Alcohol Induced Cerebellar Ataxia: A Case Report

Consumption of alcohol excessively causes dependence and leads to psychological discomfort. Motivation to drink is influenced by a variety of neurobiological and environmental variables. The proclivity of an individual to imbibe is thought to reflect a balance between alcohol’s positive reinforcing (i.e., rewarding) effects, such as euphoria and anxiety reduction (i.e., anxiolysis), and the drug’s aversive effects, which are typically associated with negative consequences of alcohol consumption (e.g., hangover or withdrawal symptoms). Neuroadaptive alterations caused by continuous alcohol use and abuse (such as tolerance and physiological dependence) are regarded to be critical in the shift from regulated alcohol use to more frequent and excessive, uncontrollable drinking which induces cerebellar degeneration considered as common type of acquired toxic ataxia. Excessive use leads to degeneration of the midline cerebellum. Progressive trunk and gait ataxia is characteristic, with little involvement of upper limbs, eyes or speech (a corollary of relative cerebellar hemispheric sparing). Abrupt termination of alcohol use after a period of heavy drinking may result in alcohol withdrawal seizures. Generalized tonic–clonic seizures are the most common and severe form of seizure in this conditions. Current case report presents complaints of astasia and slurred speech with few episodes of seizures. The diagnosis indicated Mild cerebellar atrophy. Patient was advised to undergo de-addiction and cure.