In one breath
The deep nuclei carry the cerebellum’s answer out: fastigius to the vestibular nuclei and reticular formation, interpositus to the red nucleus, and dentatus to the ventrolateral thalamus and on to the motor cortex. Through them the cerebellum keeps equilibrium, holds up muscle tone and posture, coordinates and times voluntary movement by comparing the intended movement with the actual one, and learns movements with practice. It commands no muscle itself, so its diseases cause no paralysis and no sensory loss — only clumsiness: hypotonia, ataxia, dysmetria, intention tremor, dysdiadochokinesia, nystagmus and slurred speech, all on the same side as the lesion.
Beyond your pages
This part of the chapter comes after the pages you were given: the book’s own sections on cerebellar outputs, functions, cerebellar dysfunction and cerebellar function tests are on later pages. What follows is written from standard physiology, so treat none of it as a quotation from your book, and check the wording of any list against your own copy before an exam. It is examinable content: two past papers have asked for the signs of cerebellar disease.
Builds on: Cerebellar divisions, histology and connections · Rubrospinal, vestibulospinal, reticulospinal and tectospinal tracts · Muscle spindle · Leads to: Basal ganglia: circuits and functions · Parkinson’s and Huntington’s disease · Sensory lesions and sensory function tests
Cerebellar outputs
Every deep nucleus sends its axons to the brainstem or the thalamus, and each one therefore steers a particular descending pathway:
| Deep nucleus | Projects to | Pathway it steers |
|---|---|---|
| Fastigius | Vestibular nuclei, reticular formation | Vestibulospinal, reticulospinal |
| Interpositus | Red nucleus (+ thalamus) | Rubrospinal |
| Dentatus | Ventrolateral thalamus | Corticospinal, via motor cortex |
- Fastigial output leaves largely through the inferior cerebellar peduncle; it reaches the axial and proximal muscles and so serves equilibrium, posture and tone.
- Interposital and dentate output leaves through the superior cerebellar peduncle and crosses the midline in the midbrain.
- The dentate loop is the long one: dentate → ventrolateral thalamus (Thalamus: nuclei, functions and thalamic syndrome) → motor and premotor cortex → corticospinal tract. This is the loop that lets the cerebrocerebellum shape a movement before and while the cortex issues it (Cortical integration and motor cortex, Corticospinal (pyramidal) tract).
Why cerebellar signs are ipsilateral
The cerebellar output crosses once in the midbrain, and the corticospinal tract it finally influences crosses again in the medulla. Two crossings return the influence to the side it started from, so a right cerebellar lesion gives right-sided signs. Contrast a capsular lesion, which gives contralateral signs (Upper vs lower motor neuron lesions). Examiners ask this as “on which side are cerebellar signs, and why”.
Functions of the cerebellum
Equilibrium
- The vestibulocerebellum works in a two-way loop with the vestibular nuclei and, through the vestibulospinal tract, keeps the body balanced against gravity and against movement of the head.
- It also calibrates the vestibulo-ocular reflex, so that the eyes stay on a target while the head moves.
Muscle tone
- The cerebellum facilitates the tone of muscles, largely through the fastigial projection to the vestibular nuclei and reticular formation (Inverse stretch reflex and muscle tone).
- It adjusts the γ motor neuron drive to the muscle spindles, and so sets the gain of the stretch reflex (Stretch reflex).
- Losing that facilitation is why a cerebellar lesion causes hypotonia, not spasticity.
Posture
- The vermal spinocerebellum projects to the brainstem centres for axial and proximal muscles, keeping the trunk and girdles steady while the limbs work.
Coordination of voluntary movement
This is the cerebellum’s central job, and it does it as a comparator:
- The motor cortex sends a copy of the intended movement to the cerebellum through the pontine nuclei.
- The spinocerebellar tracts report, continuously, what the limb is actually doing.
- The cerebellum computes the error between the two and corrects it within the movement, through the thalamocortical and brainstem loops.
From that one mechanism come several named functions:
- Smoothing (damping): without it a limb overshoots, swings back and oscillates. Damping is what prevents the oscillation.
- Timing, or the turn-on and turn-off signal: the cerebellum decides when a movement starts and, above all, when the braking must begin so that the hand stops on the target and not beyond it.
- Synergy: it sequences the muscles of a multi-joint movement so that the movement looks like one act and not a chain of separate ones.
- Prediction (feedforward): it predicts where a moving limb, or a moving object, will be a moment from now, and acts on the prediction rather than waiting for feedback.
Planning and programming
- The cerebrocerebellum, in its loop with the cortex, takes part in planning and programming a movement before it is executed, and in sequencing rapid movements one after another.
Motor learning
- Repeating a movement rewires the cerebellar circuit, most of all the strength of the parallel fibre synapses on Purkinje cells, with the climbing fibre acting as the error signal that drives the change.
- This is how a skill becomes automatic, and it is the same mechanism as the learned adjustment of the vestibulo-ocular reflex.
Speech and eye movements
- Speech needs rapid, precisely timed movements of the tongue, lips and larynx, so it is a cerebellar function; its failure is dysarthria.
- Smooth pursuit and accurate saccades need cerebellar calibration, which is why lesions cause nystagmus and inaccurate eye movements.
Signs of cerebellar disease
There is no paralysis, no sensory loss and no Babinski sign. What appears is disordered execution, on the same side as the lesion:
| Sign | What is seen |
|---|---|
| Hypotonia | Flabby muscles, reduced resistance to passive movement |
| Asthenia | Weak, easily tired muscles |
| Ataxia | Irregular, uncoordinated movement |
| Dysmetria | Movement stops short of, or beyond, the target |
| Intention tremor | Tremor that appears on moving, worst near the target |
| Dysdiadochokinesia | Rapid alternating movements are slow and clumsy |
| Dysarthria | Slurred, staccato, “scanning” speech |
| Nystagmus | Coarse horizontal oscillation of the eyes |
| Pendular knee jerk | The leg swings to and fro after the tap |
| Rebound phenomenon | Loss of the checking of a suddenly released limb |
| Decomposition | A movement is performed joint by joint |
| Ataxic gait | Wide-based, reeling, veering to the side of the lesion |
| Titubation | Rhythmic nodding of the head and trunk |
The reasoning behind the main ones:
- Hypotonia and the pendular knee jerk: the cerebellum’s facilitation of the motor neuron pool is lost, so tone falls, and a hypotonic limb has nothing to damp the swing of a tendon reflex.
- Dysmetria and intention tremor: the braking signal is late or absent, so the limb overshoots, is corrected, overshoots the other way, and oscillates as it closes on the target.
- Ataxia and decomposition: the sequencing of muscles across joints is lost, so a smooth act falls apart into its components.
- Rebound (Stewart–Holmes sign): the check that normally stops a contracting limb when resistance is suddenly removed fails, so the forearm flies up and strikes the patient.
- Dysarthria: the same timing failure applied to the muscles of speech.
The three cerebellar syndromes
| Syndrome | Part affected | Picture |
|---|---|---|
| Archicerebellar | Flocculonodular lobe | Truncal ataxia, nystagmus, falls |
| Paleocerebellar | Anterior lobe, vermis | Gait ataxia, legs worse than arms |
| Neocerebellar | Hemisphere | Limb ataxia, intention tremor, hypotonia |
- The archicerebellar syndrome is the one of medulloblastoma in children, a midline tumour near the roof of the fourth ventricle: the child cannot sit or stand steadily, though the limbs may test almost normally.
- The paleocerebellar syndrome is the classic picture of anterior lobe degeneration in chronic alcoholism: a staggering gait with relatively spared arms.
- The neocerebellar syndrome follows a tumour, infarct or abscess of one hemisphere, and gives the full set of limb signs on that side.
Cerebellar ataxia is not sensory ataxia
In cerebellar ataxia the patient is unsteady with the eyes open and with them closed: closing the eyes adds little, so Romberg’s sign is negative. In sensory (posterior column) ataxia the patient manages with the eyes open and then sways or falls when they close, which is a positive Romberg (Abnormalities of dorsal column sensations). The cerebellar patient also looks at the ground while walking, but for a different reason: vision is standing in for coordination, not for proprioception.
Three tremors, told apart
- Intention tremor: absent at rest, appears during movement, worst as the target nears → cerebellar.
- Resting (pill-rolling) tremor: present at rest, disappears on movement, with rigidity and bradykinesia → Parkinsonism (Parkinson’s and Huntington’s disease).
- Titubation: a rhythmic tremor of the head and trunk while sitting or standing → a midline cerebellar lesion.
The same page also separates hypotonia (cerebellar) from the hypertonia of a UMN lesion and the rigidity of basal ganglia disease.
Cerebellar function tests
These need nothing but a bed and a hand, so they are favourite practical and viva items. Test both sides and compare.
| Test | How | Cerebellar result |
|---|---|---|
| Finger–nose | Touch nose from arm’s length, eyes open then shut | Dysmetria, intention tremor |
| Finger–nose–finger | Alternate own nose and examiner’s finger | Overshoot, past-pointing |
| Past-pointing | Raise arms, then bring index fingers together | Fingers miss on the affected side |
| Heel–shin | Run the heel down the opposite shin | The heel wavers off the line |
| Rapid alternating | Rapidly pronate and supinate on the palm | Slow, irregular: dysdiadochokinesia |
| Rebound (Holmes) | Pull the flexed forearm, release suddenly | Forearm flies up, no check |
| Knee jerk | Tap the patellar tendon | Pendular swinging |
| Romberg | Stand with feet together, eyes open then shut | Sways both ways: Romberg negative |
| Tandem walking | Walk heel to toe along a straight line | Cannot keep the line, reels |
| Gait | Walk across the room and turn | Wide-based, staggering, veers |
| Speech | Repeat a long test phrase | Slurred, staccato, scanning |
| Handwriting | Write a sentence and compare with old writing | Large, irregular letters |
| Tone | Move the joints passively; shake the limb | Flabby, floppy, wide excursion |
- Also look for nystagmus on lateral gaze, and test the accuracy of eye movements.
- Because all these signs are ipsilateral, a one-sided abnormality localises the lesion to that cerebellar hemisphere.
Applied: reading a cerebellar case
A middle-aged man reels to the right when he walks and reaches past his cup with the right hand. On examination the right arm is hypotonic, the right finger–nose test shows a tremor that worsens near the nose, rapid pronation–supination is clumsy on the right, the right knee jerk is pendular, there is nystagmus worst on looking right, and speech is slurred. Power, sensation and the plantar response are normal.
- Diagnosis: a right neocerebellar lesion, in the right cerebellar hemisphere.
- What clinches it: normal power and sensation with a normal plantar exclude a corticospinal lesion; hypotonia with a pendular reflex excludes a UMN lesion; the signs being on the same side as the reeling gait points to the cerebellum and not the internal capsule.
- Mechanism to quote: lost dentate output → no braking or timing signal for the right limbs, and lost facilitation of tone.
Draw it: the cerebellum as a comparator
Draw three boxes in a triangle and one at the bottom:
- Motor cortex at the top left. Cerebellum at the top right. Spinal cord and muscle at the bottom.
- Arrow cortex → cord → muscle: label it the command.
- Arrow cortex → pontine nuclei → cerebellum: label it copy of the plan.
- Arrow muscle and joint → spinocerebellar tracts → cerebellum: label it what is actually happening (feedback).
- Inside the cerebellum box write plan − performance = error.
- Arrow out of the cerebellum, splitting in two: one through dentate → ventrolateral thalamus → motor cortex, the other through fastigius and interpositus → brainstem nuclei → descending tracts. Label both correction.
- Mark the single crossing in the midbrain on the outflow, and the second crossing in the medulla on the corticospinal tract: write beside them two crossings, so signs are ipsilateral.
The same figure explains dysmetria and intention tremor: rub out the correction arrow and the limb has no way to stop on target.
Exam-answer skeleton: "Describe the signs of cerebellar disease, with their physiological basis, and the tests used to elicit them" (short note)
- One line on what the cerebellum does: comparator and coordinator, with no direct command over muscle, so a lesion gives clumsiness without paralysis or sensory loss, on the same side.
- Say why it is ipsilateral: the outflow crosses in the midbrain and the corticospinal tract crosses again in the medulla.
- The signs, as a list: hypotonia, asthenia, ataxia, dysmetria, intention tremor, dysdiadochokinesia, dysarthria, nystagmus, pendular knee jerk, rebound, decomposition of movement, ataxic gait, titubation.
- Basis of four of them: hypotonia (lost facilitation of the motor neuron pool), intention tremor and dysmetria (lost braking and timing), pendular reflex (hypotonia leaves the swing undamped), rebound (lost check on a released limb).
- The tests, paired to the signs: finger–nose, heel–shin, rapid alternating movements, rebound test, knee jerk, tandem walking and gait, speech, handwriting, tone.
- Romberg: negative in cerebellar ataxia, positive in sensory ataxia; use it to separate the two.
- Localise it: archicerebellar (truncal ataxia, medulloblastoma), paleocerebellar (gait ataxia, alcohol), neocerebellar (limb signs).
- Finish with the contrast against a UMN lesion and against Parkinsonism, in one line each.
Asked in exams
- Signs of cerebellar disease: Dec 2015, 4 marks · Jan 2021, 2 marks