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The Australian and New Zealand Journal... Mar 2016Given the sensitivity of individuals with mood disorders to circadian disruption, transmeridian travel would likely be a high-risk endeavour leading to onset or relapses... (Review)
Review
OBJECTIVES
Given the sensitivity of individuals with mood disorders to circadian disruption, transmeridian travel would likely be a high-risk endeavour leading to onset or relapses in mood. A systematic review was undertaken to identify the evidence of the impact of transmeridian travel on people with mood disorders.
METHODS
Databases search included the following: CINAHL, MEDLINE, PsycINFO and manual searching using the keywords jetlag, transmeridian travel, circadian rhythm disruption, mood disorder, bipolar, major depression, seasonal affective disorder, depression, mania and hypomania.
RESULTS
Only three studies were identified that related to transmeridian travel and jetlag in people with mood disorders. There is some suggestion that transmeridian travel does appear to precipitate mood episodes with an increased rate of episodes of depression with westward compared with an increased rate of manic/hypomanic episodes with eastward travel. Individuals with a previous history of mood disorder appear to be more vulnerable if adherence to medication is compromised.
CONCLUSION
Given the limited evidence that transmeridian travel precipitates mood episodes, this poses difficulties in identifying suitable ways to mitigate the effects of transmeridian travel in mood disorders. However, in the absence of mood-specific guidelines, some guidance can be given based on our current understanding of the relevance of circadian disruption to both jetlag and mood disorders. Further research is required to identify more focused strategies to mitigate the impact of transmeridian travel for individuals with mood disorders.
Topics: Humans; Jet Lag Syndrome; Mood Disorders; Travel
PubMed: 26268923
DOI: 10.1177/0004867415598844 -
Bipolar Disorders Jun 2007Bipolar disorder (BD) is a leading cause of disability. Systematic reviews of randomized trials for the treatment of the maintenance phase of BD are lacking. (Review)
Review
BACKGROUND
Bipolar disorder (BD) is a leading cause of disability. Systematic reviews of randomized trials for the treatment of the maintenance phase of BD are lacking.
OBJECTIVES
To determine the efficacy and tolerability of mood stabilizers and antipsychotics in the maintenance treatment of BD.
METHODS
We systematically reviewed randomized controlled trials of licensed medications for the treatment of any phase of BD. We included randomized controlled trials comparing a medication to placebo or another medication. Comprehensive searches of electronic databases were conducted to March 2005. Outcomes investigated were relapse due to mania, depression or any mood episode, and withdrawal due to any reason or due to an adverse event. Data were combined through meta-analysis.
RESULTS
Fourteen studies (n = 2,526) met the inclusion criteria. Lithium, lamotrigine, olanzapine and valproate semisodium each demonstrated evidence to support long-term use. Compared with placebo, all medications were more effective at preventing relapse because of any mood episode. Hazard ratios (HR) were 0.68 [95% confidence interval (CI) = 0.53-0.86] for lithium, 0.68 (95% CI = 0.55-0.85) for lamotrigine, and 0.82 (95% CI = 0.57-1.20) for valproate semisodium; for olanzapine, the risk ratio (RR) was 0.58 (95% CI = 0.49-0.69). Lithium and olanzapine significantly reduced manic relapses (HR = 0.53; 95% CI = 0.35-0.79 and RR = 0.37; 95% CI = 0.24-0.57, respectively). Lamotrigine and valproate semisodium significantly reduced depressive relapses (HR = 0.65; 95% CI = 0.46-0.91 and RR = 0.40; 95% CI = 0.20-0.82, respectively). Lithium significantly reduced manic relapses compared with lamotrigine (HR = 0.56; 95% CI = 0.34-0.92) and olanzapine significantly reduced manic relapses compared with lithium (RR = 1.69; 95% CI = 1.12-2.55). Withdrawal due to an adverse event was approximately twice as likely with lithium compared with valproate semisodium (RR = 1.81; 95% CI = 1.08-3.03) and lamotrigine (RR = 2.20; 95% CI = 1.31-3.70). There were few data for carbamazepine or medications given as adjunct therapy.
CONCLUSIONS
Mood stabilizers have differing profiles of efficacy and tolerability, suggesting complementary roles in long-term maintenance treatment.
Topics: Acute Disease; Anticonvulsants; Antimanic Agents; Antipsychotic Agents; Bipolar Disorder; Humans; Lithium Compounds; Randomized Controlled Trials as Topic; Treatment Outcome
PubMed: 17547586
DOI: 10.1111/j.1399-5618.2007.00490.x -
The Lancet. Psychiatry Dec 2016Inflammatory processes and neural-immune interactions have been implicated in the pathogenesis of psychiatric conditions, but studies in bipolar disorder are... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Inflammatory processes and neural-immune interactions have been implicated in the pathogenesis of psychiatric conditions, but studies in bipolar disorder are inconclusive so far. We aimed to investigate whether peripheral concentrations of C-reactive protein (CRP), an acute-phase response protein of inflammatory activity, are increased in bipolar disorder across the mood spectrum.
METHODS
In this systematic review and meta-analysis, we searched MEDLINE, the Cochrane Library, Scopus, and Web of Knowledge from database inception to Aug 14, 2016, for studies that measured serum and plasma CRP concentrations in adult patients with bipolar disorder (as defined by DSM-IV-TR) and healthy controls. We extracted data from published reports. We did three between-group meta-analyses comparing CRP concentrations in patients in mania, depression, or euthymia, with those in healthy controls (cross-sectional studies), and two within-group meta-analyses comparing changes in CRP concentrations before and after treatment of an index manic or depressive episode (longitudinal studies). We used Hedges' adjusted g to calculate effect sizes and pooled results using random-effect models. We also did meta-regression analyses by mood state to investigate possible moderators of CRP concentrations.
FINDINGS
We identified 27 studies representing 2161 patients with bipolar disorder and 81 932 healthy controls. Compared with healthy individuals, CRP concentrations were moderately increased in people with bipolar disorder during depression (g 0·67, 95% CI 0·23 to 1·11; p=0·003) and euthymia (0·65, 0·40 to 0·90; p<0·0001) and more substantially increased during mania (0·87, 0·58 to 1·15; p<0·0001). The extent of the increases in CRP concentrations in mania and depression was not related to symptom severity (p=0·256 for mania and p=0·626 for depression). CRP concentrations were moderately decreased after resolution of an index manic episode (-0·36, -0·66 to -0·05; p=0·022) and slightly decreased after resolution of an index depressive episode (-0·18, -0·30 to -0·07; p=0·002).
INTERPRETATION
CRP concentrations are increased in bipolar disorder regardless of mood state, but are higher during mania than in depression and euthymia, suggesting an increased inflammatory burden in mania.
FUNDING
None.
Topics: Bipolar Disorder; C-Reactive Protein; Humans; Randomized Controlled Trials as Topic
PubMed: 27838212
DOI: 10.1016/S2215-0366(16)30370-4 -
Journal of Affective Disorders Jun 2018Epigenetic mechanisms have been suggested to play a key role in the pathophysiology of bipolar disorder (BD), among which microRNAs (miRNAs) may be of particular... (Review)
Review
BACKGROUND
Epigenetic mechanisms have been suggested to play a key role in the pathophysiology of bipolar disorder (BD), among which microRNAs (miRNAs) may be of particular significance according to recent studies. We aimed to summarize miRNA studies in BD to identify consistent findings, limitations, and future directions of this emerging field.
METHODS
We performed a comprehensive search on PUBMED and Medline for studies investigating an association between BD and miRNAs. The included studies report miRNA alterations in postmortem brain tissues and in the periphery, cell culture and preclinical findings, genetic associations, and the effects of medications.
RESULTS
Several studies report changes in miRNA expression levels in postmortem brain and in the periphery of patients, although most of the results so far have not been replicated and are not concordant between different populations. Genetic studies also suggest that miRNA genes are located within susceptibility loci of BD, and also a putative role of miRNAs in modulating genes previously shown to confer risk of BD.
LIMITATIONS
We did not perform a systematic review of the literature, and miRNAs represent only one facet of the plethora of epigenetic mechanisms that might be involved in BD's pathophysiology.
CONCLUSIONS
miRNA findings in BD significantly vary between studies, but are consistent to suggest a key role for these molecules in BD's pathophysiology and treatment, particularly miR-34a and miR-137. Accordingly, miRNA might represent important biomarkers of illness to be used in the clinical settings, and potentially also for the development of novel therapeutics for BD in the near future.
Topics: Bipolar Disorder; Brain; Epigenomics; Genetic Markers; Humans; MicroRNAs; Transcriptome
PubMed: 28969861
DOI: 10.1016/j.jad.2017.09.025 -
The Lancet. Psychiatry Dec 2016Although mania and hypomania define bipolar disorder, depressive episodes are more common and impairing, with few proven treatments. Adjunctive therapy with... (Meta-Analysis)
Meta-Analysis Review
Safety and efficacy of adjunctive second-generation antidepressant therapy with a mood stabiliser or an atypical antipsychotic in acute bipolar depression: a systematic review and meta-analysis of randomised placebo-controlled trials.
BACKGROUND
Although mania and hypomania define bipolar disorder, depressive episodes are more common and impairing, with few proven treatments. Adjunctive therapy with second-generation antidepressants is widely used to treat acute bipolar depression, but their efficacy and safety remain controversial.
METHODS
In this systematic review and meta-analysis, we searched MEDLINE, Embase, the Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov from inception to Jan 31, 2016, for randomised, double-blind, placebo-controlled trials of second-generation antidepressants adjunctive to a mood stabiliser or an antipsychotic in patients with acute bipolar depression. We extracted data from published reports. The primary outcome was change in clinician-rated depressive symptom score; secondary outcomes were clinical response, clinical remission, treatment-emergent mania or hypomania, and tolerability (using dropout rates as a proxy). We used pooled random-effects models, subgroup comparisons, and meta-regression for analyses. We made subgroup comparisons on the basis of mood stabiliser or antipsychotic treatment and did meta-regression examining trial duration. This study is registered with PROSPERO, number CRD#42015016024.
FINDINGS
We identified six trials representing 1383 patients with bipolar depression. Second-generation antidepressants were associated with a small but significant improvement in clinician-rated depressive symptom score (standardised mean differences 0·165 [95% CI 0·051-0·278], p=0·004). However, clinical response and remission rates did not differ significantly between patients receiving adjunctive antidepressants and those receiving placebo (1·158 [0·840-1·597], p=0·371 for clinical response; 1·220 [0·874-1·703], p=0·243 for remission). Acute treatment was not associated with an increased risk of treatment-emergent mania or hypomania (0·926 [0·576-1·491], p=0·753), but 52 week extension periods were associated with an increase in risk (1·774 [1·018-3·091], p=0·043).
INTERPRETATION
Adjunctive second-generation antidepressants are associated with reduced symptoms of acute bipolar depression, but the magnitude of benefit is small because they do not increase clinical response or remission rates. However, these medications should be used only in the short term because prolonged use is associated with an increased risk of treatment-emergent mania or hypomania.
FUNDING
None.
Topics: Antidepressive Agents; Antidepressive Agents, Second-Generation; Antipsychotic Agents; Bipolar Disorder; Double-Blind Method; Humans; Randomized Controlled Trials as Topic
PubMed: 28100425
DOI: 10.1016/S2215-0366(16)30264-4 -
Canadian Journal of Psychiatry. Revue... Nov 2020Addiction comorbidity is an important clinical challenge in mood disorders, but the best way of pharmacologically treating people with mood disorders and addictions... (Meta-Analysis)
Meta-Analysis
Pharmacological Treatment of Mood Disorders and Comorbid Addictions: A Systematic Review and Meta-Analysis: Traitement Pharmacologique des Troubles de L'humeur et des Dépendances Comorbides: Une Revue Systématique et une Méta-Analyse.
OBJECTIVE
Addiction comorbidity is an important clinical challenge in mood disorders, but the best way of pharmacologically treating people with mood disorders and addictions remains unclear. The aim of this study was to assess the efficacy of pharmacological treatments for mood and addiction symptoms in people with mood disorders and addiction comorbidity.
METHODS
A systematic search of placebo-controlled randomized controlled trials investigating the effects of pharmacological treatments in people with bipolar disorder (BD) or major depressive disorder (MDD), and comorbid addictions was performed. Treatment-related effects on mood and addiction measures were assessed in a meta-analysis, which also estimated risks of participant dropout and adverse effects.
RESULTS
A total of 32 studies met systematic review inclusion criteria. Pharmacological therapy was more effective than placebo for improving manic symptoms (standardized mean difference [SMD] = -0.15; 95% confidence interval [95% CI], -0.29 to -0.02; = 0.03) but not BD depressive symptoms (SMD = -0.09; 95% CI, -0.22 to 0.03; = 0.15). Quetiapine significantly improved manic symptoms (SMD = -0.23; 95% CI, -0.39 to -0.06; = 0.008) but not BD depressive symptoms (SMD = -0.07; 95% CI, -0.23 to 0.10; = 0.42). Pharmacological therapy was more effective than placebo for improving depressive symptoms in MDD (SMD = -0.16; 95% CI, -0.30 to -0.03; = 0.02). Imipramine improved MDD depressive symptoms (SMD = -0.58; 95% CI, -1.03 to -0.13; = 0.01) but Selective serotonin reuptake Inhibitors (SSRI)-based treatments had no effect (SMD = -0.06; 95% CI, -0.30 to 0.17; = 0.60). Pharmacological treatment improved the odds of alcohol abstinence in MDD but had no effects on opiate abstinence.
CONCLUSIONS
Pharmacological treatments were significantly better than placebo in improving manic symptoms, MDD depressive symptoms, and alcohol abstinence but were not better for bipolar depression symptoms. Importantly, quetiapine was not more effective than placebo in improving bipolar depression symptoms nor were SSRI's for the treatment of MDD depression. Our findings highlight the need for further high-quality clinical trials of treatments for mood disorders and comorbid addictions.
Topics: Bipolar Disorder; Comorbidity; Depressive Disorder, Major; Humans; Mood Disorders; Selective Serotonin Reuptake Inhibitors
PubMed: 32302221
DOI: 10.1177/0706743720915420 -
Are existing self-ratings of acute manic symptoms in adults reliable and valid?-A systematic review.Bipolar Disorders Sep 2020Depression research historically uses both self- and clinician ratings of symptoms with significant and substantial correlations. It is often assumed that manic patients...
BACKGROUND
Depression research historically uses both self- and clinician ratings of symptoms with significant and substantial correlations. It is often assumed that manic patients lack insight and cannot accurately report their symptoms. This delayed the development of self-rating scales for mania, but several scales now exist and are used in research. Our objective is to systematically review the literature to identify existing self-ratings of symptoms of (hypo)mania and to evaluate their psychometric properties.
METHODS
PubMed, Web of Knowledge, and Ovid were searched up until June 2018 using the keywords: "(hypo)mania," "self-report," and "mood disorder" to identify papers which included data on the validity and reliability of self-rating scales for (hypo)mania in samples including patients with bipolar disorder.
RESULTS
We identified 55 papers reporting on 16 different self-rating scales claiming to assess (hypo)manic symptoms or states. This included single item scales, but also some with over 40 items. Three of the scales, the Internal State Scale (ISS), Altman Self-Rating Mania Scale (ASRM), and Self-Report Manic Inventory (SRMI), provided data about reliability and/or validity in more than three independent studies. Validity was mostly assessed by comparing group means from individuals in different mood states and sometimes by correlation to clinician ratings of mania.
CONCLUSIONS
ASRM, ISS, and SRMI are promising self-rating tools for (hypo)mania to be used in clinical contexts. Future studies are, however, needed to further validate these measures; for example, their associations between each other and sensitivity to change, especially if they are meant to be outcome measures in studies.
Topics: Adult; Bipolar Disorder; Female; Humans; Male; Middle Aged; Mood Disorders; Psychiatric Status Rating Scales; Psychometrics; Reproducibility of Results; Self Report
PubMed: 32232950
DOI: 10.1111/bdi.12906 -
Journal of Psychiatric Research Aug 2011Brain-derived neurotrophic factor (BDNF) plays a central role in synaptic plasticity and neurogenesis. Bipolar disorder (BD) is among the most disabling of all... (Meta-Analysis)
Meta-Analysis Review
Brain-derived neurotrophic factor (BDNF) plays a central role in synaptic plasticity and neurogenesis. Bipolar disorder (BD) is among the most disabling of all psychiatric disorders and is associated with poor outcomes. Some studies suggest that BDNF levels decrease during mood states and remain normal during euthymia, but other studies have contradicted this paradigm. Therefore, the aim of this study was to perform a meta-analysis of all studies that measured peripheral BDNF levels in adults with BD. We conducted a systematic review using electronic databases. Inclusion criteria were studies that measured BDNF in plasma or serum in vivo in adult patients with BD. The resulting studies were compiled to measure the effect sizes (ESs) of the differences in BDNF levels between BD patients in different mood states and controls. Thirteen studies were included with a total of 1113 subjects. The BDNF levels were decreased in both mania and depression when compared to controls (ES -0.81, 95% CI -1.11 to -0.52, p < 0.0001 and ES -0.97, 95% CI -1.79 to -0.51, p = 0.02, respectively). The BDNF levels were not different in euthymia when compared to controls (ES -0.20, 95% CI -0.61 to 0.21, p = 0.33). Meta-regression analyses in euthymia showed that age (p < 0.0001) and length of illness (p = 0.04) influenced the variation in ES. There was also an increase in BDNF levels following the treatment for acute mania (ES -0.63, 95% CI -1.11 to -0.15, p = 0.01). In conclusion, BDNF levels are consistently reduced during manic and depressive episodes and recover after treatment for acute mania. In euthymia, BDNF decreases with age and length of illness. These data suggest that peripheral BDNF could be used as a biomarker of mood states and disease progression for BD.
Topics: Antidepressive Agents; Bipolar Disorder; Brain-Derived Neurotrophic Factor; Databases, Factual; Humans; Regression Analysis
PubMed: 21550050
DOI: 10.1016/j.jpsychires.2011.03.002 -
Psychosomatics 2014The gamma-aminobutyric acid type B receptor agonist baclofen is approved for spasticity and is used off-label for diverse types of addictive disorders, notably alcohol... (Review)
Review
BACKGROUND
The gamma-aminobutyric acid type B receptor agonist baclofen is approved for spasticity and is used off-label for diverse types of addictive disorders, notably alcohol dependence. Baclofen may induce numerous neuropsychiatric adverse drug reactions, including behavioral disinhibition. However, this precise adverse drug reaction has never been assessed using either a validated causality algorithm or a scale for manic symptoms.
METHODS
We report a case of a 49-year-old male patient who exhibited de novo mania during treatment with baclofen for alcohol dependence. Symptoms were evaluated using the Young Mania Rating Scale, and the causality of baclofen was determined using the Naranjo algorithm. This case was also compared with other cases of baclofen-induced mania through a systematic literature review.
RESULTS
Mr. X, taking 180 mg/d of baclofen, presented with mania and scored 24 of 44 on the Young Mania Rating Scale, and the imputability of baclofen was "probable" using the Naranjo algorithm (8 of 13). In addition, 4 other cases of baclofen-induced mania were reported in the literature; 3 cases had a bipolar I disorder history. Baclofen-induced manic symptoms occurred mostly during the dose-escalation phase.
CONCLUSION
Baclofen-induced manic symptoms may appear in patients with or without bipolar disorder. Particular attention is required during the dose-increase phase and in patients with a history of mood disorders.
Topics: Alcoholism; Baclofen; Bipolar Disorder; GABA-B Receptor Agonists; Humans; Male; Middle Aged
PubMed: 24751117
DOI: 10.1016/j.psym.2014.02.003 -
BJPsych Open May 2024Identification of the predominant polarity, i.e. hypomanic/manic (mPP) or depressive predominant polarity (dPP), might help clinicians to improve personalised management... (Review)
Review
BACKGROUND
Identification of the predominant polarity, i.e. hypomanic/manic (mPP) or depressive predominant polarity (dPP), might help clinicians to improve personalised management of bipolar disorder.
AIMS
We performed a systematic review and meta-analysis to estimate prevalence and correlates of mPP and dPP in bipolar disorder.
METHOD
The protocol was registered in the Open Science Framework Registries (https://doi.org/10.17605/OSF.IO/8S2HU). We searched main electronic databases up to December 2023 and performed random-effects meta-analyses of weighted prevalence of mPP and dPP. Odds ratios and weighted mean differences (WMDs) were used for relevant correlates.
RESULTS
We included 28 studies, providing information on rates and/or correlates of mPP and dPP. We estimated similar rates of mPP (weighted prevalence = 30.0%, 95% CI: 23.1 to 37.4%) and dPP (weighted prevalence = 28.5%, 95% CI: 23.7 to 33.7%) in bipolar disorder. Younger age (WMD = -3.19, 95% CI: -5.30 to -1.08 years), male gender (odds ratio = 1.39, 95% CI: 1.10 to 1.76), bipolar-I disorder (odds ratio = 4.82, 95% CI: 2.27 to 10.24), psychotic features (odds ratio = 1.56, 95% CI: 1.01 to 2.41), earlier onset (WMD = -1.57, 95% CI: -2.88 to -0.26 years) and manic onset (odds ratio = 13.54, 95% CI: 5.83 to 31.46) were associated with mPP ( < 0.05). Depressive onset (odds ratio = 12.09, 95% CI: 6.38 to 22.90), number of mood episodes (WMD = 0.99, 95% CI: 0.28 to 1.70 episodes), history of suicide attempts (odds ratio = 2.09, 95% CI: 1.49 to 2.93) and being in a relationship (odds ratio = 1.98, 95% CI: 1.22 to 3.22) were associated with dPP ( < 0.05). No differences were estimated for other variables.
CONCLUSIONS
Despite some limitations, our findings support the hypothesis that predominant polarity might be a useful specifier of bipolar disorder. Evidence quality was mixed, considering effects magnitude, consistency, precision and publication bias. Different predominant polarities may identify subgroups of patients with specific clinical characteristics.
PubMed: 38708573
DOI: 10.1192/bjo.2024.51