[Alcohol and epilepsy: a case report between alcohol withdrawal seizures and neuroborreliosis].

OBJECTIVES

This work consists in a study of the links between alcohol, a psychoactive substance and different related epileptic manifestations in order to clarify predominant factors both on conceptual, clinical and therapeutic levels.

BACKGROUND

If alcohol is a frequent risk factor for seizures, its scientific evidence is less clear and ad hoc literature is rich in controversies and not firmly supported by systematic surveys. Alcohol has variable roles in the physiopathological determinism of seizures, the nosographical status of which needs to be clarified: alcohol withdrawal seizures, alcoholic epilepsy, and sometimes symptomatic epilepsy caused by coincidental disorders.

METHODS

A synthesis of relevant literature describing the links between alcohol and epilepsy is illustrated by a clinical case: a patient admitted in our psychiatric ward for chronic alcoholism had had two seizures questioning their nosographical status. An infectious process with protean neurological manifestations, neuroborreliosis, was diagnosed.

DISCUSSION

Three distinct clinical pictures illustrate the links between alcohol and epilepsy: the first, convulsive inebriation corresponds to a seizure during severe acute alcohol intoxication. The second deals with alcohol withdrawal seizures following a partial or complete sudden withdrawal of alcohol; these are the clinical features the most documented in the literature representing, with delirium tremens, the main complication of alcohol withdrawal. The third clinical picture, alcoholic epilepsy, is characterized by repetitive seizures in patients presenting alcohol abuse without former history of epilepsy or other potentially epileptic disorder, and without relationship to alcohol withdrawal or acute alcohol intoxication. Acute and chronic effects of alcohol on central nervous system have been depicted, while a unified classification of alcohol related seizures has been recently established by Bartolomei. This classification based on the Ballenger hypothesis of kindling (1978) could explain withdrawal and hazardous seizures as clinical expressions of the same epileptogenic process over different stages. Although theoretically criticized, such a model offers a conceptual interest while able to unify the varied understanding of convulsive crises related to alcohol, and a practical one, whilst being a basis for a therapeutic approach. Our clinical case illustrates the delay in the diagnosis established after two iterative generalized seizures, 72 hours after the beginning of a programmed weaning of a patient presenting alcohol dependency. If the withdrawal seizure hypothesis was underlined, some data led to symptomatic epilepsy. Firstly atypia, the well-supervised preventive treatment of convulsion did not avoid seizures. Secondly, the EEG showed focal anomalies strongly linked in the literature with a cerebral disorder, which was confirmed by MRI; thirdly, cognitive alterations, which are not usual in alcohol dependency, were observed clinically and confirmed by neuropsychological tests. Finally a neuroborreliosis was diagnosed, while the main neuropsychiatric complications of Lyme disease were described. In accordance with the recommendations made by some authors, it appeared legitimate to consider neuroborreliosis as a potential differential diagnosis of every atypical psychiatric disorder, the interest of such an identification laying in the existence of a specific treatment.