ALTERED GLUCOSE-METABOLISM IN THE HIPPOCAMPAL HEAD IN MEMORY IMPAIRMENT

Objective: To evaluate the relevance of hypometabolism in the hippocam pal head to the pathophysiology of memory impairment. Background: Neur ofunctional imaging studies with an image reslicing technique provided by using software suggest that dysfunction of the amygdalohippocampal system causes memory impairment. However, metabolic and morphologic p rofiles of the whole hippocampal formation have not been evaluated in detail. Methods: By tilting the gantry of a high-resolution PET scanne r in a plane parallel to the hippocampal longitudinal axis determined beforehand by MRI, we performed quantitative measurement of glucose me tabolism in the subdivisions of the hippocampal formation (head, body, tail) in 10 patients of normal intelligence with pure amnesia, in eig ht patients with AD, and in eight normal subjects. Results: Although t he volumes of the amygdala and hippocampal formation in pure amnesics were not different significantly from those of normal subjects, glucos e metabolism in the head of the hippocampus was significantly lower in pure amnesics. In patients with AD, marked hypometabolism was found e xtending to the amygdala, the hippocampal head, and the parietotempora l cortex, along with amygdalohippocampal atrophy. Conclusion: Hippocam pal head dysfunction plays an important role in memory impairment in a mnesic patients. Further metabolic impairment over the amygdalohippoca mpal system and the surrounding association cortex reflects the pathop hysiology of AD.