Sergei Korsakoff (1854–1900), a Russian neuropsychiatrist, published in 1887 the first of several papers on a special form of psychic disorder which occurs in conjunction with peripheral neuritis. He mentioned as characteristic such symptoms as irritable weakness, rapid fatiguing, sleeplessness,
memory disturbance, preoccupation with fantasy, and fearfulness. In its modern use the term 'Korsakoff syndrome' refers to a group of symptoms — known alternatively as the amnesic syndrome — which includes inattentiveness, memory defect for recent events, retrograde
amnesia and other disorders of recall and recognition, and disorientation in time, place, and situation. Confabulation, grandiose ideas, and an inappropriate cheerfulness are prominent symptoms in some cases. The syndrome can occur without peripheral neuritis, for example as a stage in recovery after trauma to the brain. When it is combined with peripheral neuritis, the term 'Korsakoff psychosis' tends to be used.
The Korsakoff syndrome develops most often in chronic alcoholics who fail to take an adequate diet. This may cause an acute deficiency of thiamine (vitamin B
1), which produces an acute delirious illness known as
Wernicke's encephalopathy. When or if the patient recovers he will probably be left with the typical features of the Korsakoff syndrome.
The syndrome has seized the interest of neurologists and psychologists because it throws light on normal processes of recall and recognition, although many of the questions it raises have yet to be given precise answers. The memory defect is revealed in the difficulty the patient shows in finding his way about, his forgetfulness in simple matters, and especially his failure to retain information. Also, presented with an object he has been shown a few minutes before, he tends to respond to it as not identical or as in some manner changed. A learning disability can readily be demonstrated in such tests as 'paired associates' and in the delayed recall of pictures of everyday objects. There is a tendency to persist in giving wrong answers, and to fail to 'unlearn'. The deficiency in recalling recent events has been attributed to partial or total derangement of the consolidation of sensory impressions as a permanent memory trace, or engram, or, to put it another way, to a failure to transfer information from a short-term to a long-term memory store. Explanation along these lines has to be qualified by the observation that the patient sometimes recalls after a few hours what he has not recalled after a few minutes.
Some of the symptoms have been attributed to lack of insight or lack of self-critique. A patient with severe memory loss will generally confabulate when questioned about recent activities. That is to say, he will answer incorrectly by describing events that could not possibly have happened. This may give the impression that he is fabricating replies to cover the gaps in his memory. In fact he is doing nothing of the kind. His replies are often accounts of occasions in his more distant past life which are now transposed into the immediate past. He is unaware of the absurd nature of his replies as he is unconscious of the fact that he is answering incorrectly. As Barbizet so neatly put it, 'Confabulation is due to the patient's inability to remember that he can't remember'. If his memory improves he ceases to confabulate and merely replies that he does not know the correct answer to the question that has been put to him.
The lack of self-critique is shown too when he 'entertains incompatible propositions'. He says, for instance: 'I am 52 years old. I was born in 1920. It is now 1975.' The item most likely to be correct is the year of birth. He does not apply tests to check the correctness of what he has said, as a healthy person tends to do. One reason may be indolence or passivity. However, by insisting on the incompatibility of the propositions the observer may provoke a 'catastrophic reaction', and this suggests that false propositions are held to as a defence against
anxiety.
Neuropathological studies of patients who have shown the syndrome have contributed to knowledge of the brain structures concerned in memory processes. The floor of the third ventricle is usually affected. The lesion tends to be localized in subcortical structures. The hippocampal region and the mamillary bodies are involved, it has been claimed, in all cases. Recent work has shown that damage is not confined to these structures. There is also evidence of atrophy of the frontal lobes and dilatations of the cerebral ventricles. This structural damage of the brain has been reported not only in chronic alcoholics but also in young heavy drinkers and may help to explain why it is so difficult for these subjects to learn new ways of dealing with their drinking problems.
(Published 1987)— Derek Russell Davis
Bibliography- Kopleman, M. D. (1995). 'The Korsakoff syndrome'. British Journal of Psychiatry, 166/2.
- Paller, K. A., Acharya, A., and Richardson, B. (1997). 'Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff syndrome'. Journal of Cognitive Neuroscience, 9.
- Victor, M., and Yakovlev, P. I. (1955). 'S. S. Korsakoff's psychic disorder in conjunction with peripheral neuritis'. Neurology, 5. (A translation of Korsakoff's original article.)
