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      Management of bipolar I depression: clinical utility of lurasidone

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          Abstract

          Lurasidone is a benzisothiazol derivative second-generation antipsychotic. It has been approved in the United States and Europe for treatment of acute schizophrenia and bipolar depression. In type I bipolar subjects, treatment with lurasidone monotherapy of adjunctive therapy to lithium or valproic acid with doses of 20 to 120 mg once daily with food, results in statistically and clinically significant reduction of depressive symptoms. Patients experience relatively few side effects, which include somnolence, akathisia, nausea, and other gastrointestinal upset. Dopamine related side effects, such as Parkinsonism and elevated prolactin, are rare and mild. Longer term safety data obtained in 6 months long, open continuation observation periods, suggest that metabolic related elevations in weight, glucose, and lipids are absent or minimal. The mechanism of action of lurasidone is not known, but the data are compatible with antagonism of the serotonin 7 receptor. Lurasidone is a new option for the treatment of bipolar depression with relatively few side effects.

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          Most cited references 57

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          The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity.

          Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges.
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            The International Society for Bipolar Disorders (ISBD) task force report on antidepressant use in bipolar disorders.

            The risk-benefit profile of antidepressant medications in bipolar disorder is controversial. When conclusive evidence is lacking, expert consensus can guide treatment decisions. The International Society for Bipolar Disorders (ISBD) convened a task force to seek consensus recommendations on the use of antidepressants in bipolar disorders. An expert task force iteratively developed consensus through serial consensus-based revisions using the Delphi method. Initial survey items were based on systematic review of the literature. Subsequent surveys included new or reworded items and items that needed to be rerated. This process resulted in the final ISBD Task Force clinical recommendations on antidepressant use in bipolar disorder. There is striking incongruity between the wide use of and the weak evidence base for the efficacy and safety of antidepressant drugs in bipolar disorder. Few well-designed, long-term trials of prophylactic benefits have been conducted, and there is insufficient evidence for treatment benefits with antidepressants combined with mood stabilizers. A major concern is the risk for mood switch to hypomania, mania, and mixed states. Integrating the evidence and the experience of the task force members, a consensus was reached on 12 statements on the use of antidepressants in bipolar disorder. Because of limited data, the task force could not make broad statements endorsing antidepressant use but acknowledged that individual bipolar patients may benefit from antidepressants. Regarding safety, serotonin reuptake inhibitors and bupropion may have lower rates of manic switch than tricyclic and tetracyclic antidepressants and norepinephrine-serotonin reuptake inhibitors. The frequency and severity of antidepressant-associated mood elevations appear to be greater in bipolar I than bipolar II disorder. Hence, in bipolar I patients antidepressants should be prescribed only as an adjunct to mood-stabilizing medications.
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              Efficacy of olanzapine and olanzapine-fluoxetine combination in the treatment of bipolar I depression.

              Despite the longer duration of the depressive phase in bipolar disorder and the frequent clinical use of antidepressants combined with antipsychotics or mood stabilizers, relatively few controlled studies have examined treatment strategies for bipolar depression. To examine the use of olanzapine and olanzapine-fluoxetine combination in the treatment of bipolar I depression. Double-blind, 8-week, randomized controlled trial. Eighty-four sites (inpatient and outpatient) in 13 countries. Patients A total of 833 randomized adults with bipolar I depression with a Montgomery-Asberg Depression Rating Scale (MADRS) score of at least 20. Intervention Patients were randomly assigned to receive placebo (n = 377); olanzapine, 5 to 20 mg/d (n = 370); or olanzapine-fluoxetine combination, 6 and 25, 6 and 50, or 12 and 50 mg/d (n = 86). Changes in MADRS total scores using mixed-effects model repeated-measures analyses. During all 8 study weeks, the olanzapine and olanzapine-fluoxetine groups showed statistically significant improvement in depressive symptoms vs the placebo group (P or =15 subsequently) did not differ among groups (placebo, 6.7% [23/345]; olanzapine, 5.7% [19/335]; and olanzapine-fluoxetine, 6.4% [5/78]). Adverse events for olanzapine-fluoxetine therapy were similar to those for olanzapine therapy but also included higher rates of nausea and diarrhea. Olanzapine is more effective than placebo, and combined olanzapine-fluoxetine is more effective than olanzapine and placebo in the treatment of bipolar I depression without increased risk of developing manic symptoms.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2015
                08 January 2015
                : 11
                : 75-81
                Affiliations
                [1 ]College of Nursing, University of Kentucky, Lexington, KY, USA
                [2 ]Department of Psychiatry and Behavioral Sciences, University of Louisville School of Medicine, Louisville, KY, USA
                Author notes
                Correspondence: Rif S El-Mallakh, 401 E. Chestnut Street, Suite 610, Department of Psychiatry and Behavioral Sciences, University of Louisville School of Medicine, Louisville, KY 40202, USA, Email rselma01@ 123456louisville.edu
                Article
                tcrm-11-075
                10.2147/TCRM.S57695
                4293929
                © 2015 Findlay et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Review

                Medicine

                adjunctive therapy, bipolar depression, bipolar disorder, lurasidone

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