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Clinical and anatomical report of a post traumatic amnestic syndrome (Korsakoff's syndrome), associating anterograde amnesia persisting for fifteen years, with temporal disorientation, false recognitions, initially intense transitory confabulation and secondarily bursts of confabulation, intact remote memory and persistence of old learnings. Death after twelve years from mesenteric infarction. Anatomically, post-traumatic sequellae are limited to both cingulate gyri in their anterior part. This cingula involvement is easy to understand if one knows that post-traumatic Korsakoff's syndrome appears after severe cranial traumatisms, with at least three days of coma, and develops constantly, even if transitory, after long duration comas with 20 to 30 days of loss of consciousness. Anatomical explanation depends on the fact that Korsakoff's syndromes from various etiologies need, to be produced, a bilateral damage of the limbic circuit and that severe head traumatisms, when dying early in the evolution without possibility of a neuro-psychological investigation, have always a destruction of corpus callosum or cingulate gyri or both, resulting from crushing of these structures by the edge of the faulx cerebri. Consistent with these constatations, it is logical that a Korsakoff's syndrome develops after severe head traumas with bilateral lesions of the limbic circuit and especially of the cingulate gyri. But anatomical evidence remains rare, because early fatal evolution does not permit psychological evaluation and, reversely, long survivals who may die from another pathology would not have brain examination. We prefer the name of "Korsakoff's syndrome" rather than that of "amnesic syndrome" to denominate the anterograd amnesia (amnésie des faits récents) encountered in nutritional disorders due to B1 deficiency in true Korsakoff's disease, but also with other etiologies such as cerebral tumours, vascular cerebral disorders, post-commital anoxia, herpetic encephalopathy, head traumas, all of them developing amnesia for recent events, formerly classified under the title of "korsakowian syndrome" or "mental syndrome of Korsakoff" and more recently under the denomination of "amnesic syndrome". But whatever is the etiology of the memory disorder, the amnesic syndrome remains identical and the advanced small differences, such as euphoria in alcoholics or mood depression in tumours, are often fallacious, so that the only way of differentiation deals with accessory symptoms such as intracranial hypertension in tumours, sudden onset in vascular etiologies or polyneuritis in B1 deficiency. Post-traumatic Korsakoff's syndrome joins with this scheme, for its clinical aspect is so similar to that of nutritional disorders that it might be difficult to reach the exact diagnosis when an alcohol addict develops, after a head trauma, an amnesia which could be the consequence of the trauma but also of a nutritional disorder developed after the accident with inadequate parenteral treatment. Our case, which is the first well documented observation of this disease reported with long clinical survey and final pathological examination, was presented in 1981 at a joint meeting of the French and Dutch neurological societies. It gives the proof of the importance, in limbic circuit, of the cingulate gyri. A comparison is made with four other clinical cases of post traumatic amnestic syndrome with MNR procedures which show, for two of them, cingula lesions explaining the clinical features, for one of them a bilateral lesion of Ammon's homs and for the last one extra-limbic lesions, with destruction of the inferior part of both frontal lobes, associated with a possible deafferentation of the right cingula cortex.