Brain-behavior relationships in aphasia studied by positron emission tomography.
Positron emission tomography allows for the study of human brain physiology and chemistry including cerebral blood flow, oxygen or glucose metabolism. We applied PET to study glucose metabolism using aphasia as a model of neurobehavior. The most striking observation was that the extent of cerebral glucose metabolic changes in aphasic patients consistently involve brain regions that are not structurally damaged. The remote metabolic effects can be predicted depending on the location and extent of structural damage. Two observations were made: (1) In our experience, all right-handed aphasic patients with left hemisphere structural lesions have metabolic abnormalities in the left temporoparietal region, and (2) metabolic abnormalities are variably found in undamaged, left prefrontal lobe, basal ganglia, and thalamus. Variations in clinical aphasic syndromes were found to relate to these frontal metabolic changes, suggesting that aspects of the aphasia result from differences in prefrontal function rather than directly from structural damage to perisylvian or deep structures.
Metter
E J
EJ
Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224.
D001037:Aphasia / Q000000981:diagnostic imaging / Q000378:metabolism*; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism*; D002561:Cerebrovascular Disorders / Q000378:metabolism; D003847:Deoxyglucose / Q000031:analogs & derivatives / Q000378:metabolism; D019788:Fluorodeoxyglucose F18; D005625:Frontal Lobe / Q000000981:diagnostic imaging / Q000378:metabolism; D007839:Functional Laterality; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D014055:Tomography, Emission-Computed
D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose; D005947:Glucose