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PubMed2006

Pathological gambling and mood disorders: clinical associations and treatment implications.

BACKGROUND: The rapidly expanding gambling business has resulted in an increasing number of gamblers, and the problem is likely to get worse in the future. Traditionally, mood and gambling symptoms have been known to overlap. In the present review we attempt to examine the diagnostic associations and implications for treatment. METHOD: Selected published papers on the frequencies of mood disorders among patients who have gambling disorder or gambling disorder among patients who have mood disorder have been reviewed. Recently emerging new treatment methods for gambling disorder have been reviewed and a brief summary has been added. RESULTS: SCID based study results show a close link between gambling and mood disorders. The prevalence of manic disorder reaches to approximately one fourth of the pathological gambling disorder population. The prevalence of depression is much higher, reaching to over half of the population in some studies. LIMITATIONS: The studies included in the present paper involve inpatients, outpatients, subjects recruited through advertisements and prison populations. Thus the data need to be interpreted as such. Standardized assessment instruments are not used in all studies. Methodological issues such as primary or secondary nature of depression have not been addressed adequately in these studies. The findings, however, offer new insights for the assessment and treatment of complicated gambling disorder cases. CONCLUSIONS: A high prevalence rate of manic and depressive disorders has been recorded among pathological gambling disorder patients. A rational treatment approach to each defined subset of complicated gambling disorder is discussed.

Bipolar Disorder↗
PubMed2004

Polymorphisms in wolframin (WFS1) gene are possibly related to increased risk for mood disorders.

Wolfram syndrome gene (WFS1) has been suggested to have a role in the susceptibility for mood disorders. A 26-fold increased risk for psychiatric disorders in WFS1 mutation carriers has been suggested. In this study we tested the hypothesis that the WFS1 gene is related to the risk for mood disorders. We analysed 28 single-nucleotide polymorphisms (SNPs) of the WFS1 gene in 224 unrelated patients with major depressive disorder and bipolar disorder and in 160 healthy control subjects. Patients were further stratified according to their comorbidity with anxiety disorders. We applied arrayed primer extension (APEX)-based genotyping technology followed by association and haplotype analysis. Five SNPs in the WFS1 gene were associated with major depressive disorder, and three SNPs with bipolar disorder. Haplotype analysis revealed a common GTA haplotype, formed by SNPs 684C/G, 1185C/T and 1832G/A, conferring risk for affective disorders. Specifically, for major depression the GTA haplotype has an OR of 1.59 (p = 0.01) and for bipolar disorder an OR of 1.89 (p = 0.03). These results support the hypothesis that the WFS1 gene is involved in the genetic predisposition for mood disorders.

Adult↗
PubMed1997

Epidemiologic questions on mood disorders in old age.

To study factors associated with different mood disorders in old age, researchers need clear and meaningful definitions. "Major depression" is too broad and heterogeneous a category, and the boundaries of "dysthymia" are ill-defined, yet epidemiologic studies have focused on these disorders. Depressions in old age are commonly associated with medical conditions; prevalence rates of depression in cases of stroke, Parkinson's disease, dementia, and disabilities (all much commoner in old age) range upward from about 20%. Depressions are attributed to both psychological and biological reactions. Mania, too, can be precipitated by cerebral and other medical factors. The proportion of psychiatric inpatients who have depressions with melancholic and/or psychotic features is higher among elderly subjects, and this has been linked with white matter lesions and other brain changes that become commoner in old age. The prognostic relevance of these brain changes, and implications for treatment of mood disorders, require clarification.

Aged↗
PubMed2004

Possible association between a haplotype of the GABA-A receptor alpha 1 subunit gene (GABRA1) and mood disorders.

BACKGROUND: The gamma-aminobutyric acid (GABA) neurotransmitter system has been implicated in the pathogenesis of mood disorders. The GABRA1 gene encodes one of the subunits of GABA-A receptor and is located on human chromosome 5q34-q35, which is a region reportedly linked to mood disorders. We examined the GABRA1 gene as a candidate for mood disorders. METHODS: We performed mutation screening of GABRA1 in 24 Japanese bipolar patients and evaluated associations in Japanese case-control subjects consisting of 125 patients with bipolar disorder, 147 patients with depressive disorders, and 191 healthy control subjects. Associations were confirmed in the National Institute of Mental Health (NIMH) Initiative Bipolar Pedigrees, which consists of 88 multiplex pedigrees with 480 informative persons. RESULTS: We identified 13 polymorphisms in the GABRA1 gene. Nonsynonymous mutations were not found. Association of a specific haplotype with affective disorders was suggested in the Japanese case-control population (corrected p=.0008). This haplotype association was confirmed in the NIMH pedigrees (p=.007). CONCLUSIONS: These results indicate that the GABRA1 gene may play a role in the etiology of bipolar disorders.

Alleles↗
PubMed2005

Lithium in the prevention of suicidal behavior and all-cause mortality in patients with mood disorders: a systematic review of randomized trials.

OBJECTIVE: Observational studies suggest that long-term lithium treatment has a strong antisuicidal effect in mood disorders, but it is uncertain whether this association is a genuine therapeutic effect or is due to confounding factors in nonrandomized studies. The authors conducted a systematic review and meta-analysis of randomized trials to investigate the effect of lithium, compared to placebo and other active treatments, on the risk of suicide, deliberate self-harm, and all-cause mortality in patients with mood disorder. METHOD: The data source was the Cochrane Collaboration Depression, Anxiety and Neurosis Controlled Trials Register, incorporating results of searches of MEDLINE (1966-June 2002), EMBASE (1980-June 2002), CINAHL (1982-March 2001), PsycLIT (1974-June 2002), PSYNDEX (1977-October 1999), and LILACS (1982-March 2001). The Cochrane Central Register of Controlled Trials (CENTRAL) was searched with the term "lithium" for new records entered into the database from 1999 to 2003. Studies selected included randomized, controlled trials comparing lithium with placebo or all other compounds used in long-term treatment for mood disorders (unipolar depression, bipolar disorder, schizoaffective disorder, dysthymia, and rapid cycling, diagnosed according to DSM or ICD criteria). Of 727 references identified in the search, 52 articles were marked as possibly relevant on the basis of the abstract, and 32 randomized, controlled trials were eligible for inclusion in the review. Two independent reviewers extracted the data, and disagreements were resolved by consensus with a third reviewer. Methodological quality was assessed according to the criteria of the Cochrane Collaboration. When the outcomes of interest were not reported, an attempt was made to obtain the required data from the original authors. RESULTS: In 32 trials, 1,389 patients were randomly assigned to receive lithium and 2,069 to receive other compounds. Patients who received lithium were less likely to die by suicide (data from seven trials; two versus 11 suicides; odds ratio=0.26; 95% confidence interval [CI]=0.09-0.77). The composite measure of suicide plus deliberate self-harm was also lower in patients who received lithium (odds ratio=0.21; 95% CI=0.08-0.50). There were fewer deaths overall in patients who received lithium (data from 11 trials; nine versus 22 deaths; odds ratio=0.42, 95% CI=0.21-0.87). CONCLUSIONS: Lithium is effective in the prevention of suicide, deliberate self-harm, and death from all causes in patients with mood disorders.

Cause of Death↗
PubMed2002

Structural alterations in depression: cellular mechanisms underlying pathology and treatment of mood disorders.

Basic and clinical studies over the past 10 years have lead to a fundamental shift in our understanding of mood disorders. These studies demonstrate that mood disorders and stress are accompanied by structural alterations in the brain; moreover, these structural alterations are reversible with antidepressant treatment. These alterations include changes in the length and number of neuronal processes, the number of neurons and glia, and even the rate of neurogenesis in the adult brain. Work is also being conducted to identify the molecular mechanisms underlying these changes and the adaptations that are critical to the therapeutic actions of antidepressant treatment. Some of the intracellular targets include second messengers, gene transcription factors, and neurotrophic factors that could oppose the actions of stress and depression. Taken together, this exciting new work describes and details structural alterations of limbic brain regions that are extremely dynamic and adaptive. Further understanding of the abnormalities in these systems that lead to mood disorders will provide more efficacious and possibly faster-acting therapeutic interventions.

Journal Article↗
PubMed1995

Results of the DSM-IV mood disorders field trial.

OBJECTIVE: The DSM-IV mood disorders field trial, a multisite collaborative study, was designed to explore the reliability of a course-based diagnostic classification system for major depression, evaluate the symptom criteria for dysthymia, and explore the need for additional diagnostic categories for milder forms of mood disorder (e.g., minor and recurrent brief depression). METHOD: Five hundred twenty-four depressed subjects were recruited from inpatient, outpatient, and community settings at five sites and evaluated with structured interviews according to DSM-III and DSM-III-R criteria, with careful attention to longitudinal course. Within- and across-site interrater reliability studies and 6-month test-retest reliability studies were also conducted on subsets of the sample. RESULTS: For evaluations of major depression and dysthymia, intrasite reliability was good to excellent and intersite reliability was fair to good; 6-month test-retest reliability was fair for dysthymia and poor to fair for major depression. Interrater reliability for six course of illness specifiers was fair to good, and almost all subjects could be assigned to a specific type of course. CONCLUSIONS: The results supported the use of a course-based classification system for major depression. They also suggested that the content validity of the DSM-III-R symptom criteria for dysthymia could be improved by emphasizing cognitive and social/motivational symptoms, although such changes are unlikely to sharpen the distinction between dysthymia and major depression. Finally, 91% of the subjects met the criteria for current or lifetime major depression or dysthymia, suggesting that additional categories for milder forms of depression are not needed.

Adult↗
PubMed1998

Electroencephalographic findings in patients with DSM-IV mood disorder, schizophrenia, and other psychotic disorders.

BACKGROUND: Although numerous electroencephalographic (EEG) studies have been performed in psychiatric populations, and some have identified specific abnormalities within groups of functional psychoses, differences in EEG findings among subgroups of functional mental illness need to be evaluated with careful consideration of the nosologic systems employed in each study. In the present study, we examined whether there might be EEG differences among subgroups of functional psychoses defined by DSM-IV. METHODS: A total of 143 patients, whose discharge diagnoses met the DSM-IV criteria for mood disorder, schizophrenia, and other psychotic disorders, were studied. EEG findings were compared among seven diagnostic categories: mood disorder without, with mood-congruent, and with mood-incongruent psychotic features; schizoaffective disorder; schizophreniform disorder; brief psychotic disorder; and schizophrenia. RESULTS: The frequency of epileptiform variants, including the phantom spike and wave, positive spikes, and small sharp spikes, was significantly higher among patients with mood-incongruent psychotic mood disorder (33%), schizoaffective disorder (33%), and schizophreniform disorder (30%), as compared with patients with nonpsychotic mood disorder (3.2%) and schizophrenia (0%). CONCLUSIONS: Our results imply that patients with "atypical" psychoses that are located between typical mood disorder and schizophrenia have similar biological vulnerability, represented by epileptiform EEG variants.

Adult↗
PubMed2005

Effects of suppression and acceptance on emotional responses of individuals with anxiety and mood disorders.

The present investigation compared the subjective and physiological effects of emotional suppression and acceptance in a sample of individuals with anxiety and mood disorders. Sixty participants diagnosed with anxiety and mood disorders were randomly assigned to one of two groups. One group listened to a rationale for suppressing emotions, and the other group listened to a rationale for accepting emotions. Participants then watched an emotion-provoking film and applied the instructions. Subjective distress, heart rate, skin conductance level, and respiratory sinus arrhythmia were measured before, during, and after the film. Although both groups reported similar levels of subjective distress during the film, the acceptance group displayed less negative affect during the post-film recovery period. Furthermore, the suppression group showed increased heart rate and the acceptance group decreased heart rate in response to the film. There were no differences between the two groups in skin conductance or respiratory sinus arrhythmia. These findings are discussed in the context of the existing body of research on emotion regulation and current treatment approaches for anxiety and mood disorders.

Adolescent↗
PubMed2000

The implications of genetics studies of major mood disorders for clinical practice.

BACKGROUND: This article is a selective review and synthesis of relevant research findings from genetic studies of major mood disorders and the application of these to clinical practice. METHOD: The article discusses the application of genetic research findings in major mood disorders, including epidemiologic and family study risk estimates, risk modifiers, and the concepts of etiologic and phenotypic heterogeneity, to 3 clinical domains: risk counseling, diagnosis, and treatment prediction. RESULTS: Epidemiologic and family studies have provided general risk estimates useful in counseling mood-disordered patients and their relatives. A complete and accurate family pedigree provides more individualized risk estimates for specific cases and is useful in identifying the phenotypic spectrum of the disorder being transmitted in the family. Both proband course parameters and familial loading for psychiatric illnesses may be relevant for the prediction of treatment response. However, the hypothesis of inherited pharmacologic selectivity remains to be proven. CONCLUSION: Genetic studies of mood disorders have not yet provided conclusive evidence of specific susceptibility genes or their pattern of inheritance. However, they have generated information that is useful to clinical practice.

Adult↗
PubMed1994

Hypersomnia associated with mood disorders: a new perspective.

Thirty-six subjects affected with hypersomnia associated with mood disorders, 31 with a diagnosis of dysthymia, 4 with a diagnosis of bipolar disorder and one with a diagnosis of major recurrent depression underwent standardized polysomnographic procedures including night 1, MSLT and night 2 (uninterrupted). 36.1% of these subjects had a reduced or intermediate mean sleep latency on the MSLT and 13.8% slept over 9 hr at night. In addition 17 of these subjects underwent prolonged polysomnography during day 2. In comparison with eight subjects affected with idiopathic hypersomnia, mean sleep latency on the MSLT was significantly longer and total sleep time during night 2 and during night 2 plus day 2 was significantly lower in subjects affected with hypersomnia associated with mood disorders. It is concluded that a positive diagnosis of hypersomnia associated with a mood disorder requires both behavioral observation and polysomnography. Among these subjects there may be subjects with well-documented hypersomnia and subjects with anergia facilitating or mimicking sleep.

Adult↗
PubMed2000

Postmortem studies in mood disorders indicate altered numbers of neurons and glial cells.

The influence of stress and glucocorticoids on neuronal pathology has been demonstrated in animal and clinical studies. It has been proposed that stress-induced changes in the hippocampus may be central to the development of depression in genetically vulnerable individuals. New evidence implicates the prefrontal cortex (PFC) in addition to the hippocampus as a site of neuropathology in depression. The PFC may be involved in stress-mediated neurotoxicity because stress alters PFC functions and glucocorticoid receptors, the PFC is directly interconnected with the hippocampus, and metabolic alterations are present in the PFC in depressed patients. Postmortem studies in major depression and bipolar disorder provide the first evidence for specific neuronal and glial histopathology in mood disorders. Three patterns of morphometric cellular changes are noted: cell loss (subgenual PFC), cell atrophy (dorsolateral PFC and orbitofrontal cortex), and increased numbers of cells (hypothalamus, dorsal raphe nucleus). The relevance of cellular changes in mood disorders to stress and prolonged PFC development and a role of neurotrophic/neuroprotective factors are suggested, and a link between cellular changes and the action of therapeutic drugs is discussed. The precise anatomic localization of dysfunctional neurons and glia in mood disorders may reveal cortical targets for novel antidepressants and mood stabilizers.

Atrophy↗
PubMed1998

GABAA alpha-1 subunit gene not associated with depressive symptomatology in mood disorders.

Considerable evidence implicates the neurotransmitter gamma-aminobutyric acid (GABA) in the biochemical pathophysiology of mood disorders. In this study, we investigated the possibility that the gene for the gamma-aminobutyric acid type A (GABAA) receptor alpha-1 subunit (GABRA1) might be associated with depressive symptomatology in a sample of mood disorder subjects. Sixty-seven inpatients affected by unipolar (n = 37) and bipolar (n = 30) disorder (DSMIV) were assessed at admission by the Hamilton depression rating scale (HAMD) and were typed using polymerase chain reaction (PCR) techniques. GABRA1 variants were not associated with depressive symptomatology, and consideration of possible stratification effects such as sex, psychiatric diagnosis and illness severity did not reveal any association either. GABAA alpha-1 subunit gene is not, therefore, associated with depressive symptomatology in mood disorder subjects.

Adult↗
PubMed2006

Adherence to treatment in mood disorders.

PURPOSE OF REVIEW: Nonadherence to medication is common in mood disorders. Improving adherence should decrease risk of relapse, improve outcome and lessen costs. Here we review recent qualitative and quantitative work in this area. RECENT FINDINGS: Themes that emerged from qualitative studies for nonadherence are discomfort about psychiatric diagnoses, including denial of the illness, problematic side effects, fears around dependency and the view that medication was unhelpful following resolution of the acute phase. The psycho-educational intervention model alone has shown little improvement in adherence. The collaborative managed care model for improving outcomes in depression in primary care is of limited benefit in increasing adherence or indeed outcomes. Psychological approaches have been most successful when concentrating on the patient-clinician alliance when attitudes and experience are explored, recognizing the importance of the patient's opinion in treatment decisions. Psycho-pharmaceutical interventions such as changing medication preparations have potential efficacy. SUMMARY: There are difficulties in assessing adherence and developing interventions. The majority of both qualitative and quantitative studies indicate that a collaborative approach when patients are involved in the decision-making process appear to be the most effective. The focus on trial driven, specialty-specific interventions may not be the most helpful way to investigate or improve adherence. This is a fertile area for qualitative work. Interventions that focus on the structure of care alongside increasing patient involvement in treatment have the most potential to improve adherence and hence outcome in mood disorders.

Drug Therapy↗
PubMed2006

Prevalence and effects of mood disorders on work performance in a nationally representative sample of U.S. workers.

OBJECTIVE: Research on the workplace costs of mood disorders has focused largely on major depressive episodes. Bipolar disorder has been overlooked both because of the failure to distinguish between major depressive disorder and bipolar disorder and by the failure to evaluate the workplace costs of mania/hypomania. METHOD: The National Comorbidity Survey Replication assessed major depressive disorder and bipolar disorder with the World Health Organization (WHO) Composite International Diagnostic Interview (CIDI) and work impairment with the WHO Health and Work Performance Questionnaire. A regression analysis of major depressive disorder and bipolar disorder predicting Health and Work Performance Questionnaire scores among 3,378 workers was used to estimate the workplace costs of mood disorders. RESULTS: A total of 1.1% of the workers met CIDI criteria for 12-month bipolar disorder (I or II), and 6.4% meet criteria for 12-month major depressive disorder. Bipolar disorder was associated with 65.5 and major depressive disorder with 27.2 lost workdays per ill worker per year. Subgroup analysis showed that the higher work loss associated with bipolar disorder than with major depressive disorder was due to more severe and persistent depressive episodes in those with bipolar disorder than in those with major depressive disorder rather than to stronger effects of mania/hypomania than depression. CONCLUSIONS: Employer interest in workplace costs of mood disorders should be broadened beyond major depressive disorder to include bipolar disorder. Effectiveness trials are needed to study the return on employer investment of coordinated programs for workplace screening and treatment of bipolar disorder and major depressive disorder.

Absenteeism↗
PubMedDate not supplied

Psychological factors in the development of mood disorders with a seasonal pattern.

The psychiatric records of a 7-year period were searched for cases with seasonal mood disorders. Among 358 cases with a mood disorder there were 41 patients with 3 or more admissions, 4 of which were demonstrating a seasonal pattern. It was found that the depressive or manic episodes of these patients were anniversary reactions associated with intense traumatic experiences in childhood, adolescence or adulthood. The seasonal pattern of the depressive episodes fulfilled the DSM-IV diagnostic criteria. The time and sometimes the place of the traumatic event acted as triggers eliciting the clinical symptoms. This study showed that anniversary reactions may constitute a subgroup of seasonal mood disorders manifesting both depressive and manic episodes, which are precipitated primarily by psychological factors rather than climatic conditions.

Adjustment Disorders↗
PubMed2003

Prevalence of mood disorders in a national sample of young American adults.

BACKGROUND: Availability of nationally representative mood disorder prevalence estimates in the United States, based on structured psychiatric interviews is limited. This report estimates overall lifetime prevalence of major depressive episode, dysthymia, and bipolar disorder using the Third National Health and Nutrition Examination Survey (NHANES III) and compares these estimates to the Epidemiologic Catchment Area Study (ECA) conducted 10 years earlier. Additionally, prevalence estimate breakdowns by selected sociodemographic and health characteristics are investigated. METHODS: NHANES III, conducted from 1988 to 1994, is a large nationally representative cross-sectional sample of the United States. A population-based sample of 8,602 men and women 17-39 years of age were eligible to participate, of whom 7,667 (89.1 %) completed interviews. Mood disorder assessments came from the Diagnostic Interview Schedule (DIS) administered as one component of the NHANES III. RESULTS: Lifetime prevalence estimates were assessed for six mood measures: 1) major depressive episode (MDE) 8.6%, 2) major depressive episode with severity (MDE-s) 7.7%, 3) dysthymia 6.2%, 4) MDE-s with dysthymia 3.4%, 5) any bipolar disorder 1.6%, and 6) any mood disorder 11.5%. All estimates except for MDE and MDE-s were significantly higher than comparable ECA estimates. CONCLUSIONS: These data provide recent national prevalence estimates. Based on their overall magnitudes, subgroup excesses, and observed increases compared to the ECA, continued monitoring of these estimates is warranted.

Adolescent↗