Abstract

Cerebellum and particularly Purkinje neurons of cerebellum are significantly affected from intoxication and poisoning. Many drugs and toxic factors may cause cerebellar damage. Of these, alcohol is the most significant. Alcoholic cerebellar degeneration is one of the most frequent causes of chronic cerebellar ataxia and the most frequently observed of acquired toxic ataxias. Clinical findings generally occur in middle-aged males and a history of alcohol use disorder is obtained. The most significant clinical finding is gait ataxia. Drug-dependent ataxias generally have acute or subacute onset (rarely chronic) and usually improve with drug withdrawal. These characteristics are significant in terms of differentiation from insidious onset and progressive hereditary/degenerative cerebellar ataxias. It is considerably important to question the drugs used by a patient with ataxia. In such case, the picture may be reversed by immediate drug withdrawal. Also, by this way, further investigations and invasive diagnostic tests may not be required. In this article, we discussed the ataxia occurring due to use of phenytoin, carbamazepine, and lithium and which we frequently encounter in neurology practice. Among metabolic disorders, the most significant disease leading to ataxia is Wernicke encephalopathy which is caused by vitamin B1 deficiency. Wernicke encephalopathy is a rare but significant disease with acute or subacute onset, presenting with ocular findings and clinical findings of ataxia and mental state changes. It should be kept in mind that Wernicke encephalopathy should be diagnosed early and administered timely treatment since it may evolve to Korsakoff syndrome, cause permanent sequelae, or even be fatal when not treated.