Chronic alcohol consumption seems to be associated with severe executive function deficits, which are still present after a protracted period of alcohol abstinence. These data support the idea that the cognitive deficits in recently detoxified sober alcoholic subjects are due, at least partly, to frontal lobe dysfunctioning.

Inhibition and working memory deficits, associated with low levels of CBF in the medial frontal gyrus, are related to the difficulty of maintaining short-term abstinence from alcohol.

Recently detoxified non-neurological alcoholic patients appear to be impaired in cognitive tasks measuring inhibitory processes as well as working memory (involving storage and manipulation of information). The aim of this study was to investigate in alcoholic participants the relationship between these two cognitive functions and regional cerebral blood flow (rCBF) studied at rest in regions of interest selected on the basis of recent PET studies which explored inhibitory and working memory in normal subjects. Twenty non-neurological alcoholic patients and 20 normal volunteers were selected for a neuropsychological exploration, including assessment of inhibition processes (by means of the Hayling test) and working memory (by means of the Alpha-span task). rCBF of alcoholics was also evaluated with a semi-quantitative method using a 99mTc-Bicisate single photon emission computed tomography (SPECT) procedure. Alcoholic patients performed worse than controls in the alphabetical condition of the Alpha-span task (involving manipulation and storage of information), and on the Hayling test. Significant correlation emerged between inhibition performance and both the bilateral inferior (left BA 47, r = -0.40; right BA 47, r = -0.599) and median frontal gyrus (left BA 10, r = -0.55; right BA 10, r = -0.59), but not with the region of reference (occipital/cerebellum, r = -0.13). Coordination of storage and manipulation was correlated with bilateral median frontal (left BA 10/46, r = -0.50; right BA 10/46, r = -0.45), but not with bilateral parietal area (left BA 7, r = -0.12, right BA 7, r = -0.18). These results suggest a relationship between inhibition and working memory deficits in alcoholic patients, and regional rCBF measured in frontal areas. Clinical implications of these data related to alcohol relapse are discussed.

The basis of amnesia in alcoholic Wernicke-Korsakoff syndrome (WKS) has been generally associated with diencephalic lesions and more specifically with lesions of the anterior thalamic nuclei. These brain structures are considered to be involved in encoding/consolidation processes of episodic memory. However, frontal lobe damage responsible for executive function deficits has also been documented. The present report details the nature and extent of amnesia in an alcoholic patients with WKS and which appears to be mainly due to frontal lobe (executive) deficits.

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