Classical postmortem neuropathology studies identified damage to nodes of the frontocerebellar circuit in cases of chronic alcoholism. On the gross pathology level, the frontal cortex sustains notable shrinkage, due in part to cell loss, in contrast to the relatively spared motor cortex (Kril and Harper, 1989; Harper, 1998). Atrophy of the cerebellar vermis has been reported in alcoholics and even more frequently in alcoholics with exceptionally high levels of alcohol consumption (Karhunen et al., 1994) or thiamine deficiency (35–50% Victor et al., 1959). On the cellular level, Purkinje cells (Pentney, 1993) and cells in the granular and molecular layers of the cerebellar cortex (Phillips et al., 1987) are particularly affected, especially in alcoholics with a history of thiamine deficiency (Baker et al., 1999). Whether caused by neurotoxic effects of alcohol per se or to secondary events such as dietary deficiencies, excessive alcohol consumption adversely affects the pons (Adams et al., 1959) and thalamus (Kril and Butterworth, 1997; Harding et al., 2000). The pons sustains reduction of numbers of serotonergic (Halliday et al., 1993) and noradrenergic neurons (Arango et al., 1994).
