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European Archives of Psychiatry and... Jun 2015In the classification of mood disorders, major depressive disorder is separate from bipolar disorders whereas mania is not. Studies on pure mania are therefore rare. Our... (Review)
Review
In the classification of mood disorders, major depressive disorder is separate from bipolar disorders whereas mania is not. Studies on pure mania are therefore rare. Our paper reviews the evidence for distinguishing pure mania (M) and mania with mild depression (Md) from bipolar disorder. Two large epidemiological studies found a prevalence of 1.7-1.8% of M/Md in adolescents and adults. Several clinical follow-up studies demonstrated good stability of the diagnosis after a previous history of three manic episodes. Compared to bipolar disorder, manic disorder is characterised by a weaker family history for depression, an earlier onset, fewer recurrences and better remission, and is less comorbid with anxiety disorders. In addition, mania is strongly associated with a hyperthymic temperament, manifests more psychotic symptoms and is more often treated with antipsychotics. Twin and family studies find mania to be more heritable than depression and show no significant transmission from depression to mania or from mania to depression. Cardiovascular mortality is elevated among patients with mood disorders generally and is highest among those with mania. In non-Western countries, mania and the manic episodes in bipolar disorder are reported to occur more frequently than in Western countries.
Topics: Bipolar Disorder; Diagnosis, Differential; Diagnostic and Statistical Manual of Mental Disorders; History, 19th Century; History, 20th Century; History, 21st Century; Humans; Mood Disorders
PubMed: 25631618
DOI: 10.1007/s00406-015-0577-1 -
The Australian and New Zealand Journal... Jul 2022Evidence indicates that mood disorders often co-occur with substance-related disorders. However, pooling comorbidity estimates can be challenging due to heterogeneity in... (Meta-Analysis)
Meta-Analysis
BACKGROUND AND OBJECTIVES
Evidence indicates that mood disorders often co-occur with substance-related disorders. However, pooling comorbidity estimates can be challenging due to heterogeneity in diagnostic criteria and in the overall study design. The aim of this study was to systematically review and, where appropriate, meta-analyse estimates related to the pairwise comorbidity between mood disorders and substance-related disorders, after sorting these estimates by various study designs.
METHODS
We searched PubMed (MEDLINE), Embase, CINAHL and Web of Science for publications between 1980 and 2017 regardless of geographical location and language. We meta-analysed estimates from original articles in 4 broadly defined mood and 35 substance-related disorders.
RESULTS
After multiple eligibility steps, we included 120 studies for quantitative analysis. In general, regardless of variations in diagnosis type, temporal order or use of adjustments, there was substantial comorbidity between mood and substance-related disorders. We found a sixfold elevated risk between broadly defined mood disorder and drug dependence (odds ratio = 5.7) and fivefold risk between depression and cannabis dependence (odds ratio = 4.9) while the highest pooled estimate, based on period prevalence risk, was found between broadly defined dysthymic disorder and drug dependence (odds ratio = 11.3). Based on 56 separate meta-analyses, all pooled odds ratios were above 1, and 46 were significantly greater than 1 (i.e. the 95% confidence intervals did not include 1).
CONCLUSION
This review found robust and consistent evidence of an increased risk of comorbidity between many combinations of mood and substance-related disorders. We also identified a number of under-researched mood and substance-related disorders, suitable for future scrutiny. This review reinforces the need for clinicians to remain vigilant in order to promptly identify and treat these common types of comorbidity.
Topics: Comorbidity; Humans; Mood Disorders; Odds Ratio; Prevalence; Substance-Related Disorders
PubMed: 34708662
DOI: 10.1177/00048674211054740 -
The European Journal of Neuroscience May 2022Regulation of emotions is generally associated exclusively with the brain. However, there is evidence that peripheral systems are also involved in mood, stress... (Review)
Review
Regulation of emotions is generally associated exclusively with the brain. However, there is evidence that peripheral systems are also involved in mood, stress vulnerability vs. resilience, and emotion-related memory encoding. Prevalence of stress and mood disorders such as major depression, bipolar disorder, and post-traumatic stress disorder is increasing in our modern societies. Unfortunately, 30%-50% of individuals respond poorly to currently available treatments highlighting the need to further investigate emotion-related biology to gain mechanistic insights that could lead to innovative therapies. Here, we provide an overview of inflammation-related mechanisms involved in mood regulation and stress responses discovered using animal models. If clinical studies are available, we discuss translational value of these findings including limitations. Neuroimmune mechanisms of depression and maladaptive stress responses have been receiving increasing attention, and thus, the first part is centered on inflammation and dysregulation of brain and circulating cytokines in stress and mood disorders. Next, recent studies supporting a role for inflammation-driven leakiness of the blood-brain and gut barriers in emotion regulation and mood are highlighted. Stress-induced exacerbated inflammation fragilizes these barriers which become hyperpermeable through loss of integrity and altered biology. At the gut level, this could be associated with dysbiosis, an imbalance in microbial communities, and alteration of the gut-brain axis which is central to production of mood-related neurotransmitter serotonin. Novel therapeutic approaches such as anti-inflammatory drugs, the fast-acting antidepressant ketamine, and probiotics could directly act on the mechanisms described here improving mood disorder-associated symptomatology. Discovery of biomarkers has been a challenging quest in psychiatry, and we end by listing promising targets worth further investigation.
Topics: Animals; Antidepressive Agents; Bipolar Disorder; Brain; Inflammation; Mood Disorders
PubMed: 33876886
DOI: 10.1111/ejn.15239 -
Handbook of Clinical Neurology 2021Degenerative dementias such as Alzheimer's disease and frontotemporal dementia result in distinct alterations in emotional processing, emotional experiences, and mood.... (Review)
Review
Degenerative dementias such as Alzheimer's disease and frontotemporal dementia result in distinct alterations in emotional processing, emotional experiences, and mood. The neuropathology of these dementias extends to structures involved in emotional processing, including the basolateral limbic network (orbitofrontal cortex, anterior temporal lobe, amygdala, and thalamus), the insula, and ventromedial frontal lobe. Depression is the most common emotion and mood disorder affecting patients with Alzheimer's disease. The onset of depression can be a prodromal sign of this dementia. Anxiety can also be present early in the course of Alzheimer's disease and especially among patients with early-onset forms of the disease. In contrast, patients with behavioral variant frontotemporal dementia demonstrate hypoemotionality, deficits in the recognition of emotion, and decreased psychophysiological reactivity to emotional stimuli. They typically have a disproportionate impairment in emotional and cognitive empathy. One other unique feature of behavioral variant frontotemporal dementia is the frequent occurrence of bipolar disorder. The management strategies for these alterations of emotion and mood in degenerative dementias primarily involve the judicious use of the psychiatric armamentarium of medications.
Topics: Alzheimer Disease; Emotions; Empathy; Frontotemporal Dementia; Humans; Magnetic Resonance Imaging; Mood Disorders; Neuropsychological Tests
PubMed: 34389121
DOI: 10.1016/B978-0-12-822290-4.00012-8 -
Advances in Experimental Medicine and... 2018Mood disorders are heterogeneous conditions characterized by complex genetics, unclear pathophysiology, and variable symptomatology. Currently, there is no biomarker for... (Review)
Review
Mood disorders are heterogeneous conditions characterized by complex genetics, unclear pathophysiology, and variable symptomatology. Currently, there is no biomarker for the diagnosis or prognosis of mood disorders, and the treatments are of limited efficacy in a significant proportion of patients. Furthermore, the disease models are not able to recapitulate their complexity. In this scenario, stem cells may have different applications in mood disorders. Circulating stem cells may be regarded as potential biomarkers. Mesenchymal stem cells are a promising therapeutic strategy for mood disorders as they promote neurogenesis and increase the expression of neurotrophic factors that enhance the survival and differentiation of neurons. In addition, induced pluripotent stem cells, cells reprogrammed from somatic cells of healthy subjects or patients, offer a great opportunity to recapitulate both normal and pathological development of human brain tissues, thereby opening a new avenue for disease modeling and drug development in a more disease-relevant system.
Topics: Brain; Cell Differentiation; Humans; Induced Pluripotent Stem Cells; Mesenchymal Stem Cells; Mood Disorders; Nerve Growth Factors; Neurogenesis; Neurons
PubMed: 30051319
DOI: 10.1007/5584_2018_250 -
Journal of the American Academy of... Jul 2021It is well established that family history is the most important known risk factor for the development of a mood disorder. Approximately 25% of at-risk offspring will...
It is well established that family history is the most important known risk factor for the development of a mood disorder. Approximately 25% of at-risk offspring will develop a mood disorder; yet, this is only slightly higher than the lifetime rate of a mood disorder overall of 21.4%. These statistics suggest heterogeneity within mood disorders generally and within people at familial risk. More information, particularly in the form of trait-level biomarkers, is sorely needed to accurately predict mood disorder risk and development. Trait-level biomarker identification may also help to decrease the well-known delay in accurately diagnosing bipolar disorders specifically, which could ultimately improve treatment and outcomes. Nimarko et al. aimed to identify trait-level biological markers of social reward-related neural vulnerability that distinguish youths genetically at risk for mood disorder. Nimarko and colleagues reported a well-designed study consisting of extremely well-matched youths who, by virtue of parentage, were at risk of bipolar disorder, were at risk of major depressive disorder, or were healthy (control group). The sample sizes reflected the challenges associated with doing this type of research with children, but the importance of the relationships was clear and strong. Specifically, the results showed reduced bilateral putamen activity (left: z = 4.39, p = .003; right: z = 4.56, p < .001) and reduced left putamen connectivity with right posterior cingulate cortex (z = 4.04, p < .01) and left anterior cingulate cortex (z > 3.64, p < .001) during an emotional face social reward task as potential trait markers that distinguished at-risk samples. In another study, similarly reduced reward-related connectivity in genetically at-risk youths for bipolar disorder relative to at-risk and healthy groups was shown to monetary reward and loss. Importantly, in both of these studies, reward-related connectivity group differences were observed before threshold symptoms developed, suggesting that early identification and intervention may be possible. In addition, this reduced reward-related connectivity was not related to subthreshold symptoms in either study. Taken together, these findings suggest that social reward and monetary reward and loss may be interconnected at a neural level in youths genetically at risk for bipolar disorder before symptom development. Exploratory analyses in Nimarko et al. also showed that reduced reward-related connectivity may be a trait-level biomarker of risk of future conversion to an Axis I disorder over time (bipolar disorder risk: hazard ratio = 8.28, p < .01); major depressive disorder risk: hazard ratio = 2.31, p = .02). Although Acuff et al. did not address the longitudinal question of conversion directly, the authors speculated that reduced reward-related connectivity was related to increased risk of future bipolar disorder. This serendipitous independent replication of reward-related connectivity is a promising lead, but repeated testing in independent samples is needed. However, direct independent sample testing is uncommon in psychiatry and in psychiatric neuroscience. This is partially due to factors such as time and money, but also to the value placed on innovation, which is prized by funding agencies, journal editors, and society. Independent sample testing is not, by definition, innovative, and while innovation is an important cornerstone of science and should be encouraged, we also need to test previously identified findings using independent samples.
Topics: Adolescent; Bipolar Disorder; Child; Depressive Disorder, Major; Humans; Magnetic Resonance Imaging; Mood Disorders; Reward
PubMed: 33220431
DOI: 10.1016/j.jaac.2020.11.007 -
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 -
Expert Opinion on Pharmacotherapy Aug 2016Obesity and mood disorders co-occur more often than expected by chance alone. As no randomized, controlled pharmacotherapy trials have been conducted in obese patients... (Review)
Review
INTRODUCTION
Obesity and mood disorders co-occur more often than expected by chance alone. As no randomized, controlled pharmacotherapy trials have been conducted in obese patients with an active mood disorder, it is unclear how to use medication to treat this patient group.
AREAS COVERED
We briefly overview the relationship between obesity and mood disorders; the effects of psychotropic medications commonly used in mood disorders on body weight; the psychiatric effects of available anti-obesity medications; and highlight the few treatment studies of medications in obese patients with mood disorders or depressive symptoms. As binge eating and psychotropic-induced weight gain are common correlates of obese patients with mood disorders, we also provide brief overviews of the pharmacotherapy of these conditions.
EXPERT OPINION
When treating a patient with a mood disorder and obesity, both conditions need to be a focus of clinical attention. Psychotropic medications that have minimal weight gain effects should be used if possible. Weight-loss agents can probably be used in some mood disorder patients, but must be done so cautiously and with a full understanding of their potential psychiatric effects and interactions with psychotropic medications. Knowledge of the pharmacotherapy of binge eating and psychotropic-induced weight gain is also crucial.
Topics: Anti-Obesity Agents; Binge-Eating Disorder; Depression; Humans; Mental Disorders; Mood Disorders; Obesity; Psychotropic Drugs; Weight Gain
PubMed: 27280311
DOI: 10.1080/14656566.2016.1198776 -
Journal of Affective Disorders Jan 2024Two of the most common and incapacitating mental health disorders around the world are major depressive disorder (MDD) and post-stroke depression (PSD). MDD is thought... (Review)
Review
Two of the most common and incapacitating mental health disorders around the world are major depressive disorder (MDD) and post-stroke depression (PSD). MDD is thought to result from abnormal connectivity between the monoaminergic, glutamatergic, GABAergic, and/or cholinergic pathways. Additional factors include the roles of hormonal, immune, ageing, as well as the influence of cellular, molecular, and epigenetics in the development of mood disorders. This complexity of factors has been anticipated by the Swiss psychiatrists Paul Kielholz and Jules Angst who introduced a multimodal treatment of MDD. Depression is the predominant mood disorder, impacting around one-third of individuals who have experienced a stroke. MDD and PSD share common underlying biological mechanisms related to the disruption of monoaminergic pathways. The major contributor to PSD is the stroke lesion location, which can involve the disruption of the serotoninergic, dopaminergic, glutamatergic, GABAergic, or cholinergic pathways. Additionally, various other disorders such as mania, bipolar disorder, anxiety disorder, and apathy might occur post-stroke, although their prevalence is considerably lower. However, there are differences in the onset of MDD among mood disorders. Some mood disorders develop gradually and can persist for a lifetime, potentially culminating in suicide. In contrast, PSD has a rapid onset because of the severe disruption of neural pathways essential for mood behavior caused by the lesion. However, PSD might also spontaneously resolve several months after a stroke, though it is associated with higher mortality. This review also provides a brief overview of the treatments currently available in medical practice.
Topics: Humans; Depressive Disorder, Major; Mood Disorders; Bipolar Disorder; Stroke; Cholinergic Agents
PubMed: 37827260
DOI: 10.1016/j.jad.2023.10.037 -
Advances in Experimental Medicine and... 2019Mood disorders include all types of depression and bipolar disorder, and mood disorders are sometimes called affective disorders. We will discuss newly developing two...
Mood disorders include all types of depression and bipolar disorder, and mood disorders are sometimes called affective disorders. We will discuss newly developing two issues in affective disorders in children and adolescents. Those are the new diagnostic challenges using neuroimaging techniques in affective disorders and the introduction of disruptive mood dysregulation disorder (DMDD). During the 1980s, mental health professionals began to recognize symptoms of mood disorders in children and adolescents, as well as adults. However, children and adolescents do not necessarily have or exhibit the same symptoms as adults. It is more difficult to diagnose mood disorders in children, especially because children are not always able to express how they feel. Child mental health professionals believe that mood disorders in children and adolescents remain one of the most underdiagnosed mental health problems. We are currently trying to introduce the new diagnostic technique-machine learning in children and adolescents with MDD. We will discuss the current progress in the clinical application of machine learning for MDD. After that, we would also discuss a new challenging diagnosis-DMDD. We are still suffering from a lack of evidence when trying to treat the patients with DMDD. In addition, there are some debates about the diagnostic validity of DMDD. We will explain the current situation of DMDD studies and the future directions in the study of DMDD.
Topics: Adolescent; Adult; Attention Deficit and Disruptive Behavior Disorders; Bipolar Disorder; Child; Depression; Emotions; Humans; Machine Learning; Mood Disorders; Neuroimaging
PubMed: 31705498
DOI: 10.1007/978-981-32-9721-0_12