Makindo Medical Notes

🧠 The cerebellum coordinates movement, balance, and motor learning. Cerebellar signs may arise not only from the cerebellum itself, but also from its connections with the brainstem, vestibular system, and spinal cord. Damage produces distinctive motor syndromes that are typically ipsilateral to the lesion.

📍 Cerebellar Cortex

• 3-layered outer cortex:
  • Molecular Layer: Dendritic network, few cell bodies.
  • Purkinje Cell Layer: Large Purkinje neurons → main inhibitory output to deep nuclei.
  • Granular Layer: Packed with granule cells → excitatory input relay.

🎯 Deep Cerebellar Nuclei

Clusters in white matter (dentate, emboliform, globose, fastigial). Receive inhibition from Purkinje cells & excitatory inputs → output to motor and cognitive systems.

🔗 Cerebellar Peduncles

• Superior: Output → midbrain & thalamus (motor control).
• Middle: Largest, input from cerebral cortex via pons.
• Inferior: Input from spinal cord & vestibular system, output to vestibular nuclei.

⚙️ Functions

• Coordination: Fine-tunes voluntary movement, timing, accuracy.
• Balance & Posture: Uses vestibular + proprioceptive feedback to stabilise stance & gait.
• Motor Learning: Adjusts movement patterns with practice (e.g. cycling, piano). 🎹🚲
• Non-Motor Roles: Contributes to attention, language, problem-solving.

🧩 Key Structures & Roles

🧠 Clinical Features of Cerebellar Lesions

• 🚶‍♂️ Ataxic gait: broad-based, unsteady; truncal ataxia if vermis lesion, limb ataxia if hemispheric lesion.
• ↔️ Dysdiadochokinesia: impaired rapid alternating movements.
• 🎯 Dysmetria / Past-pointing: overshoot on finger–nose or heel–shin testing.
• 👀 Nystagmus: coarse, horizontal, towards lesion side.
• 🖐️ Riddoch’s sign: over-pronation of outstretched hand.
• 🗣️ Scanning dysarthria: slow, slurred, staccato speech.
• 📉 Hypotonia & Pendular reflexes: reduced tone, swinging reflexes.
• ✋ Intention tremor: worsens as target is approached.
• ❌ Motor learning failure: inability to acquire new motor skills.

⚖️ Symmetry of Signs

• Unilateral signs → MS plaques, infarct (PICA, AICA, SCA), tumour.
• Bilateral signs → Alcohol, drugs, inherited ataxias, multiple demyelinating foci.
• Truncal ataxia ± gait ataxia with intact limb coordination → midline vermis lesion.

🩺 Causes of Cerebellar Dysfunction

• 🧨 Vascular: Infarcts/bleeds (PICA, AICA, SCA).
• 🧬 Inherited: Friedreich’s ataxia (AR), Spinocerebellar ataxias (AD), Ataxia-telangiectasia, Refsum’s disease.
• 🧒 Developmental: Arnold-Chiari malformation, Dandy-Walker malformation.
• 🧫 Demyelination: Multiple sclerosis, other demyelinating diseases.
• 🎗️ Neoplasia: Posterior fossa tumours (children), CPA tumours (adults), secondary metastases (lung, breast, bowel).
• 🦠 Infectious: Varicella zoster, EBV, HIV, Mycoplasma, Legionella.
• 💊 Toxic/Drug: Alcohol, anticonvulsants, CO poisoning.
• 🧪 Paraneoplastic: Anti-Yo (SCLC), Hodgkin-associated degeneration.
• 🧓 Neurodegenerative: Multiple System Atrophy – cerebellar type (MSA-C).
• 🦠 Prion disease: e.g. Gerstmann-Sträussler-Scheinker.

💡 Exam Pearl: – Cerebellar lesions cause ipsilateral signs. – Midline lesions → truncal ataxia, hemisphere lesions → limb ataxia. – Always exclude alcohol, drugs, and paraneoplastic causes in subacute bilateral syndromes.