Identifying patients at risk of perinatal mood disorders

Perinatal mental illness influences obstetric outcomes, mother-baby interactions and longer term emotional and cognitive development of the child. Psychiatric disorders have consistently been found to be one of the leading causes of maternal deaths, often through suicide. Postnatal depression and puerperal psychosis are two disorders most commonly associated with the perinatal period. The most efficient strategy to identify patients at risk relies on focussing on clinically vulnerable subgroups: enquiries about depressive symptoms should be made at the usual screening visits. Attention should be paid to any sign of poor self-care, avoidance of eye contact, overactivity or underactivity, or abnormalities in the rate of speech. Particular care should be taken to ask about suicidal ideation and thoughts of harming others, including the baby. One of the most important risk factors is a previous history of depression. The degree of risk is directly correlated with severity of past episodes. Both antenatal and postnatal depression are being increasingly recognised in men. Puerperal psychosis is rare (1 to 2 per 1,000). Sixty per cent of women with puerperal psychosis already have a diagnosis of bipolar disorder or schizoaffective disorder. Women with a personal history of postpartum psychosis or bipolar affective disorder should be considered as high risk for postpartum psychosis. All pregnant women who are identified as being at high risk should have a shared care plan for their late pregnancy and early postnatal psychiatric management. Women with current mood disorder of mild or moderate severity who have a first-degree relative with a history of bipolar disorder or postpartum psychosis should be referred for psychiatric assessment.     

The nurse's role in the assessment and treatment of bipolar disorder

The prevalence of bipolar disorder is underestimated, and the condition is often misdiagnosed as depression. Because bipolar disorder does not appear to respond to standard treatments for depression, misdiagnosed patients may suffer increased morbidity and mortality. Nurses have the ability to significantly impact the successful care of these patients by recognizing and assessing bipolar disorder, managing treatment with appropriate mood stabilizers and therapies, and educating patients and their families. Bipolar disorder diagnosis, the consequences of misdiagnosis and mismanagement, lifestyle factors that may increase the risk for episode recurrence, and useful interventions are discussed.     

Bipolar disorder and weight gain: a multifactorial assessment

Obesity is highly prevalent in persons with bipolar disorder. This results in increased physical morbidity and poorer psychiatric outcomes. Multiple variables have been identified as potentially responsible for the weight gain in these individuals. Efforts to use successful treatment strategies require an understanding of these variables and methods that clinicians and their clients can use to reduce or minimize these risk factors. This article will review the emerging findings related to primary and secondary weight gain in bipolar disorder. The sequelae of weight gain on psychiatric and medical morbidity will be discussed. Lastly, a model for nursing assessment will propose methods for modifying risk factors and encouraging healthy lifestyle changes. The goal is to improve this component of quality of life for persons with bipolar disorder. J Am Psychiatr Nurses Assoc, 2008; 13(6), 345-352. DOI: 10.1177/1078390307310145.     

Behavioral Approach System (BAS)-Relevant Cognitive Styles in Individuals with High Versus Moderate BAS Sensitivity: A Behavioral High-Risk Design

This study used a behavioral high-risk design to evaluate cognitive styles relevant to the Behavioral Approach System (BAS) among individuals at high (n = 171) versus low (n = 119) risk of first onset of bipolar disorder based on BAS sensitivity, a known risk factor for bipolar disorder. Cognitive styles in high-BAS participants paralleled those implicated in bipolar disorder. Linear regressions indicated that individuals with high BAS sensitivity exhibited greater levels of goal striving, positive overgeneralization, rumination on positive affect, depressive brooding, perfectionism, and hypomanic personality. Furthermore, of the cognitive styles, emotion-focused rumination on positive affect mediated the association between BAS sensitivity and current levels of hypomanic symptoms. These results provide evidence that individuals at risk for the development of bipolar disorder have higher levels of BAS-relevant cognitive styles and hypomanic personality than do individuals with lower risk, indicating that these styles are not simply markers of prior (hypo)manic episodes.     

Molecular biology of depressive disorders

Heritability of major depression from twin studies is estimated as -40% that is relatively small as compared with -80% for schizophrenia and -90% for bipolar affective disorder. It suggests that genetic as well as environmental factors contribute to the aetiology of major depression. Approximately 800 association studies on candidate genes of depression have been published, and among them, several genes were confirmed as risk for vulnerability to major depression by meta-analyses. Recent investigations on pathophysiology of depression have focused on hippocampus as a modulator of Hypothalamus-Pituitary-Adrenal (HPA) glands axis. Molecular biological studies on the interaction between stress, hippocampus and HPA axis reveal glucocorticoid and brain-derived neurotrophic factor(BDNF) are key molecules developing and recovering from depressive disorder.     

双相情感障碍共病酒精使用障碍患者的临床特征及影响因素

【目的】分析双相情感障碍患者共病酒精使用障碍患者的临床特征及其影响因素。【方法】以河北省精神卫生中心住院的双相情感障碍患者为研究对象,根据是否共病酒精使用障碍将其分为共病组(n=51)和非共病组(n=97)。以美国精神障碍诊断与统计手册-第5版修订版(DSM-5)为诊断标准,对研究对象进行再次诊断。同时采用一般情况调查表、应对方式问卷对研究对象进行调查并进行相关因素分析。【结果】共病组与非共病组在性别、受教育程度、家庭关系、职业、病前性格、嗜酒家族史、起病形式等方面存在差异(P<0.05)。在各种风险评估方面,共病组冲动行为及自伤行为均高于非共病组,差异有统计学意义(P<0.05)。共病组应对方式采用解决问题的评分低于非共病组,而采用自责的应对方式评分高于较非共病组高,差异均有统计学意义(P<0.05)。非条件多因素Logistic回归分析,结果显示男性、有冲动行为、急性及亚急性起病是共病酒精使用障碍的危险性因素(P<0.05);而小学及以下、高中/中专受教育程度、工人、农民、病前性格内向是共病酒精使用障碍的保护性因素(P<0.05)。【结论】住院双相情感障碍患者共病酒精使用障碍的比例不低,共病患者较少采用解决问题的应对方式,发生冲动行为风险较高。     

Bipolar disorder and aggression

Aims: In clinical practice, overt aggressive behaviour is frequently observed in patients diagnosed with bipolar disorder. It can be dangerous and complicates patient care. Nevertheless, it has not been adequately studied as a phenomenon that is separate from other symptoms such as agitation. The aim of this review is to provide information on the prevalence, clinical context, and clinical management of aggression in patients with bipolar disorder. Methods: MEDLINE and PsycInfo data bases were searched for articles published between 1966 and November 2008 using the combination of key words ‘aggression’ or ‘violence’ with ‘bipolar disorder’. For the treatment searches, generic names of mood stabilisers and antipsychotics were used in combination with key words ‘bipolar disorder’ and ‘aggression’. No language constraint was applied. Articles dealing with children and adolescents were not included. Results: Acutely ill hospitalised bipolar patients have a higher risk for aggression than other inpatients. In a population survey, the prevalence of aggressive behaviour after age 15 years was 0.66% in persons without lifetime psychiatric disorder, but 25.34% in bipolar I disorder. Comorbidity with personality disorders and substance use disorders is frequent, and it elevates the risk of aggression in bipolar patients. Impulsive aggression appears to be the most frequent subtype observed in bipolar patients. Clinical management of aggression combines pharmacological and non‐pharmacological approaches. Discussion: A major problem with the evidence is that aggression is frequently reported only as one of the items contributing to the total score on a scale or a subscale. This makes it impossible to ascertain specifically aggressive behaviour. Large controlled head‐to‐head randomised controlled studies comparing treatments for aggressive behaviour in bipolar disorder are not yet available. There is some evidence favouring divalproex, but it is not particularly strong .We do not know if there are any efficacy differences among antipsychotics for this indication.     

Lamotrigine for the treatment of bipolar disorder

OBJECTIVE: To describe the available data regarding the clinical efficacy of lamotrigine for the treatment of bipolar disorder. SUMMARY: Anticonvulsants have emerged as alternative mood-stabilizing agents for patients with bipolar disorder who do not respond to lithium. Data regarding the efficacy of lamotrigine have been generated primarily from case reports, small open trials, and one large, randomized, placebo-controlled trial. These reports suggest that lamotrigine may be effective for the management of bipolar disorder. CONCLUSIONS: Although current data are limited, treatment-refractory patients with bipolar disorder may benefit from lamotrigine therapy. Several studies are currently underway to determine the appropriate role of lamotrigine in the treatment of bipolar disorder.     

Candidate gene studies of bipolar disorder

Genetic factors undoubtedly play an important role in determining vulnerability to bipolar disorder but the task of finding susceptibility genes is not trivial. Candidate gene studies, usually employing the association approach, offer the potential to discover the genes of relatively modest effect size that are expected for a complex genetic disorder. Candidate gene approaches depend crucially on our current understanding of disease pathophysiology, and attention has consequently been focussed on a limited range of neurotransmitter systems implicated by the action of drug treatments. Despite no unequivocal, consistently replicated findings, a number of intriguing results have emerged in the literature, both for bipolar disorder in general and for subtypes such as bipolar affective puerperal psychosis and rapid cycling bipolar illness. Genes of particular current interest include those encoding the serotonin transporter, monoamine oxidase A (MAOA) and catechol-O-methyl transferase (COMT). As susceptibility genes are found and knowledge of aetiology advanced it is likely that many more candidate genes in novel biological systems will attract attention.     

Mitochondrial involvement in psychiatric disorders

Recent findings of mitochondrial abnormalities in brains from subjects with neurological disorders have led to a renewed search for mitochondrial abnormalities in psychiatric disorders. A growing body of evidence suggests that there is mitochondrial dysfunction in schizophrenia, bipolar disorder, and major depressive disorder, including evidence from electron microscopy, imaging, gene expression, genotyping, and sequencing studies. Specific evidence of dysfunction such as increased common deletion and decreased gene expression in mitochondria in psychiatric illnesses suggests that direct examination of mitochondrial DNA from postmortem brain cells may provide further details of mitochondrial alterations in psychiatric disorders.     

Mitochondrial involvement in psychiatric disorders

Recent findings of mitochondrial abnormalities in brains from subjects with neurological disorders have led to a renewed search for mitochondrial abnormalities in psychiatric disorders. A growing body of evidence suggests that there is mitochondrial dysfunction in schizophrenia, bipolar disorder, and major depressive disorder, including evidence from electron microscopy, imaging, gene expression, genotyping, and sequencing studies. Specific evidence of dysfunction such as increased common deletion and decreased gene expression in mitochondria in psychiatric illnesses suggests that direct examination of mitochondrial DNA from postmortem brain cells may provide further details of mitochondrial alterations in psychiatric disorders.     

Psychiatric comorbidity of migraine

Migraine affects nearly 12% of the adult population in the United States and causes significant lost productivity and decrements in health-related quality of life. The burden of migraine and the challenge in managing it are increased by the comorbid psychiatric conditions that occur in association with it. Studies in both clinical and community-based settings have demonstrated an association between migraine and a number of specific psychiatric disorders. This review will focus on the relationships between migraine and depression, generalized anxiety disorder, panic disorder, and bipolar disorder. In large scale population-based studies, persons with migraine are from 2.2 to 4.0 times more likely to have depression. In longitudinal studies, the evidence supports a bidirectional relationship between migraine and depression, with each disorder increasing the risk of the other disorder. Migraine is also comorbid with generalized anxiety disorder (Odds Ratio [OR] 3.5 to 5.3), panic disorder (OR 3.7), and bipolar disorder (OR 2.9 to 7.3). A diagnosis of migraine should lead to a heightened level of diagnostic suspicion for these comorbid psychiatric disorders. Similarly, a diagnosis of one of these psychiatric disorders should increase vigilance for migraine. Treatment plans for migraine should be mindful of the comorbid conditions.     

A Novel Home Sleep Monitoring Device and Brief Sleep Intervention for Bipolar Disorder: Feasibility, Tolerability, and Preliminary Effectiveness

Sleep disturbance is common in bipolar disorder and negatively impacts its course of illness. The purpose of this study is to assess the feasibility and tolerability of a novel EKG-based home sleep monitoring device (M1) as well as a brief (two session) psychosocial sleep intervention for individuals with bipolar disorder. The sleep intervention is individually tailored for patients with insomnia or hypersomnia and extends skills designed for non-psychiatric populations as well as includes specific considerations for sleep disturbance in bipolar disorder. We found that both the M1 device and the sleep intervention were feasible and well tolerated. Participants’ sleep duration improved after the brief sleep intervention, but their sleep was more unstable as measured by the M1. Self-reported sleepiness, sleep quality, and mood symptoms improved; however, only some measures reached statistical significance (i.e., duration of sleep, dysfunction due to sleepiness). These data suggest that the M1 device is a feasible means to obtain objective sleep quality and quantity data in individuals with bipolar disorder. A brief sleep intervention may be helpful in improving sleep in a bipolar population at risk for substantial sleep disturbance, but larger, longitudinal studies are warranted.     

Addressing Methodological and Ethical Challenges of Qualitative Health Research on Persons With Schizophrenia and Bipolar Disorder

Qualitative studies of persons with schizophrenia and bipolar disorder may affect clinical practice and social policy. However, methodological and ethical challenges may present during studies of persons with these specific mental illnesses. The purpose of this paper is to increase transparency about how researchers addressed these challenges during a recent grounded theory study about engagement in primary care. As the researchers addressed the challenges, they increased understanding about persons with schizophrenia and bipolar disorder. They also gained insight about the challenges of studying persons with these specific mental illnesses and about the rigor and credibility of qualitative methods.     

No association between bipolar disorder risk polymorphisms in ANK3 and CACNA1C and common migraine

(Headache 2011;51:713‐725) Background.— Migraine and bipolar disorder are characterized by a high level of co‐morbidity, and a common familial–genetic basis has recently been hypothesized for the 2 disorders. Genome‐wide association studies have reported strong evidence of association between the polymorphisms rs10994336[T] in the ANK3 gene and rs1006737[A] in the CACNA1C gene and risk of bipolar disorder. Objective.— The aim of this study was to evaluate the hypothesis of a genetic linkage between migraine and bipolar disorder by investigating the familial transmission of the 2 bipolar disorder risk polymorphisms, in a sample of family trios with probands with childhood migraine, and unrelated controls. Methods.— Our sample comprised 192 family trios, each with a proband with childhood migraine (137 migraine without aura, 44 migraine with aura) and 228 unrelated controls. The markers rs10994336 and rs1006737 were genotyped using a TaqMan single nucleotide polymorphism Genotyping Assay. The transmission disequilibrium test analysis for the family trios and the case–control analysis were performed using the program UNPHASED. Results.— The allelic and genotypic transmission disequilibrium test analysis did not show any evidence of transmission distortion of the 2 markers in both migraine overall (rs10994336: OR = 1.61, P = .11; rs1006737: OR = 1.12, P = .49) and in the migraine without aura and migraine with aura subgroups. Likewise, the case–control analysis of alleles and genotypes frequencies did not show any evidence of association. Conclusion.— In the present study, we did not find evidence for association between the bipolar disorder risk polymorphisms rs10994336 in the ANK3 gene and rs1006737 in the CACNA1C gene in migraine. However, as these are variants that have a small effect on the risk of bipolar disorder (OR < 1.5), we cannot exclude a similar small effect on migraine susceptibility with the present sample size.     

Parenting with a diagnosis bipolar disorder

Title.  Parenting with a diagnosis bipolar disorder.
Aim.  This paper is a report of a study of the ways in which bipolar disorder is constructed in the DSM-IV and popular texts, and how parents who have been diagnosed as having a bipolar disorder construct their role as parent.
Background.  Research into parenting and mental illness has typically taken a deficit-based approach that focuses on the risks to children when a parent has a mental illness. Literature that considers parenting specifically in the context of bipolar disorder retains a focus on the increased risk to their children of psychopathology or psychosocial difficulties.
Method.  A critical discourse analysis was conducted using interviews with five parents who had received a diagnosis of bipolar disorder. These interviews were examined in relation to the text that constructs the diagnosis of bipolar disorder (DSM-IV) and the popular texts from which the parents drew their understandings of parenting.
Findings.  The need to monitor and moderate emotions was a dominant theme that emerged from the analysis. For these parents this also involved teaching moderation to their children and monitoring it in their children's development. The consequence of this for these parents was a heightened sense of the need for self-surveillance.
Conclusion.  The challenge for people working with parents who have been diagnosed with a bipolar disorder is to support them to feel confident in the management of their bipolar disorder and their ability to parent effectively.     

LOW-DOSE MAINTENANCE CLOZAPINE TREATMENT IN THE PROPHYLAXIS OF BIPOLAR AFFECTIVE DISORDER

SUMMARY A chronically relapsing middle-aged man with bipolar affective disorder responded poorly to different forms of conventional pharmacotherapy, including depot antipsychotic medication and lithium. The addition of clozapine to lithium, even at doses as low as 25mg/day, led to a stabilisation of his mood. The withdrawal of low-dose clozapine led to a relapse within a few days. It is concluded that maintenance low-dose clozapine should be considered in bipolar disorders resistant to other treatments.     

Differential effects of DAAO on regional activation and functional connectivity in schizophrenia, bipolar disorder and controls

Recent studies have identified DAAO as a probable susceptibility gene for schizophrenia and bipolar disorder. However, little is known about how this gene affects brain function to increase vulnerability to these disorders. We examined the impact of DAAO genotype (rs3918346) on brain function in patients with schizophrenia, patients with bipolar I disorder and healthy controls. We tested the hypothesis that a variation in DAAO genotype would be associated with altered prefrontal function and altered functional connectivity in schizophrenia and bipolar disorder. We used functional magnetic resonance imaging to measure brain responses during a verbal fluency task in a total of 121 subjects comprising 40 patients with schizophrenia, 33 patients with bipolar disorder and 48 healthy volunteers. We then used statistical parametric mapping (SPM) and psycho-physiological interaction (PPI) analyses to estimate the main effects of diagnostic group, the main effect of genotype, and their interaction on brain activation and on functional connectivity. Inferences were made at p<0.05, after correction for multiple comparisons across the whole brain. In the schizophrenia group relative to the control group, patients with one or two copies of the T allele showed lower deactivation in the left precuneus and greater activation in the right posterior cingulate gyrus than patients with two copies of the C allele. This diagnosis×genotype interaction was associated with differences in the functional connectivity of these two regions with other cortical and subcortical areas. In contrast, there were no significant effects of diagnosis or of genotype in comparisons involving bipolar patients. Our results suggest that genetic variation in DAAO has a significant impact on both regional activation and functional connectivity, and provide evidence for a diagnosis-dependent pattern of gene action.     

Clinical,genetic, and brain imaging predictors of risk for bipolar disorder in high-risk individuals

ABSTRACT

Introduction: Early detection and intervention in bipolar disorder (BD) might reduce illness severity, slow its progression, and, in specific cases, even ward off the full-blown disorder. Therefore, identifying at-risk individuals and targeting them promptly before the illness onset is of the utmost importance. In the last decades, there has been a significant effort aimed at identifying genetic and molecular factors able to modulate risk and pharmacological outcomes.

Areas covered: We performed a narrative review of articles aimed at identifying clinical, genetics, molecular, and brain imaging markers of BD specifically focusing on samples of individuals at high-risk for BD. Special emphasis was put on studies applying an integrative design, e.g. studies combining different markers such as genetic and brain imaging.

Expert opinion: Findings from studies in risk individuals are still too sparse to allow drawing definite conclusions. However, the high potentiality of longitudinal studies in individuals considered at risk to develop BD supports the need for more efforts. Future investigations should focus on more homogeneous subpopulations and evaluate the cross-linking between clinical, genetic, and brain morphostructural/functional neuroimaging characteristics as predictors of risk for BD.     

Normal amygdala activation but deficient ventrolateral prefrontal activation in adults with bipolar disorder during euthymia

Functional neuroimaging studies have implicated the involvement of the amygdala and ventrolateral prefrontal cortex (vlPFC) in the pathophysiology of bipolar disorder. Hyperactivity in the amygdala and hypoactivity in the vlPFC have been reported in manic bipolar patients scanned during the performance of an affective faces task. Whether this pattern of dysfunction persists during euthymia is unclear. Using functional magnetic resonance imaging (fMRI), 24 euthymic bipolar and 26 demographically matched healthy control subjects were scanned while performing an affective task paradigm involving the matching and labeling of emotional facial expressions. Neuroimaging results showed that, while amygdala activation did not differ significantly between groups, euthymic patients showed a significant decrease in activation of the right vlPFC (BA47) compared to healthy controls during emotion labeling. Additionally, significant decreases in activation of the right insula, putamen, thalamus and lingual gyrus were observed in euthymic bipolar relative to healthy control subjects during the emotion labeling condition. These data, taken in context with prior studies of bipolar mania using the same emotion recognition task, could suggest that amygdala dysfunction may be a state-related abnormality in bipolar disorder, whereas vlPFC dysfunction may represent a trait-related abnormality of the illness. Characterizing these patterns of activation is likely to help in understanding the neural changes related to the different mood states in bipolar disorder, as well as changes that represent more sustained abnormalities. Future studies that assess mood-state related changes in brain activation in longitudinal bipolar samples would be of interest.