Chronic alcohol abuse and/or dependence may result in cognitive decline, ranging from isolated amnesia and/or mild cognitive impairment to full-blown dementia. The underlying mechanisms include deficiency of nutritional factors (such as B-complex vitamins) resulting in Wernicke-Koraskoff's syndrome, and/or pellagrous encephalopathy, liver failure, Marchiafava-Bignami disease and cerebrovascular disease or combinations of the above. However, it has been suggested that progressive cognitive impairment can occur in the absence of the above-established syndromes, and has been attributed to the direct toxic effect of ethanol on the brain. Basic and clinical research has been shown that alcohol may be directly toxic to nerve cells via interplay of oxidative stress, excitotoxicity, mitochondrial damage and apoptosis.
The term "alcoholic dementia", formerly used to describe this concept, has cast doubt on its existence due to the absence of validated clinical, neuropathological and radiological criteria. A broader definition, such as "alcohol related dementia" (ARD) has been introduced to encompass a broader spectrum of alcohol related cognitive disorder. Current diagnostic criteria for ARD are based almost exclusively on clinical grounds. Oslin et al. (1998) proposed clinical diagnostic criteria for ARD based on epidemiologic and neuropathologic evidence to support these clinical criteria, which require validation. We present clinical, imaging and neurochemical characteristics of our group of elderly alcoholic partients fullfiling the above proposed criteria. The increased risk of dementia in older individuals often presents a dilemma for the clinician in the differential diagnosis, especially when dealing with elderly patients with a long and heavy history of alcohol abuse. Since alcohol effects on cognition and on the brain may be reversible in contrast to other dementias, mainly Alzheimer's disease renders the early differentiation of these disorders clinically significant.