L’implication de l’hippocampe dans la mémoire est reconnue par la forte association de l’amnésie aux lésions hippocampiques. Ces lésions peuvent être limitées, mais suffisantes pour provoquer des troubles de la mémoire épisodique consciente et de la mémoire procédurale. Une des étiologies fréquentes du syndrome amnésique pur par lésion hippocampique est l’anoxie cérébrale. L’évolution de ces lésions dépend de leur étendue, de l’âge du patient, du début de l’installation des troubles et du diagnostic précoce. Le cas clinique présenté dans ce travail s’intéresse à une jeune patiente ayant présenté un syndrome amnésique pur suite à l’inhalation accidentelle du monoxyde de carbone. Cette amnésie est accompagnée par un syndrome anxieux et un syndrome subconfusionnel et est de type antérograde. Le scanner a montré une hypodensité bilatérale hippocampique et un œdème diffus. L’évolution est marquée par la stagnation des scores de la Galveston orientation and amnesia test (GOAT) et la régression de l’œdème et des hypodensités. Ce cas clinique sera accompagné d’une revue de la littérature.

Carbon monoxide (CO) intoxication is still one of the most frequent conditions causing brain damage as a result of hypoxia in Morocco, and the main area of brain damage is the hippocampus. The role of the hippocampus in the memory process has been known for long and we usually associate hippocampus damage with anterograde amnesia. Nevertheless, the pure amnesic syndrome is retrieved in the isolated damage of the hippocampus as is seen in the anoxia caused by CO intoxication. The outcome of the patterns depends on the extent of brain damage, the age of onset and the early diagnosis.

This study presents the case of a young female patient who presented with anterograde amnesia after massive and prolonged accidental exposition to CO that presented disproportional radiological and clinical outcome. Primary care was in the intensive care unit during 24hours and based on oxygen therapy and diuretics. The psychiatric examination found an acute stress disorder and symptoms of delirium in the form of reduced awareness and memory deficit. The amnesia was anterograde and the patient exhibited diminished ability to remember time, space and persons. The Galveston orientation and amnesia test (GOAT) score on awakening in the intensive care unit was 46. The laboratory findings did not provide direct physiological disturbances. The brain computed tomography (CT) scan revealed bilateral hippocampus low-density in the cerebral white and grey matter. The clinical and the radiological outcome of this pattern were not correlated. The GOAT scores were 46 on the 10th day and 50 when the patient was discharged three weeks later, although the brain CT scan showed a decrease of the low-density in the hippocampus. Forty-five days later, the GOAT score was still 49 and the brain CT scan did not show any low-density lesion. Clinical symptoms of a major depressive episode were installed.

These results are correlated to the findings of several series in which the CT scans in CO intoxication show common characteristic features that are symmetrical low-density lesions in the cerebral white matter in some specific brain structures such as the globus pallidus and the hippocampus. The early diagnosis is usually difficult because the brain CT scan findings do not always provide morphological changes and fail approximately one half of the time to detect low-density in the white matter of the hippocampus, and the use of MRI is not as easy as the CT scan. The long period of unconsciousness, the white matter damage and the late diagnosis result in complications in the outcome.