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AN60.1-3 | Cerebellum — Self-Directed Learning

CLINICAL SCENARIO

A 7-year-old boy from Madurai is brought with a 3-week history of headache, vomiting (worse in the morning), unsteady gait, and difficulty holding objects. He falls to both sides when walking. Examination: nystagmus, intention tremor in both hands, dysdiadochokinesia, hypotonia, ataxic (wide-based) gait. MRI brain shows a midline posterior fossa mass in the 4th ventricle with hydrocephalus.

Diagnosis: Medulloblastoma.

Why does a midline cerebellar tumour cause these specific deficits? Why is gait affected more than limb coordination when the midline (vermis) is involved?

WHY THIS MATTERS

Cerebellar anatomy is clinically essential:

  • Medulloblastoma — most common malignant brain tumour in children in India; arises in the cerebellar vermis; causes hydrocephalus by blocking the 4th ventricle
  • Cerebellar ataxia — a common presentation in Indian neurology: causes include alcohol (India's second most common cause of cerebellar syndrome), vitamin B1 deficiency, paraneoplastic, MS, strokes
  • Posterior fossa surgery — cerebellar tumours require knowledge of the peduncles, vermis, and tonsillar herniation
  • Chiari malformation — cerebellar tonsillar herniation through foramen magnum; causes syringomyelia (discussed in spinal cord module)

RECALL

Before we begin, recall:

  • The cerebellum occupies the posterior fossa, below the tentorium cerebelli
  • It connects to the brainstem via three pairs of cerebellar peduncles
  • Functionally: coordinates movement, maintains posture, and regulates muscle tone
  • It does NOT initiate movements; it modulates them

Part 1: External and Internal Features (AN60.1)

External Features

  • Two hemispheres + central vermis (worm-shaped midline strip)
  • Folia — transversely oriented ridges on the cerebellar surface (equivalent to gyri)
  • Fissures separate lobes:
  • Primary fissure — separates anterior lobe from posterior lobe
  • Posterolateral fissure — separates flocculonodular lobe from the posterior lobe

Three Lobes:

LobeLocationFunctional Zone
Anterior lobeAbove primary fissureSpinocerebellum (muscle tone, posture)
Posterior lobe (largest)Between primary + posterolateral fissuresPontocerebellum (skilled movements)
Flocculonodular lobeBelow posterolateral fissureVestibulocerebellum (balance, eye movements)

Three Functional Zones (phylogenetic):

ZoneRegionInputFunctionDeep Nucleus
Vestibulocerebellum (archicerebellum)Flocculonodular lobeVestibular nucleiBalance, VOR, eye movementsNo deep nucleus (→ vestibular nuclei directly)
Spinocerebellum (paleocerebellum)Anterior lobe + vermis of posterior lobeSpinal cord (spinocerebellar tracts)Posture, gait, muscle toneFastigial (medial vermis), Interposed (intermediate)
Pontocerebellum (neocerebellum)Lateral hemispheresCerebral cortex via ponsSkilled fine voluntary movementsDentate nucleus

Internal Structure:
• Surface: 3-layered cerebellar cortex (molecular, Purkinje, granular layers)
• Deep white matter (arbor vitae — "tree of life" on sagittal section)
Intracerebellar nuclei (medial → lateral): Fastigial, Globosus, Emboliformis, Dentate
- Mnemonic: "Feel Good Every Day" (Fastigial, Globosus, Emboliformis, Dentate)
- Dentate = largest; output for voluntary fine movement (via superior cerebellar peduncle)
- Fastigial = balance, posture
- Globosus + Emboliformis = together called the Interposed nuclei

Part 2: Connections of the Cerebellum (AN60.2)

Three Cerebellar Peduncles — Input and Output Pathways

Inferior Cerebellar Peduncle (Restiform body + Juxtarestiform body)
Inputs (afferents):
• Posterior spinocerebellar tract (from Clarke's column, proprioception)
• Cuneocerebellar tract (upper limb proprioception)
• Vestibulocerebellar fibres (balance input from CN VIII)
• Olivocerebellar fibres (from inferior olivary nucleus — error signals)

Output (efferents):
• Cerebellovestibular fibres (fastigial nucleus → vestibular nuclei)

Middle Cerebellar Peduncle (Brachium pontis) — INPUT ONLY
• Corticopontocerebellar: cerebral cortex → pontine nuclei → cross → middle cerebellar peduncle → cerebellar hemisphere
• This is the largest peduncle; carries cerebrocerebellar information for skilled movements

Superior Cerebellar Peduncle (Brachium conjunctivum) — MAINLY OUTPUT
Output (efferents):
• Dentatorubrothalamic tract: Dentate nucleus → crosses in the midbrain → red nucleus → VL thalamus → motor cortex
• This is the main cerebellar OUTPUT pathway; it decussates in the midbrain tegmentum

Input (afferents):
• Anterior spinocerebellar tract

Cerebellar Cortex Circuitry:
Purkinje cells — the only OUTPUT neurons of the cerebellar cortex; INHIBITORY (GABA-ergic) → inhibit intracerebellar nuclei
Climbing fibres (from inferior olivary nucleus) — 1:1 synapse with Purkinje cells; carry error signals; cause long-term depression (LTD) of parallel fibre-Purkinje synapses
Mossy fibres (all other inputs) → granule cells → parallel fibres → multiple Purkinje cells
Granule cells — EXCITATORY; the most numerous neurons in the CNS

Part 3: Cerebellar Dysfunction (AN60.3)

Cardinal Signs of Cerebellar Dysfunction — "DANISH"
Dysdiadochokinesia — inability to perform rapid alternating movements
Ataxia (gait) — wide-based, staggering gait; falls TOWARD the side of lesion
Nystagmus — fast phase TOWARD side of lesion (opposite to peripheral nystagmus)
Intention tremor — tremor that worsens on approaching target (vs resting tremor = Parkinson's)
Speech — dysarthria (scanning/staccato speech)
Hypotonia — decreased muscle tone; pendular reflexes

Additional signs:
Past pointing (dysmetria) — inability to accurately point to a target
Rebound phenomenon — loss of check reflex; limb overshoots when resistance released
Titubation — rhythmic oscillation of the trunk or head

Localising Value of Cerebellar Signs:

StructureSignsExample Disease
Vermis (spinocerebellum)Truncal ataxia, wide-based gait, titubationMedulloblastoma (children), alcoholic cerebellar degeneration
Hemispheres (pontocerebellum)Ipsilateral limb ataxia, intention tremor, dysdiadochokinesiaPICA stroke, tumour
Flocculonodular lobe (vestibulocerebellum)Gait ataxia, nystagmus, balance disturbanceMidline posterior fossa tumours

Why ipsilateral signs?
• Cerebellum controls IPSILATERAL limbs (unlike cerebral cortex which is contralateral)
• Double-crossing pathway: cerebellum → superior cerebellar peduncle → crosses to contralateral red nucleus/thalamus → motor cortex → crosses again in corticospinal tract → back to ipsilateral limb

Common causes in India:
Alcoholic cerebellar degeneration — selective vermis degeneration (anterior lobe); gait ataxia predominates, arm ataxia minimal
Medulloblastoma — children; midline; vermis → gait ataxia + hydrocephalus
PICA territory infarct — lateral medullary + ipsilateral cerebellar hemisphere
Paraneoplastic cerebellar degeneration — lung, breast, ovarian cancer in adults

SELF-CHECK — Self-Check: Cerebellum

The ONLY output neurons of the cerebellar cortex are:

A. Granule cells

B. Purkinje cells

C. Basket cells

D. Golgi cells

Reveal Answer

Answer: B. Purkinje cells


The dentate nucleus output travels through which cerebellar peduncle?

A. Inferior cerebellar peduncle

B. Middle cerebellar peduncle

C. Superior cerebellar peduncle

D. Both superior and inferior peduncles equally

Reveal Answer

Answer: C. Superior cerebellar peduncle


A 60-year-old alcoholic presents with wide-based gait ataxia but relatively preserved arm coordination. This pattern suggests preferential degeneration of the:

A. Cerebellar vermis (anterior lobe)

B. Dentate nucleus

C. Cerebellar hemispheres bilaterally

D. Flocculonodular lobe

Reveal Answer

Answer: A. Cerebellar vermis (anterior lobe)

CLINICAL PEARL

Differentiating Cerebellar Ataxia from Sensory Ataxia (Posterior Column)

FeatureCerebellar AtaxiaSensory Ataxia (Post. Column)
Romberg testNegative (falls even with eyes open)Positive (sways/falls when eyes closed)
GaitWide-based, staggering, cannot correctWide-based, "stamping" gait, improves with visual feedback
NystagmusPresentAbsent
Intention tremorPresentAbsent
ReflexesPendular (hypotonia)Absent (posterior column + peripheral neuropathy)
SensationNormalVibration + proprioception lost

Romberg test: Patient stands with feet together, arms at sides. Eyes open first. Then close eyes. POSITIVE = sways with eyes closed (sensory ataxia — relies on vision to compensate for lost proprioception). Cerebellar ataxia: cannot stand steadily EVEN with eyes open → Romberg not informative.

REFLECT

Return to the hook case — the 7-year-old with medulloblastoma:

  1. Why does a midline vermis tumour cause truncal ataxia and wide-based gait rather than limb coordination problems?
  2. The child has nystagmus. Which part of the cerebellum controls eye movements and balance?
  3. Why does medulloblastoma in the 4th ventricle cause hydrocephalus? Trace the CSF pathway to identify the blockage.
  4. He has morning vomiting and headache — explain anatomically why morning is worse.

Discussion: (1) Vermis = spinocerebellum (gait, posture); hemispheres = limb coordination. (2) Flocculonodular lobe (vestibulocerebellum). (3) Tumour blocks CSF outflow through foramina of Magendie/Luschka from 4th ventricle → obstructive hydrocephalus. (4) ICP is highest in the morning after lying flat all night (CO2 accumulation + increased intracranial venous pressure in recumbency → worsens cerebral oedema) → morning headache and vomiting.

KEY TAKEAWAYS

Key Takeaways — Cerebellum

  • Three lobes: Anterior (spinocerebellum, posture), Posterior (pontocerebellum, skilled movements), Flocculonodular (vestibulocerebellum, balance)
  • Deep nuclei (medial→lateral): Fastigial, Globosus, Emboliformis, Dentate (mnemonic: FGED)
  • Peduncles: Inferior = input (spinocerebellar, olivocerebellar, vestibular). Middle = input only (corticopontocerebellar). Superior = MAIN OUTPUT (dentatorubrothalamic, crosses in midbrain)
  • Purkinje cells = only cortical output, INHIBITORY (GABA)
  • Ipsilateral control of limbs (double crossing)
  • DANISH signs: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Speech (dysarthria), Hypotonia
  • Vermis lesion → truncal/gait ataxia. Hemisphere lesion → ipsilateral limb ataxia