[Neuropathology of amnesic syndromes in man]

Controversies exist about the type of lesions observed in Korsakoff's syndrome or amnestic syndromes. A review of clinicopathologic data in the literature and findings in a personal series of 31 patients with amnestic syndromes (14 with alcoholism and nutritional deficiency, 8 with tumors including 2 with craniopharyngiomas, 5 with Pick's disease and presbyophrenic manifestations, 2 with vascular affections and one each with anoxia and herpetic encephalitis) were used to determine most frequently responsible lesions. Although it is generally accepted that there must be bilateral lesions divergent opinions are found with regard to the significance of limbic-hippocampomammillary circuit lesions. Some authors refute any specific role for the limbic circuit, and particularly any part played by Ammon's horn, in favor of a role for the temporal isthmus while others reject the possible role of the mammillary bodies and implicate the dorsomedian nucleus of the thalamus. The present study confirmed the importance of the limbic-hippocampomammillocingulus circuit in the maintenance of long-term memory. Involvement of the hippocampus appears obvious, particularly in disorders due to lesions of the subiculum and sommer's field. Mammillary body lesions are a constant finding in amnestic syndromes due to alcoholic nutritional deficiency and may also be present in Korsakoff's syndromes of tumoral origin e.g. a compression due to a craniopharyngioma. The rarely mentioned lesions of the cingular convolution are a further possible cause. The role of a thalamic lesion has not been totally confirmed, findings indicating equally frequent involvement of laterodorsal and dorsomedian nuclei. Clinical evidence, however, points to correlations between fabulation, false recognition and a thalamic lesion. The role of the fornix is debatable, although it is difficult to understand how destruction of the hippocampic formation or of the mammillary bodies can provoke memory disorders while an interruption in the structure that links them would have no consequences, unless it is admitted that as in animals other pathways exist that pass little or not at all through the fornix. Clinical expression of bilateral lesions of these structures differs according to whether they affect the posterior Ammon's horn region or lie more anteriorly in the trigonomammillothalamo-cingular complex. Clinical features of hippocampic amnesia include continuous anterograde amnesia with successive periods of forgetfulness, retrograde deficit of variable duration, parallel alterations of verbal and visuospatial memory and absence of fabulation.(ABSTRACT TRUNCATED AT 400 WORDS)