Positron emission tomography studies of abnormal glucose metabolism in schizophrenic illness.
Advances in psychopharmacology and neuroscience have brought into view a wide field of competing mechanisms for the etiology of schizophrenia including, but not limited to, deficits in one or more neurotransmitters (dopamine, serotonin, GABA, glutamate, and noradrenaline systems), neurodevelopmental defects in cortical connectivity, and viral infection. Genetic studies suggest heterogeneity in the illness, with multifactorial inheritance. Since cerebral metabolic activity reflects regional brain work for all neurotransmitter systems, imaging studies can provide information on the functional neuroanatomy of a deficit in the individual patient, allowing the grouping of patients for more intensive investigation in more homogeneous groups. Metabolic imaging studies allow psychopharmacological response to be regionally assessed and clinical responders to be identified, even for medications that affect more than one neurotransmitter system or have clinical effects that derive from changes in activity one synapse or more removed from the site of primary action.
Buchsbaum
M S
MS
Department of Psychiatry, Mt. Sinai School of Medicine, New York, NY 10029, USA.
D001921:Brain / Q000000981:diagnostic imaging* / Q000378:metabolism; D003847:Deoxyglucose / Q000031:analogs & derivatives / Q000378:metabolism; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D012559:Schizophrenia / Q000000981:diagnostic imaging* / Q000378:metabolism; D014055:Tomography, Emission-Computed
D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose; D005947:Glucose