The consistent dose-response relationship is rooted in plausible pathways. In particular, chronic alcohol consumption has diverse effects on the central nervous system, affecting its structure and functioning in different ways. There are several major theories explaining the effects of alcohol consumption on the development of epilepsy. One postulates a “kindling” effect [98]. According to this theory, repeated withdrawals, including natural withdrawal through sleep over the years, may lead to the gradual lowering of the epileptogenic threshold [98]. Epileptogenesis in heavy alcohol users may also be explained by cerebral atrophy [99]. Additional hypothesized causes of epilepsy in alcohol users include cerebrovascular infarctions, lesions, head traumas (from alcohol-attributable injuries), and changes in neurotransmitter systems and ionic imbalances leading to the onset of seizures [99-102]. Our analyses indicated that the strongest evidence was for the “kindling” hypothesis, for cerebral atrophy and for brain lesions each linking direct irreversible CNS changes to alcohol consumption, potentially leading to the onset of epilepsy or spontaneous seizures not immediately related to alcohol intake.
