Using positron emission tomography (PET), the regional cerebral metabolic rate of glucose consumption (rCMRGlc) was measured in 7 subjects suffering from chronic posthypoxic amnesia and in 12 controls. In 6 of the 7 patients regional decreases in rCMRGlc below normal limits were found involving the thalamus in 3 cases, the medial temporal cortex in 2 cases, and the caudate nucleus and cerebellum in one case each. No significant decrease in rCMRGlc was observed in any of the neocortical regions in any of the patients studied. Significant differences between group means of rCMRGlc were found only for the thalamus and the medial temporal cortex. These data suggest that posthypoxic amnesia stems from damage to the medial temporal cortex and its thalamic projection areas and not from neocortical dysfunction, confirming recent theories on the genesis of amnesia in man.