Effects of mood and subtype on cerebral glucose metabolism in treatment-resistant bipolar disorder

Background: Functional brain imaging studies in unipolar and secondary depression have generally found decreased prefrontal cortical activity, but in bipolar disorders findings have been more variable. Methods: Forty-three medication-free, treatment-resistant, predominantly rapid-cycling bipolar dis...

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Published inBiological psychiatry (1969) Vol. 49; no. 2; pp. 97 - 109
Main Authors Ketter, Terence A, Kimbrell, Tim A, George, Mark S, Dunn, Robert T, Speer, Andrew M, Benson, Brenda E, Willis, Mark W, Danielson, Aimee, Frye, Mark A, Herscovitch, Peter, Post, Robert M
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 2001
Elsevier Science
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Summary:Background: Functional brain imaging studies in unipolar and secondary depression have generally found decreased prefrontal cortical activity, but in bipolar disorders findings have been more variable. Methods: Forty-three medication-free, treatment-resistant, predominantly rapid-cycling bipolar disorder patients and 43 age- and gender-matched healthy control subjects had cerebral glucose metabolism assessed using positron emission tomography and fluorine-18-deoxyglucose. Results: Depressed bipolar disorder patients compared to control subjects had decreased global, absolute prefrontal and anterior paralimbic cortical, and increased normalized subcortical (ventral striatum, thalamus, right amygdala) metabolism. Degree of depression correlated negatively with absolute prefrontal and paralimbic cortical, and positively with normalized anterior paralimbic subcortical metabolism. Increased normalized cerebello-posterior cortical metabolism was seen in all patient subgroups compared to control subjects, independent of mood state, disorder subtype, or cycle frequency. Conclusions: In bipolar depression, we observed a pattern of prefrontal hypometabolism, consistent with observations in primary unipolar and secondary depression, suggesting this is part of a common neural substrate for depression independent of etiology. In contrast, the cerebello-posterior cortical normalized hypermetabolism seen in all bipolar subgroups (including euthymic) suggests a possible congenital or acquired trait abnormality. The degree to which these findings in treatment-resistant, predominantly rapid-cycling patients pertain to community samples remains to be established.
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ISSN:0006-3223
1873-2402
DOI:10.1016/S0006-3223(00)00975-6