follows the size principle — small, fatigue-resistant type I units first, because a small neuron has a higher input resistance and reaches threshold sooner. The pyramidal corticospinal tract descends through the posterior limb of the internal capsule, decussates 85 to 90% in the medullary pyramids, and mediates fine fractionated distal movement; the corticobulbar tract does the same for cranial nerve nuclei. The extrapyramidal rubrospinal, vestibulospinal, reticulospinal and tectospinal tracts govern tone and posture. An upper motor neuron lesion releases an intact reflex arc, giving spasticity, hyperreflexia and an extensor plantar without wasting; a lower motor neuron lesion destroys the arc, giving flaccidity, areflexia, wasting and fasciculation.