Unit 18 — Cerebellum & Brainstem · Question Bank

Location and general features

• Lies in the posterior cranial fossa, above and behind the pons and medulla.
• Separated from the occipital lobe above by the tentorium cerebelli (dural fold).
• Connected to the brainstem by three pairs of cerebellar peduncles (SCP, MCP, ICP).
• Surfaces: superior surface is relatively flat; inferior surface is convex with a central constriction (vallecula).

Vermis and hemispheres

• Vermis: narrow midline portion (superior vermis + inferior vermis); vermis parts include lingula, central lobule, culmen, declive, folium (superior) and nodule, uvula, pyramid, tuber (inferior).
• Hemispheres: two lateral lobes flanking the vermis. Each hemisphere's inferior surface shows the cerebellar tonsil near the foramen magnum.
• The surface is folded into many narrow ridges called folia.

Three lobes (separated by fissures)

• Anterior lobe: separated from posterior lobe by the primary fissure (V-shaped, superior surface).
• Posterior lobe: largest lobe; between primary fissure and posterolateral fissure.
• Flocculonodular lobe: separated from posterior lobe by the posterolateral fissure; consists of the flocculus (lateral) connected to the nodule (median inferior vermis) by a peduncle.

Three functional divisions

• Vestibulocerebellum = flocculonodular lobe (archicerebellum). Connected via ICP to vestibular nuclei. Function: balance and eye movement. Lesion: truncal ataxia, disequilibrium, vestibular nystagmus.
• Spinocerebellum = vermis + intermediate zone of hemisphere (paleocerebellum). Receives spinocerebellar tracts. Function: regulate muscle tone and coordination of trunk/limb movement. Lesion: hypotonia, intention tremor, ataxia, dysmetria.
• Cerebrocerebellum = lateral parts of hemispheres (neocerebellum). Connected via MCP (pontine nuclei relay cortical signals). Function: planning and coordination of skilled voluntary movements, especially distal limbs. Lesion: hypotonia, ataxia in distal limbs, slowing of movement initiation.

General principle

The cerebellum is attached to the brainstem by three pairs of peduncles (one pair per brainstem component). SCP ↔ midbrain; MCP ↔ pons; ICP ↔ medulla.

Superior cerebellar peduncle (SCP / brachium conjunctivum)

• Level: Midbrain
• Direction: Mainly output
• Output fibres: Arise from dentate nucleus and interposed (emboliform + globose) nuclei → decussate in midbrain tegmentum → terminate in VL thalamus (relays to motor cortex), red nucleus, and oculomotor nucleus.
• Input fibres: Anterior spinocerebellar tract (small component).

Middle cerebellar peduncle (MCP / brachium pontis) — LARGEST

• Level: Pons
• Direction: Exclusively input (no output fibres)
• Input fibres: Pontocerebellar fibres: cerebral cortex (wide areas) → pontine nuclei → fibres decussate → MCP → contralateral cerebellar cortex (hemispheres). These are mossy fibre afferents to the cerebrocerebellum.

Inferior cerebellar peduncle (ICP / restiform body)

• Level: Medulla
• Direction: Mainly input, some output
• Input fibres:
  • Posterior spinocerebellar tract (unconscious proprioception from lower limb)
  • Vestibular nuclei → fastigial nucleus and flocculonodular lobe
  • Inferior olivary nucleus → climbing fibres → Purkinje cells
• Output fibres: Cerebellovestibular tract → vestibular nuclei; cerebellotegmental tract → reticular formation.

Summary table mnemonic: SIM

SCP = mainly output; MCP = only input; ICP = mainly input. Fibre direction: SCP ↑, MCP ↓ (to cerebellum), ICP ↓ (mostly to cerebellum).

(a) Side of cerebellar lesion

Cerebellar lesions produce ipsilateral signs — the right upper limb signs indicate a right cerebellar hemisphere lesion. This contrasts with the corticospinal system, where lesions produce contralateral deficits. The reason: cerebellar output (dentate → SCP → decussates in midbrain → VL thalamus → motor cortex) and the corticospinal pathway from motor cortex (decussates in medullary pyramids) together form a “double decussation”, so the net effect is that each cerebellar hemisphere controls the ipsilateral limbs.

(b) DANISH sign complex

• Dysdiadochokinesia — inability to perform rapid alternating movements (e.g. pronation-supination). Tests cerebellar timing of agonist/antagonist.
• Ataxia — broad-based staggering gait; the patient tends to fall toward the side of the lesion. Limb ataxia = incoordination of voluntary movement.
• Nystagmus — involuntary rhythmic eye oscillation; horizontal; fast phase toward the side of the lesion. Due to cerebellar influence on eye movement (especially flocculonodular lobe).
• Intention tremor — tremor that worsens as limb nears a target; absent at rest. Tests finger-nose and heel-shin. Due to dentate/SCP lesion.
• Slurred/scanning speech (dysarthria) — slow, dysrhythmic, explosive or monotonous speech due to incoordination of speech musculature.
• Hypotonia — reduced muscle tone on the affected side (flaccid, pendular knee jerk). Due to loss of facilitatory cerebellar influence on motor neurons.

Important: cerebellar lesions do NOT cause paralysis, sensory loss, or hyperreflexia.

(c) Clinical tests for cerebellar function

• Finger-nose test: patient touches their own nose then examiner's moving finger; intention tremor and past-pointing (dysmetria) revealed.
• Heel-shin test: patient runs heel down opposite shin; ataxia and dysmetria of lower limb tested.
• Rapid alternating movements: pronation/supination of forearm; dysdiadochokinesia.
• Romberg test: stand with feet together, eyes open then closed; a positive Romberg (falls with eyes closed) suggests posterior column or vestibular disease, NOT pure cerebellum (cerebellar patients are unsteady with eyes OPEN too).
• Gait assessment: broad-based, staggering gait; tandem gait (heel-toe in a line) is particularly sensitive.
• Nystagmus: examine eye movements; fast phase toward lesion side.
• Tone and reflexes: hypotonia, pendular deep tendon reflexes.

(a) Three components

• Medulla oblongata: Caudal component; continuous with spinal cord at foramen magnum below; merges with pons above at the pontomedullary sulcus; ~3 cm long. Contains vital centres (respiratory, cardiovascular).
• Pons: Middle component; lies between medulla and midbrain; forms the upper part of the floor of the 4th ventricle; named for its prominent bridge-like ventral surface.
• Midbrain (mesencephalon): Rostral component; connects brainstem to diencephalon above; traversed by the cerebral aqueduct. Shortest component (~2 cm).

(b) External features

Medulla — ventral: Pyramids (longitudinal ridges, corticospinal fibres) on either side of the anterior median fissure; olives (smooth oval swellings, underlain by inferior olivary nucleus) lateral to pyramids; pyramidal decussation visible at lower end; anterolateral sulcus (XII exits); postolivary sulcus (IX, X, XI exit).

Medulla — dorsal: Gracile and cuneate tubercles (nuclei gracilis/cuneatus); posterior median sulcus; open medulla forms floor/walls of 4th ventricle (obex at inferior apex).

Pons — ventral: Large bulging basilar pons with transverse pontocerebellar fibres; basilar sulcus (basilar artery lies here); MCP laterally; CN V enters at MCP junction; CN VI, VII, VIII at pontomedullary junction.

Pons — dorsal: Forms upper rhomboid fossa (floor of 4th ventricle); medial eminence; facial colliculus (CN VII fibres over CN VI nucleus); sulcus limitans; SCP forms dorsolateral wall bridged by superior medullary velum.

Midbrain — ventral: Cerebral peduncles (crus cerebri), separated by interpeduncular fossa (CN III exits here); posterior perforated substance (posterior cerebral artery entry points) in fossa floor.

Midbrain — dorsal (tectum): Four colliculi = tectum: 2 superior colliculi (visual reflexes) + 2 inferior colliculi (auditory relay); CN IV exits just caudal to inferior colliculi (only dorsal CN exit).

(c) Cranial nerve attachment levels

• Midbrain: CN III (oculomotor — interpeduncular fossa, ventral); CN IV (trochlear — dorsal, caudal to inferior colliculi)
• Pons: CN V (trigeminal — ventrolateral, MCP junction); CN VI (abducens — pontomedullary junction, ventral); CN VII (facial — same level as VI, lateral); CN VIII (vestibulocochlear — same level, lateral)
• Medulla: CN IX (glossopharyngeal), CN X (vagus), CN XI (accessory) — postolivary sulcus; CN XII (hypoglossal) — anterolateral sulcus between pyramid and olive

Origin

Arises from upper motor neurons (UMN) in the motor cortex (precentral gyrus, area 4), premotor cortex (area 6), and some somatosensory cortex. The giant Betz cells of area 4 contribute the largest-diameter axons.

Course through the internal capsule

Fibres converge and descend through the posterior limb of the internal capsule (between the caudate/putamen and thalamus). Arranged somatotopically (face lateral, leg medial). Lacunar infarct here can cause a pure motor stroke with contralateral hemiplegia.

Cerebral peduncles (midbrain)

Fibres occupy the middle 3/5 of the crus cerebri (cerebral peduncle) on the ventral midbrain. Corticobulbar fibres (to cranial nerve motor nuclei) peel off at each brainstem level; corticospinal fibres continue. CN III emerges from the interpeduncular fossa medially.

Basilar pons

Fibres are broken into scattered bundles by the transverse pontocerebellar fibres and pontine nuclei in the basal pons. They run as multiple small fascicles (not a single compact bundle). CN VI, VII, VIII attach at the pontomedullary junction.

Medullary pyramids

Fibres reassemble into compact pyramids on the ventral medulla, flanking the anterior median fissure. The pyramids give their name to the “pyramidal tract.”

Decussation of the pyramids

At the lower border of the medulla (caudal medulla — spinal cord junction): 75–90% of fibres decussate (“pyramidal decussation”) and descend as the lateral corticospinal tract in the contralateral lateral funiculus of the spinal cord. The remaining 10–25% do not decussate here and descend as the anterior corticospinal tract in the ipsilateral anterior funiculus, crossing later at spinal cord levels.

Spinal cord — termination

Lateral corticospinal tract fibres synapse on alpha motor neurons in the ventral horn (and on interneurons), mainly for contralateral limb movements, especially fine distal movements. Most fibres terminate on interneurons; direct corticomotoneuronal synapses are proportionally more common for fine hand movements.

Clinical effects of lesions at each level

• Motor cortex / internal capsule: Contralateral hemiplegia or hemiparesis; UMN signs: spasticity, hyperreflexia, up-going plantar (Babinski sign), clonus. Face, arm, or leg depending on somatotopy.
• Cerebral peduncle: Contralateral hemiplegia + ipsilateral CN III palsy (Weber's syndrome): ptosis, dilated pupil, eye “down and out.”
• Basilar pons: Contralateral hemiplegia + ipsilateral CN VI or VII palsy. Locked-in syndrome if bilateral.
• Medullary pyramid (above decussation): Contralateral limb weakness (UMN).
• At or below decussation (spinal cord lateral corticospinal tract): Ipsilateral limb weakness below the level of the lesion; UMN signs below + LMN signs at the level (anterior horn affected).