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Alcoholic Cerebellar Degeneration — MRCPsych Paper B MCQ

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ModerateSubstance MisuseAlcoholic Cerebellar DegenerationMRCPsych Paper B

A 35-year-old man with a 10-year history of alcohol dependence develops gradually progressive unsteadiness over 8 months. Examination when sober shows marked truncal and lower-limb ataxia with a wide-based gait, but relatively preserved upper-limb coordination. He is alert and oriented, without a significant memory disorder, abnormal eye movements or asterixis. He has not recently undergone correction of hyponatraemia. Which alcohol-related neurological condition most likely explains this presentation?

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Correct answer: D — Alcohol-related cerebellar degeneration

The correct answer is **B, alcohol-related cerebellar degeneration**. Chronic heavy alcohol exposure preferentially damages the anterior superior cerebellar vermis, producing gradually progressive truncal and gait ataxia with disproportionate lower-limb involvement; upper-limb coordination and cognition may be relatively preserved. Wernicke encephalopathy is usually an acute or subacute thiamine-deficiency syndrome involving ataxia, confusion and oculomotor abnormalities, although the complete triad is often absent. Korsakoff syndrome is dominated by severe anterograde amnesia, often with confabulation. Hepatic encephalopathy causes altered attention or consciousness and commonly asterixis rather than an isolated chronic cerebellar syndrome. Central pontine myelinolysis is an acute osmotic demyelination syndrome, classically following overly rapid correction of chronic hyponatraemia.

Reference: Servais L, Bearzatto B. Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum. International Journal of Molecular Sciences. 2021;22(16):8678. https://pubmed.ncbi.nlm.nih.gov/34444449/