[FDG-PET in an amnestic and hypersomnic patient with bilateral paramedian thalamic infarction].

A 67-year-old patient was admitted to our hospital owing to coma and tetraplegia. MRI showed T2 weighed high intensity areas in the pontine tegmentum, lower aspect of the right cerebellar hemisphere, left half of medulla oblongata, and bilateral paramedian thalamus. He showed marked recovery by urokinase injection becoming able to walk in a few months, but severe amnesia and hypersomnia persisted even 5 months after onset. EEG showed diffuse alpha activity with occasional delta waves in frontal leads. Intelligence was considered normal (WAIS score; verbal IQ 97, performance IQ 102, total IQ 99), through performance on Wechsler memory Scale-R (Revised Japanese edition, WMS-R) and Benton Visual Retention Test indicated impairment of both verbal and visual memory. Verbal memory was impaired to a greater degree than visual memory (Scores of WMS-R: verbal memory index 60, visual memory index 98, index of general memory 72, attention index 95, index of delayed memory 71). He was able to finish only 0 and 1 categories on two trials of the Wisconsin Card Sorting Test. FDG (18F-fluorodeoxyglucose)-PET showed diffuse areas of decreased metabolism in bilateral thalami, frontal lobes, cingulate gyri and medial temporal lobes. The bilateral thalamic lesion seemed to affect the following structures, as judged from MRI: 1) The anterior thalamic peduncle including most of the reciprocal connections between dorsomedial nucleus of thalamus (MD nucleus) and the frontal lobe, 2) The inferior thalamic peduncle which serves as the reciprocal pathway between MD nucleus and medial temporal lobe, especially the amygdala (component of Yakovlev circuit), and 3) The inferior part of mammillothalamic tract (component of Papez circuit).(ABSTRACT TRUNCATED AT 250 WORDS)