Biological correlates of mental activity studied with PET

Article Abstract:

Positron-emission tomography (PET) is an imaging technology that provides a noninvasive way to assess the functioning of various brain regions by measuring differences in cerebral blood flow (CBF) and rates of glucose metabolism in damaged and surrounding brain areas. Measurements of glucose metabolism and CBF can monitor brain activity because of a direct relationship between CBF, glucose metabolism and the firing of brain cells. PET studies show that mental operations result from the coordinated activation of various brain regions. The signal measured by PET is the decay of radioactive (injected or inhaled) substances. PET studies have demonstrated how a dysfunction in one brain region can lead to a dysfunction in another (diaschisis). PET studies of patients with well localized lesions have helped point out the hierarchical nature of brain organization. Diaschisis seems to result from a chain reaction of disruptions along communication pathways within the brain. When one area of the brain responds to stimulation, that information is filtered, then relayed to appropriate brain areas through specific pathways. Disruption at any point in the relay process can lead to a variety of defects. In a study of speech-impaired (aphasic) patients who had suffered left-sided strokes, the majority showed slow glucose metabolism in the damaged side (left hemisphere) and less severe metabolism defects in the right hemisphere. PET has documented similar intrahemispheric disturbances in patients with localized, one-sided vein or artery damage, making it clear that trying to associate a particular brain region with a single, specific mental task is not possible. PET studies have begun to reveal physical processes which correspond with mental processes. Most studies have focused on simple mental tasks, but future investigations may lead to a clearer understanding of the complex ways in which more elaborate mental operations are carried out. (Consumer Summary produced by Reliance Medical Information, Inc.)

Usage, Blood flow, Blood flow measurement, Brain, PET imaging, Positron emission tomography

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Changes in brain glucose metabolism in cocaine dependence and withdrawal

Article Abstract:

Under conditions of cocaine availability, a user will typically continue to use the drug until he or the cocaine supply is exhausted. However, this uncontrolled use pattern is not fully explained by cocaine's euphoric effect'; even under conditions in which a user develops a tolerance to the effect, the drug is still craved and used uncontrollably. There may be chemical changes in the brain that account for this phenomenon. In the present investigation, 15 cocaine abusers and 17 normal subjects were studied. Glucose metabolism was measured in several regions of the brain using positron emission tomography (PET). Subjects were also evaluated for affective (mood) symptoms using the Beck Depression Inventory. The cocaine abusers were male and averaged 29 years old, they had abused cocaine for at least 12 months, and were in various stages of withdrawal from the drug. The normal control subjects were male and were an average age of 32 years. All but three of the cocaine-dependent subjects had symptoms of depression and all had a sense of cocaine craving. Glucose metabolism varied between the groups and by stage of cocaine withdrawal within the dependent group. Cocaine-dependent subjects who were in early withdrawal (about one week since last use) had the highest glucose metabolism and the normal control subjects had the lowest. Within two-to-four weeks of withdrawal, the differences between cocaine-dependent subjects and normal controls disappeared. It is suggested that these changes are due to changes in dopamine activity, and that the decreased dopamine activity resulting from cocaine use causes an increase in the brain's metabolism of glucose. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Cocaine abuse, Drug withdrawal symptoms, Substance withdrawal syndrome

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Dopamine blockade and clinical response: evidence for two biological subgroups of schizophrenia

Article Abstract:

It has been generally assumed that lack of response by some schizophrenic patients to neuroleptic therapy, treatment with antipsychotic drugs, indicates inadequate dosage of the drugs. This premise was challenged by investigators who concluded that this is not necessarily the case. Ten schizophrenic patients were measured for dopamine receptor occupancy and clinical response before and after dosages of haloperidol, a common antipsychotic. Reduced dopamine receptor status would have indicated that the drug was not having the desired biochemical effect of blocking the release of the hormone dopamine, a "brain messenger," and thus failing to moderate transmission of nervous signals. Results indicated that dopamine blockade was the same for patients who responded to treatment as it was for patients who did not respond. It was concluded that inadequate neuroleptic blockage of dopamine may not be responsible for the failure of the drug therapy. The possibility of the existence of other influential factors was discussed. Greater site density, i.e. the availability of more receptors, in the schizophrenic patient who did not respond was offered as an explanation. Another possibility suggested was that schizophrenia may progress in phases and that during certain phases patients are not responsive to neuroleptics. Investigators suggest that there are intrinsic differences in the pathophysiology of symptoms and a greater heterogeneity exists in schizophrenia than is generally considered.

Research, Evaluation, Drug therapy, Identification and classification, Physiological regulation, Biological control systems, Schizophrenia, Antipsychotic drugs, Antipsychotic agents, Dopamine receptors, Haloperidol, Central nervous system depressants

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