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PubMed2005

Family history of suicidal behavior and mood disorders in probands with mood disorders.

OBJECTIVE: First-degree relatives of persons with mood disorder who attempt suicide are at greater risk for mood disorders and attempted or completed suicide. This study examined the shared and distinctive factors associated with familial mood disorders and familial suicidal behavior. METHOD: First-degree relatives' history of DSM-IV-defined mood disorder and suicidal behavior was recorded for 457 mood disorder probands, of whom 81% were inpatients and 62% were female. Probands' lifetime severity of aggression and impulsivity were rated, and probands' reports of childhood physical or sexual abuse, suicide attempts, and age at onset of mood disorder were recorded. Univariate and multivariate analyses were carried out to identify predictors of suicidal acts in first-degree relatives. RESULTS: A total of 23.2% of the probands with mood disorder who had attempted suicide had a first-degree relative with a history of suicidal behavior, compared with 13.2% of the probands with mood disorder who had not attempted suicide (odds ratio=1.99, 95% CI=1.21-3.26). Thirty percent (30.8%) of the first-degree relatives with a diagnosis of mood disorder also manifested suicidal behavior, compared with 6.6% of the first-degree relatives with no mood disorder diagnosis (odds ratio=6.25, 95% CI=3.44-11.35). Probands with and without a history of suicide attempts did not differ in the incidence of mood disorder in first-degree relatives (50.6% versus 48.1%). Rates of reported childhood abuse and severity of lifetime aggression were higher in probands with a family history of suicidal behavior. Earlier age at onset of mood disorder in probands was associated with greater lifetime severity of aggression and higher rates of reported childhood abuse, mood disorder in first-degree relatives, and suicidal behavior in first-degree relatives. CONCLUSIONS: Risk for suicidal behavior in families of probands with mood disorders appears related to early onset of mood disorders, aggressive/impulsive traits, and reported childhood abuse in probands. Studies of such clinical features in at-risk relatives are under way to determine the relative transmission of these clinical features.

Adult↗
PubMed2001

Lithium for maintenance treatment of mood disorders.

BACKGROUND: Mood disorders are common, disabling and tend to be recurrent. They carry a high risk of suicide. Maintenance treatment, aimed at the prevention of relapse, is therefore of vital importance. Lithium has been used for some years as the mainstay of maintenance treatment in bipolar affective disorder, and to a lesser extent in unipolar disorder. However, the efficacy and effectiveness of prophylactic lithium therapy has been disputed. Low suicide rates in lithium-treated patients have led to claims that lithium has a specific anti-suicidal effect. If so, this is of considerable importance as treatments for mental disorders in general have not been shown convincingly to be effective in suicide prevention. OBJECTIVES: 1. To investigate the efficacy of lithium treatment in the prevention of relapse in recurrent mood disorders. 2. To examine the effect of lithium treatment on consumers' general health and social functioning, its acceptability to consumers, and the side-effects of treatment. 3. To investigate the hypothesis that lithium has a specific effect in reducing the incidence of suicide and deliberate self-harm in persons with mood disorders. SEARCH STRATEGY: The Cochrane Collaboration Depression, Anxiety and Neurosis Controlled Trials Register (CCDANCTR) and The Cochrane Controlled Clinical Trials Register (CCTR) were searched. Reference lists of relevant papers and major text books of mood disorder were examined. Authors, other experts in the field and pharmaceutical companies were contacted for knowledge of suitable trials, published or unpublished. Specialist journals concerning lithium were hand searched. SELECTION CRITERIA: Randomised controlled trials comparing lithium with placebo, where the stated intent of treatment was maintenance or prophylaxis. Participants were males and females of all ages with diagnoses of mood disorder. Discontinuation studies (in which all participants had been stable on lithium for some time before being randomised to either continued lithium treatment or placebo substitution) were excluded. DATA COLLECTION AND ANALYSIS: Data were extracted from the original reports independently by two reviewers. The main outcomes studied were related to the objectives stated above. Data were analysed for all diagnoses of mood disorder and for bipolar and unipolar disorder separately. Data were analysed using Review Manager version 4.0. MAIN RESULTS: Nine studies were included in the review, reporting on 825 participants randomly allocated to lithium or placebo. Lithium was found to be more effective than placebo in preventing relapse in mood disorder overall, and in bipolar disorder. The most consistent effect was found in bipolar disorder (random effects OR 0.29; 95% CI 0.09 to 0.93 ). In unipolar disorder, the direction of effect was in favour of lithium, but the result (when heterogeneity between studies was allowed for) did not reach statistical significance. Considerable heterogeneity was found between studies in all groups of patients. The direction of effect was the same in all studies; no study found a negative effect for lithium. Heterogeneity may have been due to differences in selection of participants, and to differing exposures to lithium in the pre-study phase resulting in variable influence of a discontinuation effect. There was little reported data on overall health and social functioning of participants under the different treatment conditions, or on the participants' own views of their treatment. Descriptive analysis showed that assessments of general health and social functioning generally favoured lithium. Small absolute numbers of deaths and suicides, and the absence of data on non-fatal suicidal behaviours, made it impossible to draw meaningful conclusions about the place of lithium therapy in suicide prevention. REVIEWER'S CONCLUSIONS: This systematic review indicates that lithium is an efficacious maintenance treatment for bipolar disorder. In unipolar disorder the evidence of efficacy is less robust. This review does not cover the relative efficacy of lithium compared with other maintenance treatments, which is at present unclear. There is no definitive evidence from this review as to whether or not lithium has an anti-suicidal effect. Systematic reviews and large scale randomised studies comparing lithium with other maintenance treatments (e.g. anti-convulsants, antidepressants) are necessary. Outcomes relating to death and suicidal behaviour should be included in all future maintenance studies of mood disorder.

Antimanic Agents↗
PubMed2006

Comorbidity studies of eating disorders and mood disorders. Critical review of the literature.

OBJECTIVE: We conducted a critical literature review of studies assessing the prevalence of mood disorders (MD) in subjects with eating disorders (ED; anorexia nervosa and bulimia nervosa). In the first part of this article, we discuss methodological issues relevant to comorbidity studies between ED and MD. In the second part, we summarize the findings of these studies in light of the methodological considerations raised. METHOD: A manual computerised search (Medline) was performed for all published studies on comorbidity between ED and MD. In order to have sufficiently homogeneous diagnostic criteria for both categories of disorders, this search was limited to articles published between 1985 and 2006. RESULTS: Too few studies include control groups, few studies compared diagnostic subgroups of ED subjects, and results are scarce or conflicting. DISCUSSION: The results are discussed in the light of the methodological problems observed. The implications when reviewing the results of published studies and planning future research are set out.

Anorexia Nervosa↗
PubMed2001

Insight into illness in schizophrenia, schizoaffective disorder, and mood disorders with psychotic features.

OBJECTIVE: Deficits in insight have been found in one study to be more common and severe in patients with schizophrenia than in patients with schizoaffective and major depression with and without psychosis but not more severe than they are in patients with bipolar disorder. The goals of this study were to replicate this finding independently and to clarify whether patients with schizophrenia differ from patients with bipolar disorder in a larger study group. METHOD: Using the Scale to Assess Unawareness of Mental Disorder, the authors evaluated 29 inpatients with schizophrenia, 24 with schizoaffective disorder, and 183 with mood disorders with psychotic features (153 with bipolar disorder and 30 with unipolar depression). RESULTS: Patients with schizophrenia had poorer insight than patients with schizoaffective disorder and patients with psychotic unipolar depression but did not differ from patients with bipolar disorder. CONCLUSIONS: The lack of significant differences between patients with schizophrenia and patients with bipolar disorder was not a result of low statistical power. This replication and more detailed examination of diagnostic group differences in insight have clinical, theoretical, and nosological implications.

Adult↗
PubMed1993

Delusional disorder and mood disorder: can they coexist?

DSM III-R acknowledges that delusional disorder and mood disturbance can coexist. The aim of the study is to analyze mood disturbances occurring within a delusional disorder. An external validator, as the increased familial risk of psychiatric disorder, is also added to clarify the relationship between the two diagnostic areas. We found a high frequency of mood disturbances in our patients (50.7%). We were able to identify a proportion of delusional patients affected by a recurrent form of mood disturbance (35.2%); in about 42% of these patients the onset of the mood disturbance preceded the onset of the delusional disorder by a considerable interval of time. Our hypothesis is that, in these cases, the observed mood disturbance could represent a codiagnosis of true mood disorder. This hypothesis is partly supported by familial data.

Adult↗
PubMed1997

The association between premenstrual dysphoric disorder and other mood disorders.

Premenstrual dysphoric disorder (PMDD) is a premenstrual mood disorder that cyclically recurs during the majority of menstrual cycles. It is included under the category of "depressive disorders not otherwise specified" in DSM-IV. Given the placement of PMDD with other mood disorders in DSM-IV, the evidence suggesting an association between PMDD and other mood disorders is examined. Primary reports on the epidemiology, phenomenology, family history, psychobiology, and treatment of PMDD were examined for features that are commonly found in other mood disorders. There is an overlap in the symptoms experienced by women with PMDD and patients with other mood disorders. As in patients with other mood disorders, past episodes of mood disorder and family history of mood disorder are common in women with PMDD. Selected biological markers differentiate women with PMDD from controls, and some but not all antidepressants are effective in the treatment of PMDD. Many features of PMDD support its inclusion in the DSM-IV category of mood disorders. However, a number of factors (biological and cognitive studies, treatment response) differentiate PMDD from other mood disorders.

Biomarkers↗
PubMed2006

Schizoaffective disorders are psychotic mood disorders; there are no schizoaffective disorders.

Schizoaffective disorder (SA D/O), introduced in 1933 by Dr. Jacob Kasanin, represented a first, modest change in our concept about the diagnoses of psychotic patients away from the beliefs of E. Bleuler, i.e., that hallucinations and delusions define schizophrenia, and toward the recognition of a significant role for mood disorders. SA D/O established a connection between schizophrenia and mood disorders, traditionally considered mutually exclusive, a connection that has strengthened progressively toward the diagnostic unity of all three disorders. A basic tenet of medicine holds that if discrepant symptoms can be explained by one disease instead of two or more, it is likely there is only one disease. The scientific justification for SA D/O and schizophrenia as disorders distinct from a psychotic mood disorder has been questioned. The "schizo" prefix in SA D/O rests upon the presumption that the diagnostic symptoms for schizophrenia are disease specific. They are not, since patients with severe mood disorders can evince any or all of the "schizophrenic" symptoms. "Schizophrenic" symptoms mean "psychotic" and not any specific disease. These data and a very low interrater reliability for SA D/O suggest that the concepts of SA D/O and schizophrenia as valid diagnoses are flawed. Clinically SA D/O remains popular because it encompasses both schizophrenia and psychotic mood disorder when there is a diagnostic question. We present a review of the literature in table form based on an assignment of each article assigned to one of five categories that describe the possible relationships between SA D/O, schizophrenia and psychotic mood disorders. We conclude that the data overall are compatible with the hypothesis that a single disease, a mood disorder, with a broad spectrum of severity, rather than three different disorders, accounts for the functional psychoses.

Affective Disorders, Psychotic↗
PubMed2006

Sex differences in the familial transmission of mood disorders.

BACKGROUND: Mood disorders exhibit familial transmission due to both environmental and genetic risk factors. Mood disorders are more common in women, yet the role of gender in the familial transmission of mood disorders is unclear. This study examines rates of mood disorder transmission to offspring based on the sex of affected parent, sex of offspring and role of clinical factors, such as childhood abuse history, comorbid psychiatric disorders, and traits of aggression and impulsivity. METHODS: Risk of transmission of mood disorder to offspring from females and males was compared in a sample of 272 probands with a major mood disorder using generalized estimating equations (GEE). Demographic and clinical characteristics of all male and female probands were compared. Characteristics that differed in probands were entered into the model to obtain an unbiased test of gender differences in transmission rate. Multivariate GEE models, one for male probands and one for female probands, were used to test for risk factors in transmission of mood disorder. RESULTS: Familial transmission rate of mood disorders from female probands was almost double that of males. There was no difference in transmission to male or female offspring. For male probands, offspring mood disorder was independently associated with earlier age of proband mood disorder onset, greater number of proband years ill, and proband history of childhood abuse. For female probands, offspring mood disorder was associated with higher aggression scores in probands. LIMITATIONS: We did not directly interview offspring and also had limited data on psychopathology in co-parents. This is a cross-sectional study and cannot account for emergence of illness in offspring in the future. CONCLUSIONS: The two-fold higher rate of maternal transmission of mood disorder may reflect differences in regulation of maternal and paternal transmission of mood disorder. Future studies need to determine the relative contribution of genetic and non-genetic factors and identify the factors responsible for higher rates of transmission of mood disorders by females with a mood disorder.

Adult↗
PubMed1996

Effects of childbearing on the natural history of panic disorder with comorbid mood disorder.

This historical prospective study included 22 women with panic disorder. They experienced 45 pregnancies associated with or after their first lifetime episode of panic disorder. Mood disorder predated or was associated with 32 of these pregnancies. The most common effect of pregnancy was No Change in symptoms from baseline during pregnancy and continued No Change postnatally for both panic attacks (n = 22; 49%) and depression (n = 19; 59%). The pattern of panic attack across gestations was consistent for only 5 of 14 multiparae. An interesting observation was that first lifetime onset of panic disorder was common postpartum (n = 4) or post-miscarriage (n = 2). First-onset depression was also common postpartum (n = 4).

Adult↗
PubMed2000

[Manic-depressive disorders in adolescence. Mood disorders and psychoses in adolescence].

DISEASE ONSET: In adolescents, the different aspects of mood disorders and psychoses are closely related. The first episode of what will become schizophrenia is often suggestive of a mood disorder. The inverse is also true. Frequently, a psychotic state is the inaugural manifestation of a mood disorder. SIGNS AND SYMPTOMS: The depressive manifestations observed in adolescents are very similar to negative psychotic symptoms. More so than in adults, the thymic disorder is expressed as severe episodes of psychosis. It would appear that in this case, the psychotic elements are related to the intensity of the thymic disorder. DIAGNOSTIC ERRORS: Misdiagnosis is probably related to the fact that mood is not sufficiently taken into account in acute psychotic states. The risk inherent in "over"-diagnosis of schizophrenic disorders is related to the therapeutic implications: prescriptions of neuroleptics can hinder the psychic work involved in the structuralization process going on in the adolescent.

Adolescent↗
PubMed1994

Mood Disorder Service Genetic Database: morbidity risks for mood disorders in 3,942 first-degree relatives of 671 index cases with single depression, recurrent depression, bipolar I, or bipolar II.

There is increasing evidence that genetic factors play a role in the etiology of mood disorders. As a result, relatives of affected individuals are more often asking about their own risks to develop a mood disorder. From 1988 to 1990, all consecutive, unrelated inpatients and outpatients (index cases) presenting to the Mood Disorders Service, Department of Psychiatry, University of British Columbia, had detailed family histories taken, thus creating the Mood Disorders Service Genetic Database. Diagnoses for index cases and their first-degree relatives were made according to Research Diagnostic Criteria and Family History Research Diagnostic Criteria respectively. Morbidity risks for mood disorders were calculated for first-degree relatives (parents, siblings, children--aged 10 and above) of all index cases with a diagnosis of single depression, recurrent depression, bipolar I, or bipolar II disorder. Morbidity risks were calculated using the maximum likelihood approach. Morbidity risk data are presented according to the sex and diagnosis for the index case in an easy reference format for risk counselling. The risks are presented twice, including and excluding data for "high-risk" families whose genetic pedigree is suggestive of "autosomal dominant" inheritance.

Age of Onset↗
PubMed1996

Association study of a null mutation in the dopamine D4 receptor gene in Italian patients with obsessive-compulsive disorder, bipolar mood disorder and schizophrenia.

Although serotonergic dysregulation is a leading pathogenetic hypothesis for obsessive-compulsive disorder (OCD), some evidence also suggests a possible dysregulation of the dopaminergic system in this disorder. Therefore, individual differences in deoxyribonucleic acid (DNA) coding for dopamine receptor proteins might contribute to the genetic background of this disorder. Previously we reported a null mutation in exon 1 of the dopamine D4 receptor gene. The variant type is characterized by a 13 bp deletion and is predicted to code for a truncated, non-functional receptor. We assessed the frequency of this polymorphism in 157 OCD patients, 196 schizophrenics, 111 bipolars and 162 healthy controls of Italian descent. Our findings do not implicate a role for this mutation in conferring a susceptibility to OCD and confirm previous negative results regarding its involvement in schizophrenia and bipolar disorder.

Bipolar Disorder↗
PubMed2006

Treatment of co-morbid obsessive compulsive disorder, mood, and anxiety disorders.

In Sumary, OCD, non-OCD anxiety disorders and mood disorders are common co-morbid psychiatric disorders are common co-morbid psychiatric disorders in clinically referred youth with TS. Emotional disorders such as anxiety and depression may be more problematic to the patient than the tics, with regard to overall illness severity and the potential for adverse outcomes, such as school and social failure. The emotional symptoms and co-morbid mood and anxiety disorders must be comprehensively identified because they will require specific intervention and treatment. Treatment must be tailored to each individual, and should ideally include education, monitoring, and prioritization of symptoms based on distress and impairment. There is growing evidence to support the use of several medications, particularly the selective serotonin reuptake inhibitors, and some cognitive behavioral techniques to treat the psychiatric co-morbid disorders.

Anxiety Disorders↗
PubMed1998

Cognitive factors differentiating attention deficit-hyperactivity disorder with and without a comorbid mood disorder.

Mood disorders and attention deficit-hyperactivity disorder (ADHD) co-occur in 20-30% of children and adolescents diagnosed in both epidemiological and clinical studies, but little information is available regarding cognitive factors that may be relevant to the expression of co-occurring mood disorders and ADHD. This study examined whether ADHD with and without a comorbid mood disorder could be differentiated on the basis of cognitive factors associated with prominent theories of depression. Children meeting diagnostic criteria for ADHD (n = 14) or ADHD and a comorbid mood disorder (n = 27) were assessed on a variety of cognitive indices. Children in the comorbid group reported more negative views of themselves and a more depressogenic attributional style. Cognitive disturbances associated with A. T. Beck's (1967) cognitive model and attributional style theories of depression differentiate ADHD children with significant mood pathology.

Adolescent↗
PubMed2001

Review of the role of progesterone in the management of postnatal mood disorders.

Postnatal mood disorders (maternity blues, postnatal depression and puerperal psychosis) are cross-cultural symptoms that are commonly seen in primary care by general practitioners and midwives, by gynecologists and obstetricians, and within the psychiatric services. One of several hypotheses for their causation is falling progesterone levels in the postpartum period. Progesterone supplements are therefore currently used in the treatment of postnatal mood disorders, both in primary and secondary health care settings. The evidence for this is reviewed. The MEDLINE and PSYCHLIT databases from 1966 to 1999 were searched. References reporting observational data on progesterone levels around delivery or therapeutic studies using progesterone were retrieved. Additional references were identified by citation tracking from these and direct contact with available authors. Eight papers were identified. Although there is some weak evidence for its role in maternity blues and some theoretical justification for its use, there is no robust primary research to support the use of progesterone in the treatment of postnatal mood disorders. Progesterone is being used to prevent recurrence of postnatal depression but the evidence supporting its efficacy is lacking. Its use in the treatment of postnatal mood disorders cannot be recommended on the basis of current evidence. Randomized controlled trials are needed to decide if it has a role in the treatment and prevention of postnatal mood disorders.

Depression, Postpartum↗
PubMed1997

Psychobiology of postpartum mood disorders.

Postpartum mood disorders are common. The clustering of mood-disorder episodes after birth compels a search for factors particularly potent during childbearing. In this article, the complex relationships between the dynamic postbirth physiological environment and mood disorder are discussed. Available studies show a lack of evidence that serum levels of gonadal hormones account for mood disturbance in women. However, substantial amounts of data demonstrate their ability to modulate other neuroendocrine systems. Alterations in hypothalamic-pituitary-adrenal (HPA) axis function attributable to childbearing show remarkable similarity to those observed in depressed women. Postpartum women are also at increased risk for hypothalamic-pituitary-thyroidal (HPT) axis dysfunction that may increase affective-disorder vulnerability. A decreased rate of postpartum recovery of HPA- and HPT-axis function may play a more central role than cross-sectional measures. Understanding the etiology of postpartum mood disorders will require integration of multiple psychosocial and biological risk factors. Further research is critically needed.

Adult↗