Cerebral computer tomography (CCT) confirmed cerebellar atrophy in about 40% of chronic alcoholics (Haan 1986). Pathological-anatomical atrophy was found in 26.8% of alcoholics (Torvik et al. 1982), with shrinking mainly of the anterior superior cerebellar vermis. The atrophy was caused by a reduction in cerebellar white matter (Harding et al. 1998) and of the molecular layer (stratum moleculare) of the cerebellar vermis and a drop in Purkinje cell density (Karhunen et al. 1994) as well as reactive proliferation of astrocytes, the Bergmann glia (Fig. 18.2). The total number and density of Purkinje cells declines, apparently a dose-dependent phenomenon (Karhunen et al. 1994). A decrease in dendritic arborization has also been shown (Ferrer et al. 1984). Cerebellar atrophy is expressed clinically in ataxia and impaired coordination, mainly of the lower extremities. Thiamine deficiency is thought to be the chief cause of the cerebellar atrophy (cf. Adams 1976), resulting from malnutrition and a daily ethanol intake of more than 140 g over 10 years, which were independently asso
ciated with the development of cerebellar shrinkage (Nicolás et al. 2000).
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Alcoholism is something that can't be formed in easy terms. Alcoholism as a whole refers to the circumstance whereby there's an obsession in man to keep ingesting beverages with alcohol content which is injurious to health. The circumstance of alcoholism doesn't let the person addicted have any command over ingestion despite being cognizant of the damaging consequences ensuing from it.