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Brain-behavior relationships in aphasia studied by positron emission tomography
1Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224.
Annals of the New York Academy of Sciences
|January 1, 1991
Summary
Positron emission tomography (PET) reveals that brain glucose metabolism changes in aphasia extend beyond damaged areas. These remote metabolic effects in undamaged regions predict aphasia severity and presentation.
Area of Science:
- Neuroscience
- Medical Imaging
- Neurology
Background:
- Positron emission tomography (PET) is a powerful tool for investigating human brain physiology and chemistry.
- PET enables the study of cerebral blood flow, oxygen, and glucose metabolism.
- Aphasia, a neurobehavioral disorder, serves as a model for understanding brain function and dysfunction.
Purpose of the Study:
- To investigate glucose metabolism in aphasic patients using PET.
- To explore the relationship between structural brain damage and remote metabolic changes.
- To determine if metabolic alterations in undamaged brain regions correlate with aphasia severity and presentation.
Main Methods:
- Application of Positron Emission Tomography (PET) to assess cerebral glucose metabolism.
- Utilizing aphasia as a model to study neurobehavioral changes.
- Correlation of metabolic data with structural lesion location and extent.
Main Results:
- Cerebral glucose metabolic changes in aphasic patients frequently involve brain regions not structurally damaged.
- Remote metabolic effects are predictable based on the location and extent of structural lesions.
- All right-handed aphasic patients with left hemisphere lesions showed temporoparietal metabolic abnormalities.
- Metabolic abnormalities in undamaged left prefrontal lobe, basal ganglia, and thalamus were variable.
- Frontal metabolic changes correlated with variations in clinical aphasic syndromes.
Conclusions:
- Structural brain lesions in aphasia induce remote metabolic changes in functionally connected, yet undamaged, brain regions.
- The extent and location of these remote metabolic alterations are predictable.
- Clinical variations in aphasia syndromes may stem from functional differences in the prefrontal cortex, rather than solely from direct structural damage.