title: Positron emission tomography findings in dementia disorders: contributions to differential diagnosis and objectivizing of therapeutic effects.
abstract: At present, positron emission tomography (PET) is the only technology affording the quantitative three-dimensional imaging of various aspects of brain function. Since glucose is the dominant substrate of the brain's energy metabolism, studies of glucose metabolism by PET of 2(18F)-fluoro-2-deoxy-D-glucose (FDG) are widely applied for investigating the participation of various brain systems in simple or complex stimulations and tasks. In focal or diffuse disorders of the brain, functional impairment of affected or inactivated brain regions is a reproducible finding. While glucose metabolism is decreased slightly with age in a regionally different degree, in most types of dementia severe changes of glucose metabolism are observed. Degenerative dementia of the Alzheimer type is characterized by a metabolic disturbance most prominent in the parietooccipito-temporal association cortex and later in the frontal lobe, while primary cortical areas, basal ganglia, thalamus, and cerebellum are not affected. By this typical pattern Alzheimer disease can be differentiated from other dementia syndromes, as e.g. Pick's disease (with the metabolic depression most prominent in the frontal and temporal lobe), multi infarct dementia (with multiple focal metabolic defects), and Huntington's chorea (with metabolic disturbance in the neostriatum). In demented patients PET studies can also be applied to the quantification of treatment effects on disturbed metabolism. Such studies demonstrated an equalization of metabolic heterogeneities in patients responding to muscarinergic cholinagonists and diffuse increase of metabolism during treatment with piracetam. The therapeutic relevance of such metabolic effects, however, must be proved in controlled clinical trials.
authors.forename: W D
authors.initials: WD
authors.lastname: Heiss
authors.forename: K
authors.initials: K
authors.lastname: Herholz
authors.forename: G
authors.initials: G
authors.lastname: Pawlik
authors.forename: I
authors.initials: I
authors.lastname: Hebold
authors.forename: P
authors.initials: P
authors.lastname: Klinkhammer
authors.forename: B
authors.initials: B
authors.lastname: Szelies
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000150:complications; D000544:Alzheimer Disease / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D002561:Cerebrovascular Disorders / Q000150:complications; D003704:Dementia / Q000139:chemically induced / Q000000981:diagnostic imaging* / Q000209:etiology / Q000378:metabolism / Q000628:therapy; D003937:Diagnosis, Differential; D004660:Encephalitis / Q000150:complications; D005947:Glucose / Q000378:metabolism; D006801:Humans; D014055:Tomography, Emission-Computed
chemical_list: D005947:Glucose