[Korsakoff amnesia syndrome]

PATHOLOGY CORRELATIONS: The Korsakoff syndrome results from cerebral lesions due to thiamine depletion, usually of alcoholic etiology. Other nutritional, or genetic factors, could be implicated. Exceptionally, it results from thalamic disease or a tumor of the third ventricle floor.

Anterograde and retrograde aspects of episodic memory are principally impaired, contrasting with the preservation of semantic and procedural memory. Opposition between explicit (impaired) and implicit (unimpaired) memory is one of the main cognitive features of this syndrome. Several cerebral structures, components of various memory systems, are simultaneously damaged. Critical lesion sites for anterograde amnesia involve the memillary bodies, the mamillotalamic tract and the anterior thalamus. Retrograde amnesia is dependent on function abnormalities of a circuit between the dorso-median thalamus and the prefrontal cortex. Impairment of retrieval and chronological disorganization of memories contribute to this extensive retrograde amnesia, probably because of frontal dysfunction. Confabulations and false recognitions are produced in the initial stage of the disease. They are, in the same way, interpreted as the consequence of frontal desafferentation due to dorso-median thalamus damage. The impact of diencephalic destruction on the frontal lobes is evidenced clinically by behavioral changes and dysexecutive syndrome. Neuroimaging studies of the brain show a decreased regional metabolic ration in the frontal areas.

Korsakoff syndrome is a serious disorder, responsible for cognitive handicap. There is no curative treatment. Preventive measures, consisting in systematic prescription of thiamine in alcoholics, is the main effective measure.