Antidepressant Treatment in Bipolar Versus Unipolar Depression

Ghaemi, S. Nassir; Rosenquist, Klara J.; Ko, James Y.; Baldassano, Claudia F.; Kontos, Nicholas; Baldessarini, Ross J.

doi:10.1176/appi.ajp.161.1.163

Cited by 239 publications

(164 citation statements)

References 9 publications

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“…Antidepressant treatment in bipolar disorder patients may only exacerbate the problem by inducing switching or rapid cycling. 14,15 The imputed prevalence was similar to rates reported for other studies of depressed patients. To our knowledge, this is the first time anyone has looked specifically at patients being treated with antidepressants.…”

Section: Discussionsupporting

confidence: 81%

Screening for Bipolar Disorder in Patients Treated for Depression in a Family Medicine Clinic

Hirschfeld¹,

Cass²,

Holt³

et al. 2005

The Journal of the American Board of Family Medicine

163

109

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Purpose:The prevalence of bipolar disorder in patients being treated for depression with antidepressants in a family medicine clinic was investigated in this study.Methods: Adult patients with depression who were treated with an antidepressant in a general outpatient family medicine clinic at the University of Texas were screened for bipolar disorder using the Mood Disorder Questionnaire (MDQ), a brief self-report inventory. A subsample of subjects received the Structured Clinical Interview based on the DSM-IV (SCID) to test the operating characteristics of the MDQ in this population.Results: of the patients taking an antidepressant for depression, 21.3% screened positive for bipolar disorder on the MDQ. These patients were somewhat younger, more likely to be white, more likely to be living alone, much less likely to be married, and less likely to be employed than those who screen negative. Nearly two thirds of those screened positive had never received diagnosis of bipolar disorder. The sensitivity and specificity of the MDQ in this population, after adjusting for the sampling protocol, were 0. The recognition, diagnosis, and treatment of depression in primary care settings has received enormous attention over the last decade. A result of this attention is the management of depressed patients in primary care settings has been improved. Unfortunately, little attention has been given to a significant subset of depressed patients-those with bipolar disorder. A notable exception has been the work of J. Sloan Manning in Tennessee, who reported that 26% of patients presenting with depression in his family practice setting had bipolar disorder.1 This prevalence is similar to that reported in the psychiatric specialty care settings. In a study conducted in France by Hantouche et al, 2 the rate of bipolar disorder in a population of patients presenting with a major depressive episode was 28%. In a study conducted in a private psychiatric practice in northern Italy, Benazzi 3 found that 49% of the outpatients presenting with depression had bipolar spectrum disorder. The prevalence of bipolar disorder in these clinical settings is substantially higher than that found in the community, which ranges from approximately 1% for bipolar I disorder to 3% to 6.5% for bipolar I and II and other disorders in the bipolar spectrum. 4The issue of misdiagnosis or inaccurate diagnosis is particularly important for patients who are being treated with antidepressants for depression. Antidepressants, particularly tricyclics and monoamine oxidase inhibitors, when administered with-

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Section: Discussionsupporting

confidence: 81%

Screening for Bipolar Disorder in Patients Treated for Depression in a Family Medicine Clinic

Hirschfeld¹,

Cass²,

Holt³

et al. 2005

The Journal of the American Board of Family Medicine

163

109

View full text Add to dashboard Cite

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“…[72][73][74] Furthermore, drugs or conditions known to induce mania in susceptible individuals 171 could be studied using 11 C-labeled AA and PET. Because antidepressants can induce switching to mania when given to a depressed bipolar disorder patient, 146,[172][173][174] we examined the selective serotonin reuptake inhibitor fluoxetine in our models. Opposite to the antimanic drugs, chronic fluoxetine increased frontal cortex cPLA 2 activity, protein and mRNA expression along with the turnover of AA in brain phospholipids of the unanesthetized rat.…”

Section: Observations Related To Aa In Bipolar Disorder Patientsmentioning

confidence: 99%

Mode of action of mood stabilizers: is the arachidonic acid cascade a common target?

et al. 2008

Mol Psychiatry

109

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Bipolar disorder is a major medical, social and economic burden worldwide. However, the mechanisms of action of effective antibipolar disorder drugs remain elusive. In this paper, we review studies using a neuropharmacological approach in unanesthetized rats, combined with kinetic, biochemical and molecular biology techniques, showing that chronic administration of three Food and Drug Administration-approved mood stabilizers (lithium, valproate and carbamazepine) at therapeutically relevant doses, selectively target the brain arachidonic acid (AA) cascade. Whereas chronic lithium and carbamazepine decrease the binding activity of activator protein-2 and in turn the transcription, translation and activity of its AA-selective calcium-dependent phospholipase A 2 gene product, valproate appears to be a non-competitive inhibitor of long-chain acyl-CoA synthetase. The net overlapping effects of the three drugs are decreased turnover of AA but not of docosahexaenoic acid in rat brain phospholipids, and decreased brain cyclooxygenase-2 and prostaglandin E 2 . Although these observations support the hypothesis proposed by Rapoport and colleagues that the AA cascade is a common target of mood stabilizers, this hypothesis is not necessarily exclusive of other targets. Targeting the AA cascade with drugs or diet may be a useful therapeutic approach in bipolar disorder, and examining the AA cascade in patients might help in better understanding the disease.

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“…Despite this, the neurobiology of bipolar depression has been only sparsely explored. The need for further research is underscored by the fact that none of the antidepressant medications approved for treatment of unipolar depression have been approved for treatment of bipolar depression and may carry risks of inducing mania (Ghaemi et al, 2004;Connolly and Thase, 2011). Conversely, the approved pharmacotherapies for bipolar depression remain limited in number, often carry significant risks of metabolic side effects, and are not approved as monotherapy for major depression (Ghaemi et al, 2004;Connolly and Thase, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…The need for further research is underscored by the fact that none of the antidepressant medications approved for treatment of unipolar depression have been approved for treatment of bipolar depression and may carry risks of inducing mania (Ghaemi et al, 2004;Connolly and Thase, 2011). Conversely, the approved pharmacotherapies for bipolar depression remain limited in number, often carry significant risks of metabolic side effects, and are not approved as monotherapy for major depression (Ghaemi et al, 2004;Connolly and Thase, 2011). Similarities of clinical presentation but the presence of differential risk of mania and treatment response suggests that bipolar and unipolar depression have both common and dissociable neurobiological substrates (Treadway and Zald, 2011;Chase et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Common and Dissociable Dysfunction of the Reward System in Bipolar and Unipolar Depression

Satterthwaite

Kable

Vandekar

et al. 2015

Neuropsychopharmacol

224

147

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Unipolar and bipolar depressive episodes have a similar clinical presentation that suggests common dysfunction of the brain's reward system. Here, we evaluated the relationship of both dimensional depression severity and diagnostic category to reward system function in both bipolar and unipolar depression. In total, 89 adults were included, including 27 with bipolar depression, 25 with unipolar depression, and 37 healthy comparison subjects. Subjects completed both a monetary reward task and a resting-state acquisition during 3T BOLD fMRI. Across disorders, depression severity was significantly associated with reduced activation for wins compared with losses in bilateral ventral striatum, anterior cingulate cortex, posterior cingulate cortex, and right anterior insula. Resting-state connectivity within this reward network was also diminished in proportion to depression severity, most notably connectivity strength in the left ventral striatum. In addition, there were categorical differences between patient groups: resting-state connectivity at multiple reward network nodes was higher in bipolar than in unipolar depression. Reduced reward system task activation and resting-state connectivity therefore appear to be a brain phenotype that is dimensionally related to depression severity in both bipolar and unipolar depression. In contrast, categorical differences in reward system resting connectivity between unipolar and bipolar depression may reflect differential risk of mania. Reward system dysfunction thus represents a common brain mechanism with relevance that spans categories of psychiatric diagnosis.

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Antidepressant Treatment in Bipolar Versus Unipolar Depression

Abstract: The findings suggest an unfavorable cost/benefit ratio for antidepressant treatment of bipolar depression.

Cited by 239 publications

References 9 publications

Screening for Bipolar Disorder in Patients Treated for Depression in a Family Medicine Clinic

Screening for Bipolar Disorder in Patients Treated for Depression in a Family Medicine Clinic

Mode of action of mood stabilizers: is the arachidonic acid cascade a common target?

Common and Dissociable Dysfunction of the Reward System in Bipolar and Unipolar Depression

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