Functional sites of neuroleptic drug action in the human brain: PET/FDG studies with and without haloperidol.
[|Wu]Objective:[|WU] The functional pathways through which antipsychotic drugs act in the brain to decrease psychosis remain unknown, despite our knowledge that their site of initial action is through blockade of dopamine D2 receptors. The authors sought to define the brain regions that are functi...
| Published in: | American Journal of Psychiatry Vol. 153; pp. 41 - 50 |
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| Main Authors: | , , |
| Format: | Article |
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American Psychiatric Publishing, Inc.
January 1996
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| Subjects: | |
| Online Access: | View this record in EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ssf&AN=512730108&site=ehost-live header: @attributes: shortDbName: ssf uiTerm: 512730108 longDbName: Social Sciences Full Text (H.W. Wilson) uiTag: AN controlInfo: bkinfo: jinfo: jid: 0002953X API jtl: American Journal of Psychiatry issn: 0002953X maglogo: N pubinfo: dt: January 1996 vid: 153 pid: 37323 pub: American Psychiatric Publishing, Inc. artinfo: ui: 512730108 ppf: 41 ppct: 9 formats: tig: atl: Functional sites of neuroleptic drug action in the human brain: PET/FDG studies with and without haloperidol. aug: au: Holcomb, Henry H. Cascella, Nicola G. Thaker, Gunvant K. su: Neuropsychopharmacology Haloperidol Brain function localization Thalamus Basal ganglia Cerebral cortex Glucose -- Metabolism Schizophrenia sug: subj: Neuropsychopharmacology Haloperidol Brain function localization Thalamus Basal ganglia Cerebral cortex Glucose -- Metabolism Schizophrenia ab: [|Wu]Objective:[|WU] The functional pathways through which antipsychotic drugs act in the brain to decrease psychosis remain unknown, despite our knowledge that their site of initial action is through blockade of dopamine D2 receptors. The authors sought to define the brain regions that are functionally altered by neuroleptic drugs. [|Wu]Method:[|WU] Regional cerebral glucose metabolism was studied in 12 subjects with schizophrenia while they were receiving a fixed dose of haloperidol, again 5 days after withdrawal of the drug, and a third time 30 days after withdrawal. Positron emission tomography with an {18F}fluorodeoxyglucose tracer was used in a within-subject design. [|Wu]Results:[|WU] The analysis demonstrated a decrease in glucose metabolism in the caudate and putamen 30 days after withdrawal, indicating that haloperidol treatment enhanced glucose utilization in these areas. The thalamus, bilaterally but only in anterior areas, showed the same response to haloperidol. Only in the frontal cortex and in the anterior cingulate had metabolism increased 30 days after withdrawal, indicating that in those two cortical areas haloperidol depressed glucose metabolism. In the 5-day drug free scans, no regions differed significantly from those in the haloperidol condition, despite numerical changes. [|Wu]Conclusions:[|WU] It appears that 5 days of neuroleptic withdrawal are inadequate to escape the effects of neuroleptic drugs on regional cerebral glucose metabolism. The pattern and localization of changes in metabolic activity between the haloperidol condition and the 30-day drug-free condition suggest that haloperidol exerts its primary antidopaminergic action in the basal ganglia. It is proposed that the additional changes in the thalamus and cortex are secondary to this primary site of drug action, mediated through classically described striato-thalamo-cortical pathways. Reprinted by permission of the publisher. pubtype: Academic Journal doctype: Article src: R language: English refInfo: copyright: @attributes: flag: N holdings: @attributes: islocal: N |
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