THE KORSAKOFF SYNDROME

Authors
Citation
Md. Kopelman, THE KORSAKOFF SYNDROME, British Journal of Psychiatry, 166, 1995, pp. 154-173
Citations number
229
Categorie Soggetti
Psychiatry,Psychiatry
ISSN journal
00071250
Volume
166
Year of publication
1995
Pages
154 - 173
Database
ISI
SICI code
0007-1250(1995)166:<154:TKS>2.0.ZU;2-N
Abstract
Background. Investigations of the Korsakoff syndrome by researchers fr om different disciplines have proliferated in recent years, making it apposite to review the various findings. Method. This review is based on the author's knowledge of reports in the major clinical and neurops ychological journals, supplemented by Medline searches to update parti cular subtopics. Results. The Korsakoff syndrome is defined as a dispr oportionate impairment in memory, relative to other aspects of cogniti ve function, resulting from a nutritional (thiamine) depletion. The in itial manifestations of the disorder are variable, and a persistent me mory impairment can result from a non-alcoholic aetiology, although th is seems to happen much less commonly than in the past-presumably beca use of generally higher standards of nutrition. Although there is agre ement on the underlying neuropathology, the critical lesion sites for memory disorder have been debated. Recent evidence suggests that the c ircuit involving the mammillary bodies, the mammillo-thalamic tract an d the anterior thalamus, rather than the medial dorsal nucleus of the thalamus, is particularly critical in the formation of new memories. T he relationship of these deficits to thiamine depletion remains a topi c of current investigation, as does the purported role of neurotransmi tter depletions in the cholinergic, glutamate/GABA and catecholamine a nd serotonergic systems. Neuro-imaging studies have confirmed autopsy findings of more widespread structural and metabolic abnormalities, pa rticularly involving the frontal robes. Conclusions. The relationship of these neuropathological, neurochemical, and metabolic abnormalities to cognitive functioning, with particular reference to specific aspec ts of memory processing, has been considered in some detail. Whereas s tructural and/or neurochemical abnormalities within the limbic/diencep halic circuits account for anterograde amnesia, some other factor, suc h as frontal robe dysfunction, must underlie the severe retrograde mem ory loss which is characteristically found in this syndrome.