In patients with uncomplicated alcoholism, MRI studies have generally confirmed postmortem studies by demonstrating that such patients have regional cortical volume deficits,64,70 especially in the frontal lobes.71,72 Among individuals with alcoholism, cerebral shrinkage is more pronounced in older patients than in younger patients, suggesting that the aging brain is especially susceptible to ARBD.70,73 Structural MRI has also demonstrated that individuals with alcoholism have significant volume deficits in the corpus callosum74,75 and cerebellar white matter.48,76 In contrast to postmortem findings, MRI has provided in vivo evidence for volume deficits in the an terior hippocampus of patients with chronic alcoholism.77,78 These deficits are potentially accounted for by a loss of non-neuronal cells; that is, glia. Altogether, use of MRI to characterize WKS structural brain changes in the context of the neuropathology of uncomplicated alcoholism has revealed a graded pattern of volume deficits (from mild deficits in ARBD to moderate or severe deficits in WKS) in the mamillary bodies, hippocampus, thalamus, cerebellum and pons (Figure 4).5 As brain regions outside those traditionally associated with thiamine depletion (for example, the frontal cortices, hippocampus and
