A different depression: Clinical distinctions between bipolar and unipolar depression [Electronic version]
Department of Psychiatry, University of Texas Health Science Center, 7703 Floyd Curl Drive, 7th Floor (Mail Code 7792), San Antonio, TX 78229-3900, USA. Journal of Affective Disorders
(Impact Factor: 3.38).
03/2005; 84(2-3):117-25. DOI: 10.1016/S0165-0327(03)00194-0
Delayed diagnosis or misdiagnosis can prolong the suffering of patients with bipolar disorder. Accurate early diagnosis is sometimes difficult, however, particularly because patients often present in the depressive phase, which can easily be mistaken for unipolar depression. Unfortunately, therapy appropriate for unipolar depression can increase the risk of manic switch or cycle acceleration in bipolar disorder, especially in those with a family history of bipolarity and suicide, although some antidepressants may be useful in some bipolar patients. In addition, most currently available mood stabilizers, though effective in managing mania, do not effectively resolve depression. In contrast, lamotrigine has shown activity in bipolar depression and has a very low risk of manic switch. Bipolar depression, compared with unipolar depression, is more likely to be associated with hypersomnia, motor retardation, mood lability, early onset, and a family history of bipolar disorder. Awareness of these distinctions can greatly improve diagnosis of bipolar disorder and provide an opportunity for effective therapeutic intervention.
Available from: Julia Becker Cretu
- "Sleep disturbance is a key feature of syndromal mood episodes, being included in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; APA, 2013) criteria for manic, hypomanic, and major depressive episodes. Thus, symptoms of syndromal bipolar depression can be associated with insomnia or hypersomnia (Bowden, 2005), whereas syndromal mania is most commonly associated with insomnia, decreased sleep duration, increased sleep latency, and decreased need for sleep (Plante and Winkelman, 2008). Sleep disturbance is common during times with residual (subsyndromal) symptoms between mood episodes. "
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ABSTRACT: Background: Sleep disturbance in bipolar disorder (BD) is common during and between mood episodes. In recovered (euthymic at least two months) BD patients, we assessed sleep compared to controls and its relationships with residual mood symptoms and mood episode recurrence. Method: Recovered Stanford University BD Clinic patients diagnosed with the Systematic Treatment Enhancement Program for BD (STEP-BD) Affective Disorders Evaluation and monitored with the STEP-BD Clinical Monitoring Form (CMF) for > 1 year and healthy controls completed the Pittsburgh Sleep Quality Index (PSQI). PSQI parameters were compared in BD patients versus controls, and the most robustly differentiating PSQI parameter was assessed in relationship to residual mood symptoms, and time to mood episode recurrence in BD patients. Results: Eighty nine recovered BD patients compared to 56 healthy controls had significantly worse PSQI global score, more sleep medication use, longer sleep latency, and worse daytime dysfunction. PSQI global score had the greatest BD patient versus control effect size, and among BD patients, correlated significantly with residual mood symptoms and predicted earlier mood episode recurrence, even after covarying for residual mood symptoms. Limitations: Use of subjective (PSQI) rather objective (polysomnography) sleep metric. Statistical power limited by small sample size. Potential psychotropic medication confound. Northern California tertiary BD clinic referral sample. Conclusion: Further research is needed to confirm that in recovered BD patients, poor sleep quality correlates with residual mood symptoms, and independently predicts mood episode recurrence. If confirmed, these observations suggest potential mood benefit for focusing on sleep quality in interventions for recovered BD patients. Published by Elsevier B.V.
Journal of Affective Disorders 01/2016; 190:162-166. DOI:10.1016/j.jad.2015.09.076 · 3.38 Impact Factor
- "The strategy for drug treatments for other disorders can vary since the symptomatology can be diverse and dynamic (Bowden 2005; Walderhaug et al. 2011). Current research focuses on other novel treatment options include the exploration of peptidergic ligands. "
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ABSTRACT: Psychiatric disorders such as unipolar depression have complex pathologies, which include disruptions in circadian and sleep-wake cycles. At the neurochemical level, psychiatric diseases can also be accompanied by changes in neuromodulator systems such as orexin/hypocretin and the monoamines. Indeed, for decades the monoamine hypothesis of depression has been instrumental in driving discoveries and developments of antidepressant drugs. Recent preclinical and clinical advancement strongly suggests that neuropeptides such as orexin can play an important part in the pathophysiology of depression. Due to the complexity and extensive connectedness of neurobiological systems, understanding the biological causes and mechanisms of psychiatric disorders present major research challenges. In this chapter, we review experimental and computational studies investigating the complex relationship between orexinergic, monoaminergic, circadian oscillators, and sleep-wake neural circuitry. Our main aim is to understand how these physiological systems interact and how alteration in any of these factors can contribute to the behaviours commonly observed in depressive patients. Further, we examine how modelling across different levels of neurobiological organization enables insight into these interactions. We propose that a multiscale systems approach is necessary to understand the complex neurobiological systems whose dysfunctions are the underlying causes of psychiatric disorders. Such an approach could illuminate future treatments.
Orexin and Sleep: Molecular, Functional and Clinical Aspects, 1 edited by Takeshi Sakurai, S.R. Pandi-Perumal, Jaime M. Monti, 01/2015: chapter 16: pages 299-322; Springer International Publishing., ISBN: 978-3-319-23078-8
Available from: Sedat Batmaz
- "Although the cognitive model of unipolar depression is extensively studied   , little is known about the distinctive features of the cognitive model of bipolar depression    . Clinical and demographic variables may be helpful to some extent in the distinction between these two different phenomenological syndromes   , but there still is a high rate of misdiagnosis   . "
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Clinicians need to make the differential diagnosis of unipolar and bipolar depression to guide their treatment choices. Looking at the differences observed in the metacognitions, and the emotional schemas, might help with this differentiation, and might provide information about the distinct psychotherapeutical targets.
Three groups of subjects (166 unipolar depressed, 140 bipolar depressed, and 151 healthy controls) were asked to fill out the Metacognitions Questionnaire-30 (MCQ-30), and the Leahy Emotional Schema Scale (LESS). The clinicians diagnosed the volunteers according to the criteria of DSM-IV-TR with a structured clinical interview (MINI), and rated the moods of the subjects with the Montgomery Asberg Depression Rating Scale (MADRS), and the Young Mania Rating Scale (YMRS). Statistical analyses were undertaken to identify the group differences on the MCQ-30, and the LESS.
The bipolar and unipolar depressed patients' scores on the MCQ-30 were significantly different from the healthy controls, but not from each other. On the LESS dimensions of guilt, duration, blame, validation, and acceptance of feelings, all three groups significantly differed from each other. There were no statistically different results on the LESS dimensions of comprehensibility, consensus, and expression. The mood disordered groups scored significantly different than the healthy controls on the LESS dimensions of simplistic view of emotions, numbness, rationality, rumination, higher values, and control.
These results suggest that the metacognitive model of unipolar depression might be extrapolated for patients with bipolar depression. These results are also compatible to a great extent with the emotional schema theory of depression.
Comprehensive Psychiatry 06/2014; 55(7). DOI:10.1016/j.comppsych.2014.05.016 · 2.25 Impact Factor
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