In addition to atrophy of the mamillary bodies, WKS reveals neuronal loss in the anterior principal and medio-dorsal nuclei of the thalamus53 and in the basal forebrain.54 In patients with alcoholism and signs of WE, a reduction in Purkinje cell density and molecular layer atrophy are noted in the cerebellum, suggesting that this brain region is selectively vulnerable to thiamine deficiency.55 In patients with uncomplicated alcoholism, microscopic studies have revealed an ≈25% loss of pyramidal neurons in the superior frontal and frontal association (dorsolateral portion) cortices.56,57 Little evidence exists for neuronal loss in the primary motor cortex in ARBD. However, a silver impregnation technique has shown that pyramidal neurons in both the superior frontal and motor cortices have dendritic arbor shrinkage,58 indicating compromise in interneuronal communication. Dendritic shrinkage has been shown to be reversible in a rodent model of alcoholism following a prolonged period of abstinence.59 Subcortical regions of brains from patients with uncomplicated alcoholism exhibit neuronal loss in the supraoptic and para ventricular nuclei of the hypothalamus that shows a positive correlation with maximum daily alcohol consumption.60 With respect
