Where is the cerebellum and how is it divided?
The cerebellum ('little brain') is the largest part of the hindbrain. It lies in the posterior cranial fossa, behind the fourth ventricle, pons and medulla, and is separated from the cerebrum by the tentorium cerebelli. It is made of two hemispheres joined by the vermis and is divided into three lobes — anterior, posterior and flocculonodular — by two transverse fissures: the V-shaped primary fissure (between anterior and posterior lobes) and the posterolateral fissure (between posterior and flocculonodular lobes).

The surface is thrown into thin, accordion-like folds (folia) with a core of white matter, the arbor vitae, which surrounds the deep nuclei. The cerebellum develops from the posterior part of the alar plates of the metencephalon; the hemispheres and vermis are formed by about the 12th week. The cerebellar tonsils lie on the undersurface of the hemispheres just below the flocculonodular lobe — the structures that herniate through the foramen magnum in raised posterior-fossa pressure.
What are the functional divisions of the cerebellum?
Functionally the cerebellum is divided into three zones that match their main inputs. Learning each zone's input, role and lesion is the most useful way to answer clinical and anatomical stems.
| Zone (anatomical part) | Main input | Function | Lesion causes |
|---|---|---|---|
| Vestibulocerebellum (flocculonodular lobe) | Ipsilateral vestibular nuclei (plus visual input) | Balance, vestibulo-ocular reflex, smooth pursuit; projects directly to vestibular nuclei, bypassing deep nuclei | Nystagmus, loss of balance and difficulty standing; reduced tone |
| Spinocerebellum (vermis and paravermis) | Spinal cord (proprioception) and trigeminal nuclei | Vermis: trunk, head, proximal limbs. Paravermis: distal limbs. Muscle tone | Truncal ataxia (vermis); wide-based gait and lower-limb incoordination |
| Cerebrocerebellum (lateral hemispheres) | Contralateral motor and supplementary motor cortex via pontine nuclei; contralateral inferior olive | Motor planning, timing and initiation of movement | Delayed initiation, limb dysmetria and dysdiadochokinesia |
- The dorsal vermis and the fastigial nuclei modulate saccades and vergence.
- The spinocerebellum acts on the rubrospinal tract (flexor tone) and the vestibulospinal tract (extensor tone).
- The vermis coordinates the midline body; the intermediate zone the distal limbs; the lateral hemispheres the planning of sequential movement and the conscious assessment of movement errors.
What are the layers of the cerebellar cortex and the deep nuclei?
The cerebellar cortex has three layers — unlike the six of the cerebral cortex: the outer molecular layer (stellate and basket cells), the middle Purkinje cell layer and the inner granular layer. Purkinje cells are large neurons whose dendrites branch in the molecular layer and whose axons descend through the granular layer to the deep nuclei. They provide the only output of the cerebellar cortex, and it is inhibitory; the deep nuclei in turn give excitatory output. Input arrives by mossy fibres and climbing fibres; mossy fibres use glutamate.
| Nucleus | Related zone | Key point |
|---|---|---|
| Fastigial | Vermis | Most medial; modulates saccades and vergence with the dorsal vermis |
| Globose and emboliform (together the nucleus interpositus) | Paravermis (intermediate zone) | Project to the contralateral red nucleus |
| Dentate | Lateral hemisphere | Largest nucleus; fibres go via the superior peduncle to the contralateral red nucleus and ventrolateral thalamus |
Which fibres run in the three cerebellar peduncles?
The cerebellum is attached to the brainstem by three paired peduncles. The middle is the largest and carries only afferent fibres; the superior is the main efferent route; the inferior carries mostly afferents from the spinal cord, olive and vestibular system.
| Peduncle | Connects with | Main contents |
|---|---|---|
| Superior | Midbrain | Efferents from the deep nuclei to the red nucleus and the motor nuclei of the thalamus (dentatorubral and dentatothalamic fibres) |
| Middle (largest) | Pons | Pontocerebellar fibres from the contralateral pontine nuclei (which receive motor and supplementary motor cortex input) |
| Inferior | Medulla | Afferents: dorsal spinocerebellar, cuneocerebellar, olivocerebellar and vestibulocerebellar tracts |

What are the signs of cerebellar dysfunction and how are they tested?
Each cerebellar hemisphere controls the same side of the body, so a lesion produces ipsilateral signs. Patients with cerebellar damage, regardless of cause or location, show persistent errors of movement on the same side as the lesion.
| Sign | How it appears | Test |
|---|---|---|
| Intention tremor | Low-frequency tremor (under 5 Hz) that worsens as the limb nears its target; absent at rest | Finger-nose test |
| Dysmetria (past-pointing) | Overshoot or undershoot of the target | Finger-nose; heel-shin |
| Dysdiadochokinesia | Slow, incomplete rapid alternating movements on the side of the lesion | Rapid pronation-supination of the forearms |
| Rebound phenomenon | Arm shoots upward and oscillates when downward pressure is suddenly released | Outstretched arms with eyes closed |
| Hypotonia | Reduced resistance to palpation; broad-based gait, leaning to the affected side | Tone testing |
| Nystagmus and abnormal saccades | Gaze-evoked nystagmus; hypometric or hypermetric saccades | Gaze test |
| Dysarthria | Slurred speech with syllables separated (scanning speech) | Speech |
| Gait (truncal) ataxia | Wide-based, 'drunken' stumbling gait; cannot tandem-walk | Gait |
How do vermis, hemisphere and flocculonodular lesions differ?
| Site | Deficit | Typical cause |
|---|---|---|
| Vermis (midline) | Truncal ataxia, incoordination of head and trunk, cannot maintain upright posture, falls | Medulloblastoma of the vermis in children |
| Cerebellar hemisphere | Ipsilateral limb ataxia (dysmetria, dysdiadochokinesia, intention tremor), dysarthria, nystagmus; delayed initiation of movement with lateral lesions | Tumour, stroke, demyelination, alcohol |
| Flocculonodular lobe (vestibulocerebellum) | Impaired standing, nystagmus, eye fixation drift followed by corrective saccade, loss of tone | Disruption of vestibular pathways to the cerebellum |
| Anterior lobe | Wide-based gait, lower-limb incoordination (anterior spinocerebellum) | Chronic alcohol use — degeneration of anterior cerebellar cortex |
The commonest cause of cerebellar dysfunction is alcohol. Other causes include trauma, multiple sclerosis, tumours and vascular disease. Autoimmune, infectious and neoplastic processes can also cause cerebellar dysfunction.
Which arteries supply the cerebellum and what does infarction cause?
Three paired arteries of the vertebrobasilar system supply the cerebellum: the superior cerebellar artery (SCA), the anterior inferior cerebellar artery (AICA) and the posterior inferior cerebellar artery (PICA). The SCA encircles the brainstem below the oculomotor nerve and above the trigeminal nerve. AICA arises from the basilar trunk, passes the abducens nerve and meets the facial and vestibulocochlear nerves at the cerebellopontine angle; it supplies the anterior-inferior cerebellum, the flocculus and the middle cerebellar peduncle. PICA, the largest branch of the vertebral artery, supplies the cerebellar nuclei, the inferior vermis and the undersurface of the hemisphere, and also the lateral medulla.
| Artery | Clinical picture |
|---|---|
| PICA (commonest cerebellar infarct) | Acute vertigo, nausea, inability to stand or walk; may give lateral medullary (Wallenberg) syndrome — ipsilateral facial pain and temperature loss, dysphagia and dysarthria, Horner syndrome, ipsilateral limb ataxia and contralateral body pain and temperature loss |
| AICA | Dysmetria, unilateral hearing loss or tinnitus, ipsilateral facial paralysis or sensory loss, contralateral hemibody pain and temperature loss |
| SCA | Ataxia, dysarthria and nystagmus; vertigo, headache and vomiting less frequent. About 15% of cerebellar infarcts |
- Sudden vertigo, vomiting and inability to walk in an older or vascular-risk patient suggests acute cerebellar infarction (or haemorrhage if headache is prominent).
- Symptoms are often more severe than the findings on examination.
- Oedema from a large infarct in the confined posterior fossa can compress the brainstem and the fourth ventricle, causing hydrocephalus and downward tonsillar herniation, which is why deterioration can be rapid.
How is the cerebellum asked in NEET PG and INI-CET?
- Side of signs — ipsilateral to the cerebellar lesion.
- Peduncle content — which tract passes through which peduncle; middle peduncle is the largest, superior carries efferents.
- Deep nuclei — order and which is the largest (dentate), and where each projects.
- Purkinje cell facts — inhibitory, only cortical output, in the middle layer.
- Lesion localisation — truncal ataxia (vermis) versus limb ataxia (hemisphere).
- Vascular syndromes — PICA and Wallenberg syndrome; AICA with hearing loss and facial palsy.