Document Detail

Prefrontal cortical-amygdalar metabolism in major depression.
MedLine Citation:
PMID:  10415674     Owner:  NLM     Status:  MEDLINE    
Functional neuroimaging studies of the anatomical correlates of familial major depressive disorder (MDD) and bipolar disorder (BD) have identified abnormalities of resting blood flow (BF) and glucose metabolism in depression in the amygdala and the orbital and medial prefrontal cortical (PFC) areas that are extensively connected with the amygdala. The amygdala metabolism in MDD and BD is positively correlated with both depression severity and "stressed" plasma cortisol concentrations measured during scanning. During antidepressant drug treatment, the mean amygdala metabolism decreases in treatment responders, and the persistence of elevated amygdala metabolism during remission is associated with a high risk for the development of depressive relapse. The orbital C metabolism is also abnormally elevated during depression, but is negatively correlated with both depression severity and amygdala metabolism, suggesting that this structure may be activated as a compensatory mechanism to modulate amygdala activity or amygdala-driven emotional responses. The posterior orbital C and anterior cingulate C ventral to the genu of the corpus callosum (subgenual PFC) have more recently been shown in morphometric MRI and/or post mortem histopathological studies to have reduced grey matter volume and reduced glial cell numbers (with no equivalent loss of neurons) in familial MDD and BD. These data suggest a neural model in which dysfunction of limbic PFC structures impairs the modulation of the amygdala, leading to abnormal processing of emotional stimuli. Antidepressant drugs may compensate for this dysfunction by inhibiting pathological limbic activity.
W C Drevets
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  877     ISSN:  0077-8923     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  1999 Jun 
Date Detail:
Created Date:  1999-08-10     Completed Date:  1999-08-10     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  614-37     Citation Subset:  IM    
Department of Psychiatry, University of Pittsburgh School of Medicine, Pennsylvania 15213, USA.
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MeSH Terms
Amygdala / drug effects,  metabolism*,  physiopathology
Antidepressive Agents / pharmacology,  therapeutic use
Bipolar Disorder / metabolism,  physiopathology
Cerebrovascular Circulation
Depressive Disorder / drug therapy,  metabolism*,  physiopathology
Hydrocortisone / blood
Prefrontal Cortex / drug effects,  metabolism*,  physiopathology
Reg. No./Substance:
0/Antidepressive Agents; 50-23-7/Hydrocortisone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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