The nucleus basalis (Ch4) in the alcoholic Wernicke-Korsakoff syndrome: reduced cell number in both amnesic and non-amnesic patients
- aDepartment of Pathology, Neuropathology Division, The University of Sydney 2006, NSW 2006, Australia, bPrince of Wales Medical Research Institute, High Street, Randwick, NSW 2031, Australia, cNeuropsychology Unit, Royal Prince Alfred Hospital, Camperdown, NSW 2050, Australia
- Dr K M Cullen, Neuroscience Unit, School of Biological Sciences A08, The University of Sydney, Sydney, NSW 2006, Australia.
- Received 27 November 1996
- Revised 27 January 1997
- Accepted 12 February 1997
Abstract
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 the memory disorder, Korsakoff’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 Korsakoff’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 differ significantly between alcoholic and non-alcoholic 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 Korsakoff’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 non-amnesic patients with Wernicke’s encephalopathy than in some patients with Korsakoff’s psychosis. The non-amnesic 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.
