Cerebellum anatomy
Cerebellum: functional divisions, cortex, peduncles, connections and lesions
Cerebellum for FCPS Part 1: functional divisions, cortical layers and cell types, mossy and climbing fibres, peduncles, blood supply and signs of disease. Covers cerebellar versus sensory ataxia, alcohol, paraneoplastic anti-Yo, posterior fossa tumours and herniation.
What the cerebellum does
- The cerebellum compares the intended movement (from cortex via the pons) with what is actually happening (from muscles, joints and the vestibular system) and corrects errors. It does not start movement; initiation depends on the cortex and basal ganglia.
- It acts on the same side of the body: its output crosses in the superior peduncle to the opposite red nucleus and thalamus, and the corticospinal tract then crosses back in the medulla.
Functional divisions
| Division | Parts | Main connections | Function | Lesion |
|---|---|---|---|---|
| Vestibulocerebellum (archicerebellum) | Flocculonodular lobe | Vestibular nuclei | Balance, eye movements | Nystagmus, truncal ataxia (medulloblastoma of the nodulus in children) |
| Spinocerebellum (palaeocerebellum) | Vermis and paravermis, anterior lobe | Spinocerebellar tracts; fastigial and interposed nuclei | Posture, tone, gait | Truncal and gait ataxia, wide-based gait; alcohol damages the anterior superior vermis |
| Cerebrocerebellum (neocerebellum) | Lateral hemispheres | Cortex to pons to hemisphere; dentate to thalamus to motor cortex | Planning, timing and coordinating limb movement | Limb ataxia, intention tremor, dysmetria, dysdiadochokinesia |
Cortex: layers and cells
| Layer | Cells | Notes |
|---|---|---|
| Molecular (outer) | Stellate and basket cells, Purkinje dendrites, parallel fibres | Inhibitory interneurones |
| Purkinje cell layer | Purkinje cells | Only output of the cortex; GABAergic, inhibitory to deep nuclei |
| Granular (inner) | Granule cells (the only excitatory, glutamatergic cortical neurone), Golgi cells | Site of mossy fibre rosettes |
- Mossy fibres (from pontine nuclei, spinal cord, vestibular nuclei) end on granule cells in the granular layer; granule axons rise as parallel fibres to many Purkinje cells.
- Climbing fibres come only from the contralateral inferior olive and wrap directly around a single Purkinje cell; they are important in motor learning.
- Purkinje cells are among the neurones most sensitive to hypoxia, along with hippocampal CA1 and cortical layers III, V and VI.
- Deep nuclei from lateral to medial: dentate, emboliform, globose, fastigial. Dentate serves the hemispheres; fastigial serves the vestibular and vermal circuits. All excite their targets.
Peduncles
| Peduncle | Main fibres | Direction |
|---|---|---|
| Superior | Dentate and interposed output to opposite red nucleus and thalamus; ventral spinocerebellar input | Mainly output |
| Middle (largest) | Pontocerebellar fibres from the opposite pontine nuclei | Input only |
| Inferior | Dorsal spinocerebellar, olivocerebellar (climbing), vestibulocerebellar input; output to vestibular nuclei | Mainly input |
Signs of cerebellar disease
| Sign | What it looks like |
|---|---|
| Ataxia | Broad-based staggering gait (vermis); clumsy limbs (hemisphere) |
| Intention tremor | Tremor worsens as the finger approaches the target |
| Dysmetria | Past-pointing; overshoot |
| Dysdiadochokinesia | Slow, irregular rapid alternating movements |
| Nystagmus | Coarse, fast phase towards the side of the lesion |
| Scanning dysarthria | Slurred, staccato, separated syllables |
| Hypotonia | Pendular knee jerk, rebound phenomenon |
- Dysarthria of any cause is a problem of articulation with normal language: the patient understands, names, repeats and writes normally. Scanning speech points to the cerebellum.
- Intention tremor, scanning speech and nystagmus together suggest multiple sclerosis in a young adult.
Cerebellar versus sensory ataxia
| Feature | Cerebellar ataxia | Sensory ataxia |
|---|---|---|
| Lesion | Cerebellum or its connections | Dorsal columns, dorsal roots, large-fibre neuropathy |
| Eyes open | Unsteady | Steadier (vision compensates) |
| Romberg test | Negative (unsteady either way) | Positive (falls on closing eyes) |
| Proprioception and vibration | Normal | Lost |
| Examples | Alcohol, stroke, MS, tumour | B12 deficiency, tabes dorsalis, diabetic neuropathy |
- An elderly woman with macrocytic anaemia and ataxia has B12 deficiency with dorsal column (sensory) ataxia.
- Vestibular disorders cause vertigo, vomiting, nystagmus and unsteadiness with intact limb coordination; Romberg may be positive.
- Friedreich ataxia (autosomal recessive GAA repeat in frataxin) combines spinocerebellar, dorsal column and pyramidal damage: ataxia, dysarthria, absent ankle jerks with extensor plantars, pes cavus and hypertrophic cardiomyopathy.
Causes
- Alcohol: anterior superior vermis; gait ataxia with relatively normal arms and speech. Also thiamine deficiency (Wernicke).
- Paraneoplastic cerebellar degeneration: subacute severe ataxia, dysarthria and nystagmus with a normal MRI early on. Anti-Yo (anti-Purkinje cell) antibodies with ovarian and breast cancer; anti-Hu and anti-VGCC with small cell lung cancer.
- Tumours: in children, pilocytic astrocytoma (cystic, Rosenthal fibres, GFAP positive, good prognosis) and medulloblastoma (small round blue cells from the external granular layer, midline vermis, drop metastases). In adults, metastases and haemangioblastoma (von Hippel–Lindau).
- Drugs (phenytoin, lithium), hypothyroidism, MS, posterior circulation stroke.
- A hemisphere lesion near the CP angle can give ataxia with ipsilateral facial palsy and deafness (vestibular schwannoma, AICA stroke).
Mass effect in the posterior fossa
- The posterior fossa is small and tight. A cerebellar haematoma or swollen infarct compresses the fourth ventricle (obstructive hydrocephalus) and the brainstem. Sudden occipital headache, vomiting and inability to stand followed by drowsiness means urgent neurosurgical decompression.
- Lumbar puncture with raised pressure from a posterior fossa mass lowers spinal CSF pressure and lets the cerebellar tonsils herniate through the foramen magnum, compressing the medulla: sudden coma and respiratory arrest. Image first when there is papilloedema or focal signs.
- Chiari I malformation: low-lying tonsils, often with syringomyelia.
Blood supply
| Artery | Origin | Territory |
|---|---|---|
| Superior cerebellar (SCA) | Basilar, top | Superior surface, dentate |
| AICA | Basilar, lower | Anterior inferior surface; inner ear via labyrinthine artery; lateral pons |
| PICA | Vertebral | Inferior surface, inferior vermis, lateral medulla |
Remember Cerebellar signs are on the same side as the lesion, and the cerebellum is unsteady with the eyes open as well as shut.
Exam trap Romberg tests proprioception, not the cerebellum: positive Romberg means sensory ataxia.
Exam trap A normal MRI does not exclude cerebellar disease: suspect paraneoplastic anti-Yo with an ovarian mass.
How FCPS asks about this
- Only output of cerebellar cortex: Purkinje cells, inhibitory (GABA).
- Mossy fibres end in: granular layer (rosettes with granule cells); climbing fibres come from the inferior olive.
- Alcoholic with broad-based gait, normal arms: anterior vermis degeneration.
- Subacute ataxia, normal MRI, ovarian mass: anti-Yo paraneoplastic degeneration.
- Collapse after LP in a patient with posterior fossa tumour: tonsillar herniation compressing the medulla.
- Cerebellar haematoma 4 cm with drowsiness: urgent surgery for brainstem compression and hydrocephalus.
- Patient sways only with eyes closed: dorsal column lesion, not cerebellar.
Test yourself on this topic
5 of the 21 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 56-year-old woman develops severe unsteadiness, slurred speech and nystagmus over six weeks. MRI of the brain is normal, but pelvic ultrasound shows a complex ovarian mass and CA-125 is raised. Which of the following antibodies is most likely to be found?
Answer: Anti-Yo (Purkinje cell) antibody
A subacute, severe pancerebellar syndrome with normal early imaging in a woman with ovarian or breast cancer suggests paraneoplastic cerebellar degeneration with anti-Yo antibodies. The tumour expresses a neuronal antigen (cdr2), and the immune response, largely T-cell mediated, destroys cerebellar Purkinje cells, so recovery is poor even after tumour removal. Anti-Hu is linked to small cell lung cancer and sensory neuronopathy, and anti-NMDA receptor encephalitis to ovarian teratoma with psychiatric features.
Paraneoplastic cerebellar degeneration
- Subacute pancerebellar syndrome
- Anti-Yo: ovarian, breast cancer
- Purkinje cells lost; poor recovery
- MRI normal early, atrophy later
Remember Woman, ovarian mass, sudden ataxia: anti-Yo.
Exam trap A normal MRI does not exclude a cerebellar cause; paraneoplastic damage is cellular at first.
Why the other options are wrong
- Anti-Hu antibody Linked to small cell lung cancer with sensory neuronopathy or encephalomyelitis.
- Anti-NMDA receptor antibody Causes encephalitis with psychosis, seizures and dyskinesia.
- Anti-GAD antibody Linked to stiff person syndrome.
- Anti-acetylcholine receptor antibody Linked to myasthenia gravis and thymoma.
A left lateral medullary infarct causes left limb ataxia. Which of the following structures is damaged?
Answer: Left inferior cerebellar peduncle
The inferior cerebellar peduncle forms part of the lateral wall of the medulla. It carries the dorsal spinocerebellar tract, olivocerebellar climbing fibres and vestibulocerebellar fibres into the cerebellum on the same side. A lateral medullary infarct damages it, giving ipsilateral limb ataxia. Because cerebellar hemispheres control the same side of the body, the ataxia is on the side of the lesion.
Cerebellar peduncles
- Inferior: medulla, input (spinal, olive)
- Middle: pons, pontocerebellar
- Superior: midbrain, main output
- Hemisphere lesion: same-side ataxia
Remember Lateral medulla carries the inferior peduncle: same-side ataxia.
Exam trap Climbing fibres from the opposite inferior olive enter through the inferior peduncle.
Why the other options are wrong
- Left superior cerebellar peduncle Leaves at the midbrain level; not in the medulla.
- Right middle cerebellar peduncle Lies in the pons, not the medulla.
- Left medial lemniscus Medial medullary; carries proprioception, not cerebellar input.
- Right dentate nucleus Deep nucleus in the cerebellum, not damaged by a medullary infarct.
A 40-year-old woman with headaches, vomiting and papilloedema has a lumbar puncture in the OPD before any scan. Twenty minutes later she becomes deeply unconscious and stops breathing. Later imaging shows a large cerebellar tumour. What is the mechanism of her collapse?
Answer: Tonsils herniated, compressing the medulla
With a posterior fossa mass, pressure is high above the foramen magnum. Removing CSF from below creates a pressure gradient that pushes the cerebellar tonsils down through the foramen magnum (coning). The tonsils compress the medulla, where the respiratory and cardiovascular centres lie, causing apnoea and death. This is why imaging is needed before lumbar puncture when raised intracranial pressure is suspected.
Tonsillar herniation
- Tonsils through foramen magnum
- Compresses medulla
- Apnoea, cardiac arrest
- Scan before LP if ICP raised
Remember LP with a posterior fossa mass can cause coning.
Exam trap Neck stiffness and head tilt can be early signs of tonsillar herniation, mimicking meningitis.
Why the other options are wrong
- Uncus herniated, compressing the midbrain Seen with supratentorial masses; pupil dilates first.
- Cingulate gyrus herniated under the falx Compresses the anterior cerebral artery; rarely causes apnoea.
- Upward herniation of the vermis Can occur with posterior fossa masses but compresses the midbrain, not the medulla.
- Spinal cord injury from the needle Needle at the lumbar level is below the cord.
A 6-year-old has a midline posterior fossa tumour. He walks with a broad-based, unsteady gait and has nystagmus, but limb coordination is fairly normal. Which part of the cerebellum is mainly affected?
Answer: Flocculonodular lobe and vermis
The flocculonodular lobe (vestibulocerebellum) and vermis control balance, posture and eye movements. Midline lesions such as medulloblastoma in children cause truncal ataxia, a wide-based gait and nystagmus, with relatively spared limbs. Hemisphere lesions cause ipsilateral limb ataxia, intention tremor and dysdiadochokinesia.
Cerebellar lesions
- Midline: truncal ataxia, nystagmus
- Flocculonodular: vestibulocerebellum
- Hemisphere: ipsilateral limb ataxia
- Child midline tumour: medulloblastoma
Remember Middle shakes the trunk; sides shake the limbs.
Exam trap Cerebellar signs are on the same side as the lesion.
Why the other options are wrong
- Lateral cerebellar hemisphere Ipsilateral limb ataxia and intention tremor.
- Dentate nucleus Limb coordination output.
- Middle cerebellar peduncle Limb ataxia.
- Cerebellar tonsil only Herniation, not this picture.
A 14-year-old boy has a progressive clumsy gait, slurred speech, absent ankle jerks with extensor plantars, pes cavus and loss of vibration sense. His echocardiogram shows hypertrophic cardiomyopathy. The most likely genetic defect is:
Answer: GAA repeat expansion in frataxin
Friedreich ataxia is an autosomal recessive disorder caused by a GAA repeat in the frataxin gene, which impairs mitochondrial iron handling. It degenerates the spinocerebellar tracts, posterior columns, corticospinal tracts and dorsal root ganglia. This explains ataxia and dysarthria, loss of vibration, areflexia from dorsal root loss, and extensor plantars from pyramidal damage. Cardiomyopathy and diabetes are common, and cardiac disease is the usual cause of death.
Friedreich ataxia
- GAA repeat, frataxin
- Ataxia + areflexia + extensor plantars
- Pes cavus, scoliosis
- Hypertrophic cardiomyopathy
Remember Absent ankle jerks with upgoing toes in a teenager: Friedreich.
Exam trap It is the only common trinucleotide disorder on this list that is autosomal recessive.
Why the other options are wrong
- CAG repeat in huntingtin Huntington disease: chorea and dementia in adults.
- CTG repeat in DMPK Myotonic dystrophy: myotonia and distal weakness.
- CGG repeat in FMR1 Fragile X: learning disability and large testes.
- Deletion in the dystrophin gene Duchenne: proximal weakness and calf hypertrophy.
Where this sits in the CPSP syllabus
- Paper 1: Neuroanatomy, Cerebellum: parts, connections and lesions
- Surgery & Allied, Paper 2: Cranium and brain, Cerebellum: parts, connections and lesions
- Medicine & Allied, Paper 2: Central nervous system, Cerebellum: parts, connections and lesions
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