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Diffuse Brain Alterations

Cortical and subcortical white matter damage is due to thiamine deficiency as well as to direct toxic effects of alcohol (Langlais and Zhang 1997). Atrophy of the cortex and white matter (Fig. 18.1) can be observed by CT, macroscopically as well as microscopically. This results in a mean loss in brain mass of 1.43-1.35 kg in males (Harper and Kril 1993). The extent of atrophy has been shown (Harding et al. 1996) to be dependent upon the amount of alcohol consumed and the duration of alcohol dependence. Atrophy is based on a reduction of cortical neurons (Fig. 18.1a, b) and of the prefrontal cerebral white matter (Kril et al. 1997) (Fig. 18.1c-e), as well as -especially - the corpus callosum (Fig. 18.1c) (Harper and Kril 1988). The cerebral white matter is usually more vulnerable than the gray matter (Hansen et al. 1991), especially the subcortical white matter. The atrophic process partly is reversible, however (see above) (Pfefferbaum et al. 1995; Trabert et al. 1995). A recent study (Pfefferbaum et al. 2002) on the effect of alcohol abuse on white matter brain macrostructure provided evidence of a correlation between a higher life-time level of alcohol consumption and smaller volumes and prolonged transverse relaxation time in the pons; an overall deficit in white matter macrostructural size is observed in alcoholic women.

A loss of neuronal elements in the cerebral cortex is seen mostly in patients with Wernicke-Korsakoff syndrome (see below) (Kril et al. 1997). Harper et al.

Fig. 18.1a-e. Chronic alcohol intoxication. a Cortical atrophy; b the atrophy is caused by a decline in nerve cell density and secondary gliosis (H&E, magnification X200); c atrophic mammillary bodies are seen associated with an extreme hydrocephalus inter-

(1987) observed a loss of neurons in the frontal cortex (Moselhy et al. 2001) chiefly involving the large pyramidal cells (Harper and Kril 1989). There is also a reduction in the number of dendritic branches in the third cortical nerve cell layer (Harper and Cor-bett 1990) and a decrease in the number of dendritic spines in the fifth cortical nerve cell layer (Ferrer et al. 1986).

A decline in nerve cell density is seen, especially a loss of vasopressin-immunoreactive neurons in the magnocellular hypothalamus, supraoptic nucleus,

nus and a reduction of the corpus callosum; d subcortical white matter atrophy, which results in an interior atrophy, e rarely associated with macroscopic visible bilateral cystic white matter involvement and paraventricular nucleus (Harding et al. 1996; Harper et al. 1997). On the other hand, secondary gliosis has only been observed in a few cases (Harper et al. 1997). The Alzheimer's type I and II astrocytes observed in the thalamus and striatum are less a direct indication of chronic alcoholism than of the accompanying impairment of liver function with subsequent brain involvement in the sense of hepatocerebral degeneration (p. 611).

nus and a reduction of the corpus callosum; d subcortical white matter atrophy, which results in an interior atrophy, e rarely associated with macroscopic visible bilateral cystic white matter involvement

Fig. 18.2a, b. Chronic alcohol intoxication. An early alteration is the cortical atrophy of the superior cerebellar vermis, which is macroscopically (a) and microscopically (b) visible, associated with an atrophy of the molecular layer and a decline of Purkinje cells

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Alcohol No More

Alcohol No More

Do you love a drink from time to time? A lot of us do, often when socializing with acquaintances and loved ones. Drinking may be beneficial or harmful, depending upon your age and health status, and, naturally, how much you drink.

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