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https://www.ncbi.nlm.nih.gov/books/NBK538167

Q.2 Cerebellum

1. Neuronal circuit of cerebellum

Cerebellar cortex has 3 layers:
  1. Molecular layer: parallel fibres, dendrites of Purkinje cells, stellate and basket cells
  2. Purkinje cell layer: Purkinje cells
  3. Granular layer: granule cells and Golgi cells

Well-labelled diagram

                    CLIMBING FIBRE
             (from contralateral inferior olive)
                           │  Excitatory (+)
                           ▼
                     PURKINJE CELL
                           │ Inhibitory (GABA)
                           ▼
      ┌─────────────────────────────────────────┐
      │ Deep cerebellar nuclei / vestibular nuclei│
      │ Dentate, interposed, fastigial nuclei     │
      └─────────────────────────────────────────┘
                           │ Excitatory output
                           ▼
      Thalamus → Motor cortex / Red nucleus /
      Vestibular nuclei / Reticular formation


MOSSY FIBRES
(from pons, spinal cord, vestibular nuclei,
reticular formation, etc.)
             │
             ├─────────────► Deep cerebellar nuclei (+)
             │
             ▼
       GRANULE CELL
             │
             ▼
      PARALLEL FIBRES (+)
       ┌─────────┼───────────┐
       ▼         ▼           ▼
  Purkinje   Stellate      Basket
    cell       cells        cells
                │             │
                └─────── Inhibitory (GABA) ─────► Purkinje cell

Golgi cell ───── inhibitory feedback ─────► Granule cell

Explanation

  • Mossy fibres arise from pontine nuclei, vestibular nuclei, spinal pathways, reticular formation, etc. They excite:
    • Granule cells
    • Deep cerebellar nuclei through collateral branches.
  • Granule cells give rise to parallel fibres, which excite Purkinje cells and inhibitory interneurons.
  • Climbing fibres arise exclusively from the contralateral inferior olivary nucleus. They make powerful excitatory synapses with Purkinje cells and also send collaterals to deep nuclei.
  • Purkinje cells are the only output neurons of cerebellar cortex. They are inhibitory and project to deep cerebellar nuclei and vestibular nuclei.
  • Deep nuclei are the main output stations. Their output is excitatory to thalamus, red nucleus, vestibular nuclei, and reticular formation.
Reference: Neuroanatomy through Clinical Cases, 3rd ed., p. 730. Guyton and Hall Textbook of Medical Physiology, p. 701.

2. Functions of cerebellum

  1. Coordination of voluntary movements
    Makes movements smooth, accurate, coordinated, and appropriately timed.
  2. Maintenance of posture and equilibrium
    Especially through the vermis and vestibulocerebellum. It helps maintain balance during standing and walking.
  3. Regulation of muscle tone
    Facilitates alpha and gamma motor neuron activity through connections with motor cortex and brainstem motor centres.
  4. Comparison and correction of movements
    Compares intended motor activity from cerebral cortex with actual performance feedback from proprioceptors. It corrects errors during movement.
  5. Motor learning and planning
    Important for acquisition and adaptation of skilled motor activities, such as writing, playing an instrument, and coordinated eye movements.
  6. Control of eye movements
    Helps maintain fixation, smooth pursuit, and vestibulo-ocular reflexes.

3. Salient features of cerebellar lesion

Cerebellar signs occur on the same side as the lesion.
  • Ataxia: incoordination of movements; broad-based, staggering gait.
  • Dysmetria: inability to judge distance, causing past pointing or overshooting in finger-nose test.
  • Intention tremor: tremor appears or increases as the target is approached.
  • Dysdiadochokinesia: inability to perform rapid alternating movements.
  • Hypotonia and pendular deep tendon reflexes.
  • Dysarthria: scanning or slurred speech.
  • Nystagmus and vertigo, particularly with flocculonodular lobe involvement.
  • Vermis lesion causes truncal and gait ataxia; hemispheric lesion causes ipsilateral limb ataxia.
Reference: Guyton and Hall Textbook of Medical Physiology, p. 701; p. 730.
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