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Results for “Mood Disorders”

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PubMed1996

Nuclear magnetic resonance spectroscopy: new insights into the pathophysiology of mood disorders.

Magnetic Resonance Spectroscopy (MRS) is a novel non-invasive approach for investigation of in vivo brain neurochemistry. In this paper, we review the initial studies conducted in mood disorders. 31P MRS studies have suggested membrane phospholipid and energy metabolism abnormalities in the frontal and temporal lobes of bipolar patients. 1H MRS studies have pointed to increase in choline resonance in the basal ganglia of patients with unipolar and bipolar disorders. Mood disorders are not associated with reductions in N-acetyl-aspartate, unlike schizophrenia and other neuropsychiatric disorders. Both 31P and 1H MRS have begun to be used to investigate the mechanisms of action of ECT. 19F and 7Li MRS offer therapeutically relevant new tools for psychopharmacological investigation, allowing the determination of brain concentrations of psychotropic drugs. Measurement of in vivo brain lithium concentrations may have clinical relevance. While several methodological limitations persist, the noninvasiveness and the unique neurochemical insights provided by MRS offer an excellent opportunity for in vivo investigation of the neurobiology of mood disorders.

Bipolar Disorder↗

PubMed1999

Serotonin-2A receptor polymorphism (102T/C) in mood disorders

Serotonergic dysfunction has been implicated in mood disorders and suicidal behaviors. This study examined the association between a serotonin-2A (5HT2A) receptor gene polymorphism (102T/C) and mood disorders. The genotype and allele frequencies did not differ between patients with mood disorders and control subjects. Furthermore, the 102T/C polymorphism was not found to be associated with suicidal history in mood disorder patients. Our results suggest that this polymorphism is unlikely to play a role in the genetic susceptibility to mood disorders.

Journal Article↗

PubMed2003

Social and economic burden of mood disorders.

Social and economic effects of mood disorders include functional impairment, disability or lost work productivity, and increased use of health services. Evidence for these impacts includes cross-sectional studies, longitudinal studies, and true experiments (randomized trials of specific treatments or treatment programs). With respect to unipolar depression, strong evidence demonstrates that depression is associated with significant functional impairment and that effective treatment helps to restore function. Studies of the effect of depression on work disability and health care costs show strong cross-sectional associations (i.e., greater disability and higher costs among those with depression) and longitudinal associations (i.e., improvement in depression is associated with reduced disability and lower costs). All of these findings regarding unipolar depression seem as consistent in the subgroup of patients with comorbid chronic medical illness as in the total population with depressive disorders. Fewer data are available regarding social and economic burden of bipolar disorder, but available data show cross-sectional associations between mood symptoms and functional impairment, disability, and health care costs. Taken together, these data describe the substantial social and economic burden of mood disorders and the potential benefits of more effective treatment. We must recall, however, that economic benefits of treatment for mood disorders are secondary to the principal objective of relieving human suffering.

Chronic Disease↗

PubMed2004

Familial transmission of mood disorders: convergence and divergence with transmission of suicidal behavior.

OBJECTIVE: Both mood disorder and suicidal behavior are familial. In this study, the authors examine the factors associated with the familial transmission of these two related conditions to learn which are shared or unique risk factors for familial transmission. METHOD: The 285 offspring of 141 probands with mood disorder were studied. Proband and offspring characteristics associated with offspring mood disorder were examined by univariate statistics, logistic and Cox regression, and path analysis. RESULTS: Parental history of sexual abuse was associated with an increased risk of offspring mood disorder. The relationship between parent sexual abuse and offspring mood disorder was mediated by offspring impulsive aggression, sexual abuse, and anxiety disorder. In offspring, higher levels of impulsive aggression were associated with earlier age at onset of mood disorder. Offspring suicide attempt was mainly related to offspring mood disorder, with additional contributions from offspring sexual abuse and impulsive aggression. CONCLUSIONS: The pathways associated with the familial transmission of mood disorder and of suicide attempt are similar but not identical. Prevention of early-onset mood disorder by targeting high- risk families may help to prevent the transmission of suicidal behavior. Because these data are cross-sectional, these results must be confirmed by prospective follow-up.

Adolescent↗

PubMed1989

Eating and mood disorders in young children.

This article addresses issues emerging from research and clinical work done with young children who develop eating and mood disorders. A literature review and vignettes of anorexia nervosa in prepubertal children are presented, and research on the relationship between eating disorders and mood disorders is examined. Three cases of prepubertal children with growth problems and features of eating and mood disorders and a developmental model of eating disorders and their relationship to mood disorders are explored. In conclusion, a series of questions and suggestions for research and therapy are posed about young children with eating and mood disorders and the relationship between them.

Adolescent↗

PubMed2006

Postpartum mood disorders may be related to a decreased insulin level after delivery.

Postpartum mood disorders are very frequent complications of delivery. The prevalence of postpartum blue syndrome is around 25% and that of postpartum depression is around 10%. These disorders greatly affect the well-being of these newly delivering mothers. Currently, the etiology of postpartum mood disorders is still unknown. Although many hormones have been investigated for their possible roles in postpartum mood disorders, the results are still inconclusive. Several studies have shown that insulin increases gradually during pregnancy. The level of insulin secretion may double by the third trimester. Insulin level reaches a maximum before delivery and returns to the level before pregnancy after delivery. The drop in the insulin level during the postpartum period appears to be more sudden and abrupt than the rise of insulin level during pregnancy. Recent studies have showed that insulin affects the secretion of serotonin in the brain. While serotonergic nervous system is well known for its important role in the development of mood disorders, decreased insulin level may induce mood disorders through the mechanism of affecting serotonin secretion in the brain. In the current paper, we propose that the rapid decrease in insulin level during the postpartum period may be one of the causes of postpartum mood disorders. If the hypothesis is valid, clinicians may be able to prevent postpartum mood disorders by carbohydrate-rich food during the postpartum period to stimulate the secretion of insulin. A carbohydrate-rich diet may also become an adjunctive therapy in the treatment of postpartum mood disorders according to the present hypothesis.

Female↗

PubMed2002

Aggression and violence in mood disorders.

As a common component of mood disorders, aggression can have many adverse effects on the child's or adolescent's life, including disrupting school performance and causing personal rejection by family, peers, and teachers. The problems of children and adolescents with mood disorders are compounded by comorbid aggressiveness. Without effective treatment for both problems, many of these aggressive, depressed children and adolescents go on to experience multiple failures in life leading to disturbances in character and the inability to establish fulfilling interpersonal relationships. This article is intended to heighten clinician awareness of the complex relationship between mood disorders and aggression.

Adult↗

PubMed1998

Postpartum mood disorders: diagnosis and treatment guidelines.

Mood disturbance occurs commonly during the postpartum period. The symptoms may be transient and relatively mild (as in postpartum blues) or may be associated with significant impairment of functioning (as in postpartum depression and puerperal psychosis). Despite the prevalence of postpartum mood disorders, depressive symptoms that emerge during the puerperium are often overlooked. Puerperal affective illness places the mother at risk for the development of recurrent depression and has also been associated with significant long-term effects on child development and behavior. Therefore, the prompt recognition and efficacious treatment of puerperal mood disorders are essential in order to avoid adverse outcomes for both mother and infant. This article discusses the evaluation of postpartum mood disturbance and offers guidelines for the treatment of affective illness during the puerperium.

Depression, Postpartum↗

PubMed2005

Symptoms of depression in late luteal phase dysphoric disorder: a variant of mood disorder?

BACKGROUND: In premenstrual syndrome, depressed mood in the luteal phase of the menstrual cycle is acknowledged, whereas the presence of symptoms of depression during the follicular phase remains in debate. METHODS: On the basis of prospective daily recording of the presence and severity of symptoms for at least two menstrual cycles, 43 women were diagnosed with Late Luteal Phase Dysphoric Disorder (LLPD) according to the criteria of the third edition revision of the Diagnostic and Statistical Manual of Mental Disorders. They were compared to a group of 85 women who showed no evidence of LLPD for two menstrual cycles. Structured psychiatric interviews were administered during the follicular phase. Only those subjects without Axis I disorders were subsequently included in the study. RESULTS: Those women with minor/moderate symptoms of depression had an odds of suffering from LLPD of 1.9 (95% CI=1.5-2.4, p<0.001) in relation to increasing severity of symptoms of depression at the total MADRS scale (1-point increase). The ORs of LLPD in relation to each dimension (1-point increase) of the emotional/affective, cognitive, and neurovegetative symptoms were 1.6 (95% CI=1.2-2.3, p=0.003), 2.8 (95% CI=0.9-8.5, p=0.077) and 3.3 (95% CI=1.9-5.9, p<0.001), respectively. LIMITATIONS: No hormonal changes that may be associated with symptoms of LLPD were determined in this study. CONCLUSIONS: LLPD is likely to represent a variant of a depressive disorder, where premenstrual psychobiological changes seem to exacerbate mild depressive symptoms and signs to which LLPD women are otherwise predisposed. This hypothesis opens new perspectives for prevention and of even treatment for LLPD. Further longitudinal studies with larger populations and evaluation of hormonal changes are needed to confirm these data.

Adult↗

PubMedDate not supplied

Tryptophan hydroxylase gene and response to lithium prophylaxis in mood disorders.

Lithium is an effective prophylactic agent in mood disorders but not all patients with mood disorders respond to lithium therapy; it is therefore necessary to identify responders prior to treatment. Clinical predictors account for about half of the variance and it is probable that genetic factors play a substantial role. The aim of this study was to investigate the possible association between the tryptophan hydroxylase (TPH) gene and prophylactic efficacy of lithium in mood disorders. One hundred and eight subjects affected by bipolar (n = 90) and major depressive (n = 18) disorder were followed prospectively for an average of 50.4 months and were typed for their TPH variant using polymerase chain reaction techniques. TPH variants were marginally associated with lithium outcome (F = 3.16; d.f.=2,105; P = 0.046). Subjects with the TPH*A/A variant showed a trend toward a worse response compared to both TPH*A/C and TPH*C/C variants. Consideration of possible stratification effects such as gender, polarity or age at onset did not influence the observed association. TPH variants may be a possible factor influencing the prophylactic efficacy of lithium in mood disorders.

Adult↗

PubMed2004

Multiple dimensions of familial psychopathology affect risk of mood disorder in children of bipolar parents.

The aim of our study was to determine whether familial loading of unipolar disorder, bipolar disorder, and substance use disorder are associated with DSM-IV mood disorders in adolescents at risk for bipolar disorder. One hundred and forty adolescents aged 12-21 years of 86 bipolar parents participated in the study. Lifetime DSM-IV diagnoses of the bipolar offspring were assessed with the Schedule for Affective Disorders and Schizophrenia for School Age Children Kiddie-SADS-Present and Lifetime Version (SADS-PL). Parents were interviewed using the Family History Research Diagnostic Criteria (FH-RDC) which were used to calculate a continuous familial loading score (FL) for unipolar disorder, bipolar disorder, and for substance use disorder in first- and second-degree relatives of the adolescents. FL for unipolar disorder and substance use disorder were strong and independent predictors for lifetime mood disorders in the adolescents. The gender adjusted hazard ratios for mood disorders in the children were 1.5 (95% confidence interval (CI) = 1.2-2.0) for FL of unipolar disorder and 1.8 (95% CI = 1.3-2.4) for FL of substance use disorder. Expression of mood disorders in children of bipolar parents varies with the degree of additional FL of unipolar disorder and substance use disorder in the extended family.

Adolescent↗

PubMed2001

Relationship of mood disturbance to cigarette smoking status among 252 patients with a current mood disorder.

BACKGROUND: The relationship between cigarette smoking and mood has received increasing attention. This retrospective study evaluated the relationship between mood disturbance and cigarette smoking status among patients with a current mood disorder. The association between level of nicotine dependence and severity of mood disturbance was also evaluated among current smokers. METHOD: Retrospective data for 252 patients (63.5% male, 85.0% white) admitted for treatment of a mood disorder at the San Diego Veteran Affairs Mental Health Clinical Research Center between November 1988 and June 1997 were studied. All current cigarette smokers at admission (N = 126) were matched with nonsmokers (N = 126) on the primary DSM-IV Axis I mood disorder diagnosis, admission status (inpatient or outpatient), gender, age (+/- 5 years), and ethnicity. The Hamilton Rating Scale for Depression (HAM-D), the Beck Depression Inventory, and the Profile of Mood States (POMS) were administered to patients on admission. Conditional logistic regression analysis for matched sets with a backward elimination was used to identify factors independently predictive of current smoking status. RESULTS: A greater number of cups of coffee consumed per day (p = .002), a history of alcoholism (p = .004), and higher POMS fatigue subscale scores (p = .007) were predictive of current smoking status. Among current smokers, the HAM-D terminal insomnia item was positively associated with mean number of cigarettes smoked per day (p = .012). CONCLUSION: Cigarette smoking should be addressed in the treatment of patients with a current mood disorder. Smokers experience greater levels of fatigue than nonsmokers. In addition, higher cigarette consumption levels are associated with mild-to-severe symptoms of terminal insomnia.

Adult↗

PubMed1997

Mood Disorders Secondary to Systemic Medical Conditions.

Evidence that secondary mood disorders are distinct clinical entities is mounting; and comparisons of mood disorders due to various medical or systemic conditions are only now beginning in earnest. Unlike mood disorders secondary to neurological illness, those secondary to medical conditions show wide variability in their prevalence rates and lack evidence of structural lesions within the central nervous system (CNS) as a pathophysiologic basis for their emergence. The authors selectively review literature published since 1990 concerning mood disorders secondary to four areas of medical illness: endocrine disorders, coronary artery disease, cancer, and end-stage renal disease. Potential pathophysiologic mechanisms for these depressions are examined, these include the role of cytokines in the CNS, subclinical cerebrovascular disease or leukoencephalopathy, altered platelet function, and dysregulation of CNS functions. Recent advances are dispelling old constructs regarding depressiosn in medical illness, but longitudinal studies of specific diseases are needed together with further work on the pathophysiology of these mood disorders.

Journal Article↗

PubMed1999

Dopamine receptor D2 and D4 genes, GABA(A) alpha-1 subunit genes and response to lithium prophylaxis in mood disorders.

Lithium is an effective prophylactic agent in mood disorders, and genetic factors are likely to modulate individual susceptibility to lithium treatment. The aim of this study is to investigate the influence of dopamine receptor D2 (DRD2), D4 exon 3 (DRD4), and gamma-aminobutyric acid type A (GABA(A)) receptor alpha-1 subunit (GABRA1) gene variants on the efficacy of lithium prophylaxis in mood disorders. Patients with mood disorders (N = 125: bipolar subtype, n = 100; major depressive disorder subtype, n = 25) were followed prospectively for an average of 53 months and were typed for DRD2 (Ser311/Cys311: n = 121, VNTR: n = 63), DRD4 (n = 125) and GABRA1 (n = 61) variants using polymerase chain reaction (PCR) techniques. DRD2, DRD4 and GABRA1 variants were not associated with response to lithium. A trend was observed toward a better outcome of DRD4* 2/4 subjects, but it was due to only two subjects. Consideration of possible stratification effects like gender, polarity, family history, age at onset and duration of lithium treatment did not reveal any association either. DRD2, DRD4 and GABRA1 variants therefore do not appear to be associated with the outcome of lithium prophylaxis in mood disorders.

Adult↗

PubMed2004

The epidemiology of mood disorders.

This review provides an overview of the epidemiology, risk factors, and genetic epidemiology of mood disorders in adults and children. The magnitude and impact of mood disorders in the community outweighs that of most other chronic diseases. Although there is substantial knowledge regarding the sociodemographic risk factors for mood disorders, our understanding of the pathogenesis and classification still is evolving. Comorbidity of mood disorders with anxiety disorders and substance abuse has been documented widely. Whereas substance abuse and mood disorders seem to be independent etiologically, anxiety and mood disorders result from partially common etiologic factors. The results of family, twin, and adoption studies reveal that a positive family history is the most potent risk factor for mood disorders, particularly bipolar disorder. However, the specific factors that are transmitted in families still are unknown. The two areas that will inform future genetic research include phenomenologic studies that refine the validity of the current phenotypic classification of mood disorders, and application of study designs to elucidate specific factors that may explain the familial transmission of these disorders.

Adult↗

PubMed2006

Genome wide gene expression studies in mood disorders.

Microarrays offer the possibility of screening in parallel virtually all genes expressed in a given tissue or to study the molecular signature associated with available treatments. As such, this technology has been increasingly used to investigate multifactorial and polygenic complex traits such as psychiatric disorders, in particular, schizophrenia and mood disorders. This review focuses on microarray studies investigating mood disorders. Study designs, methodologic approaches and limitations, subsequent follow-up strategies, and confirmation of results are discussed. Despite the apparent disparate and not always concordant results, it appears evident that this technology is a powerful and inevitable approach for the study of mood disorders, especially when phenotype-specific confounders are properly accounted for. Thus, alterations of mitochondrial, oligodendrocyte, and myelin related genes in bipolar disorder, of signaling and olidendroglial related genes in depression, and of GABA-glutamate related genes in depression and suicide have been observed and have confirmed new avenues for the study and the treatment of these complex disorders.

Gene Expression Profiling↗

PubMed2004

An overview of the genetics of psychotic mood disorders.

This article presents a conceptual review of the genetic underpinnings of psychotic mood disorders. Both unipolar and bipolar forms of mood disorder sometimes feature psychotic symptoms. Some evidence from epidemiological research suggests that psychotic forms of mood disorder specifically might be heritable. Linkage studies of mood disorders in general have also provided some support for that notion, as have associated studies involving serotonin and dopamine genes and psychotic mood disorder. Some research suggests there might be a genetic connection between schizophrenia and bipolar disorder, undermining the Kraepelinian dichotomous classification of the psychoses. Future research should continue to examine psychotic forms of mood disorder using both epidemiological and molecular approaches.

Affective Disorders, Psychotic↗

PubMed2001

Mood disorders associated with interferon treatment: theoretical and practical considerations.

OBJECTIVE: To review the theoretical and clinical aspects of mood disorders associated with interferon treatment and discuss their management. DATA SOURCES: Pertinent and selected laboratory/clinical studies, review articles, letters, abstracts, and book chapters on behavioral and mood-related adverse effects of interferons published in English-language journals in the past two decades were identified by MEDLINE (June 1980-June 2000) and manual searches. DATA SELECTION AND DATA EXTRACTION: All of the publications identified were reviewed, and the relevant data were included. Studies not using criteria for psychiatric diagnosis or instruments for psychiatnc monitoring were excluded. DATA SYNTHESIS: Clinical observations and limited research data suggest that interferon treatment may be associated with mood disorders. Mood-related symptoms induced by interferons emerge in a few days or weeks and tend to be dose dependent. Their severity may necessitate discontinuation of interferon therapy and/or the use of antidepressant or antimanic agents. The mechanisms responsible for inducing or exacerbating mood disorders in interferon-treated patients have not been elucidated. There is limited evidence implicating alterations in the serotonin system. CONCLUSIONS: While interferon therapy may trigger or induce mood-related symptoms, preexisting or stable concurrent mood disorders in remission do not necessarily constitute a contraindication to treatment with interferons. Mood disorders associated with interferon treatment can present clinical challenges. However, they may promote our understanding of mood disorders in the context of the current biologic theories of depression and mania.

Humans↗