The nucleus basalis (Ch4) in the alcoholic Wernicke-KorsakoV syndrome: reduced cell number in both amnesic and non-amnesic patients

Background—The cholinergic nucleus basalis (Ch4) is an exclusive site of neurofibrillary degeneration in alcoholic patients with Wernicke’s encephalopathy. Aim—To test the hypothesis that the loss of Ch4 neurons contributes to thememory disorder, KorsakoV’s psychosis, commonly seen in Wernicke’s encephalopathy. Methods—Magnocellular basal forebrain neurons were quantified in alcoholic patients with Wernicke’s encephalopathy, both with and without KorsakoV’s psychosis, and neurologically asymptomatic alcoholic and non-alcoholic controls. Because amnesic and non-amnesic patients with Wernicke’s encephalopathy share common periventricular lesions, both thiamine deficient groups as well as alcoholic patients with no neurological complications were included to determine the lesion specific to memory impairment. Results—Ch4 cell number did not diVer significantly between alcoholic and nonalcoholic controls and there was no correlation between cell number and lifetime alcohol intake. However, Ch4 cell number in all groups was significantly correlated with the volume of its major projection target, the cerebral cortex. Ch4 cell number in the non-amnesic Wernicke’s encephalopathy group was significantly below controls (24%), with cell number in patients with KorsakoV’s psychosis 21% below controls. There was considerable overlap in cell number between groups. On discriminant analysis, there was significantly greater cell loss in three nonamnesic patients with Wernicke’s encephalopathy than in some patients with KorsakoV’s psychosis. The nonamnesic patient with the greatest cell loss was impaired on attentional tasks. Conclusion—Whereas neurons in the nucleus basalis are at risk in thiamine deficient alcoholic patients, cell loss is minor and does not account for the profound memory disorder. (J Neurol Neurosurg Psychiatry 1997;63:315–320)