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PubMed2004

A review of mood disorders among juvenile offenders.

OBJECTIVES: This article provides an overview of what is known about the prevalence, diagnosis, and effective treatment of mood disorders among youths, particularly among juvenile offenders, and discusses the unique problems that arise for the delivery of treatment services. The relationship between mood disorders and disruptive or delinquent behaviors as well as the particular importance of proper diagnosis and treatment of mood disorders in this population are discussed. METHODS: A search was conducted of the MEDLINE and PsycINFO databases for articles that had been published since 1980 on mood disorders in the juvenile offender population as well as articles on adolescent mood disorders. RESULTS: The studies on the prevalence of mood disorders among juvenile offenders varied significantly in the methodology used and in the rates of prevalence found, although all studies showed that this population had high rates of mood disorders. The identification and effective treatment of mood disorders is critical because these disorders are a leading cause of suicide among adolescents and because mood disorders may contribute to or exacerbate delinquent and disruptive behaviors. CONCLUSIONS: Juvenile detainees have a constitutional right to needed mental health treatment. More comprehensive mental health services are required to ensure that juvenile offenders with mental illness are identified and cared for appropriately. Doing so not only will alleviate painful symptoms but may also contribute significantly to improvements in psychosocial functioning, interpersonal relations, and school performance and to decreases in delinquent, disruptive, and suicidal behaviors.

Adolescent↗

PubMed2003

The recognition and management of mood disorders as a comorbidity of epilepsy.

Mood disorders, especially as a comorbid finding in people with medical disorders in general, and in those with epilepsy in particular, have become increasingly recognized as a serious health concern. Unfortunately, affective disorders are underrecognized, and appropriate treatment is infrequent. The consequences of poor detection of mood disorders in people with epilepsy are discussed, along with a review of risk factors and the appearance of the disorder in this population. Prevalence rates of both depressive and bipolar spectrum disorders in people with epilepsy appear to be higher than in the general population. Recent data from community samples show elevated rates of both disorders in people with epilepsy, significantly above those in people with and without other chronic diseases. Assessment issues, including the positive and negative side effects of antiepileptic drugs, are reviewed. Treatment options are discussed, along with caveats concerning the use of antidepressants in people with epilepsy, with a focus on safety, utility, and drug interactions. Electroconvulsive therapy can also be used safely in people with epilepsy, and vagus nerve stimulation may have some utility in the treatment of depressive disorders as well. However, despite improved detection methods and effective treatments, implementation of this knowledge in neurology outpatient clinics is still problematic.

Anticonvulsants↗

PubMed2006

Adult mood disorders and childhood psychological trauma.

OBJECTIVE: To evaluate the association between adult mood disorders and childhood psychological trauma in a developing country. METHOD: Adults with and without mood disorders were assessed in a case-control study using the Mini International Neuropsychiatric Interview. Assessment of childhood trauma included physical and sexual abuse, frequent exposure to violence, and parental loss. RESULTS: In two independent multivariate analyses, after adjusting for potential confounding factors, we found a higher odds ratio for frequent exposure to violence in the community (p = .037) and for physical abuse by parents or caregivers during childhood/adolescence (p = .012) in the group with mood disorders than in the control group. In secondary analyses splitting the mood disorder group in two subgroups (manic episode, and major depressive episodes/ dysthymia), only manic patients showed significantly higher rates of frequent exposure to violence in the community (p = 0.01) and physical abuse during childhood (p = 0.02) than did patients in the control group. In addition, maniac patients had significantly higher rates of sexual abuse than did controls (p = .03). CONCLUSIONS: Our findings document an association between violence during childhood and adult mood disorders, especially for manic patients, in a developing country.

Adult↗

PubMed2004

Migraine headache and mood disorders: a descriptive study in an outpatient psychiatric population.

BACKGROUND: Information is sparse concerning migraine distribution in mood disorder subjects based mainly on psychiatric disorder. METHODS: In a sample of 283 normothymic mood disorder outpatients on maintenance treatment with serotonin reuptake inhibitors (SSRIs) or lithium, we investigated migraine distribution and clinical variables possibly related to comorbidity risk between mood disorder and migraine. RESULTS: Some 26.8% of the sample met criteria for migraine with migraine age of onset earlier than mood disorder age of onset; familiarity for mood disorder and migraine was strictly related to comorbidity risk in probands. Long-term treatment with lithium salts subjectively improved migraine outcome. CONCLUSIONS: These results could support the bidirectional association between the two clinical forms, considering the familial and pharmacological patterns.

Adult↗

PubMed2005

Secular trends in first hospitalizations for major mood disorders with comorbid substance use.

In the past half-century, the incidence of major mood disorders reportedly has risen, and onset age, diminished. Substance-use disorders (SUDs) are commonly comorbid with mood disorders and may influence their course and outcome. Since secular relationships of these disorders remain unknown, we evaluated medical records of 421 patients (233 men, 188 women) at first-lifetime admissions for major depression, mania or mixed bipolar episodes at a public hospital in Italy during 1978-2002, updated diagnoses to DSM-IV criteria, and compared selected factors between subjects with vs. without SUDs, seeking evidence of secular trends in SUDs in association with early mood disorders. SUD was diagnosed in 122 patients (29.0%). SUD risk was greatest in young males. Relative risk (RR) of diagnostic association with SUDs ranked: mixed states (RR 1.80), mania (RR 1.06), depression (RR 0.55). Annual rates of comorbid SUD and mood disorders increased continuously over the 25-yr epoch for all substances (r=0.640, p<0.001). Age at onset of illness and at first hospitalization (averaging 36 yr and 38 yr) were unrelated to year of hospitalization in this relatively brief sampling, but patients with SUD were younger at onset and admission, overall. Clinical Global Impression (CGI) ratings of illness severity at hospitalization and discharge were stable across years. These findings indicate a secular increase of comorbid SUD among first admissions for mood disorder, especially in young males, with a parallel increase in the proportion of bipolar disorder diagnoses over the past quarter of a century.

Adult↗

PubMed2005

[Omega-3 fatty acids in mood disorders].

The etiology and treatment of mood disorders has not yet been elucidated. Omega (omega)-3 fatty acids are essential fatty acids, which cannot be synthesized in the human body. Eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) are representative omega-3 fatty acids which are found in fish (eg., mackerel, herring, Chinook salmon) and vegetables (eg., flax, walnut, canola). The peripheral level of EPA and DHA decrease in patients with major depression, and EPA is useful for its treatment. Further research is required on omega-3 fatty acids in patients with mood disorders.

Fatty Acids, Omega-3↗

PubMed2003

Treatment-refractory mood disorders: a psychodynamic perspective.

Treatment-refractory mood disorders pose a significant problem for clinicians. Although biological approaches are usually emphasized in the treatment of patients with these disorders, preliminary findings from an ongoing, naturalistic, longitudinal study of treatment outcome support the notion that a subset of patients with treatment-refractory mood disorders may respond to careful integration of a psychodynamic therapeutic approach into the customary biological approaches. Ten psychodynamic principles that appear to be useful in work with patients with treatment-refractory mood disorders were identified based on a review of the records of 28 patients who were treated using this approach. These principles are presented, discussed, and illustrated by material from a representative case study.

Journal Article↗

PubMed1993

Seasonal mood disorders. Patterns of seasonal recurrence in mania and depression.

DSM-III-R criteria, applied retrospectively in a research-oriented psychiatric clinic, identified patients (N = 146) with a mood disorder and a seasonal pattern of recurrence (seasonal mood disorder). The seasonal mood disorder syndrome was not rare (10% of all mood disorders); diagnostic distribution was as follows: recurrent depression, 51%, and bipolar disorder, 49%, with 30% of the latter having mania (bipolar disorder type I) and 19% having hypomania (bipolar disorder type II). Most patients were women (71%); onset age averaged 29 years, with a mean of eight cycles in 12 years of illness; mean episode duration was 5.0 months. Mood disorder was found in a high proportion (68%) of the families. All but one patient followed one of two seasonal patterns in equal frequency: type A, fall-winter depression with or without spring-summer mania or hypomania; and type B, spring-summer depression with or without fall-winter mania or hypomania. Both types showed consistent times of onset and remission. These results emphasize that DSM-III-R seasonal mood disorder includes severe cases of recurrent depression and bipolar disorder and support a distinction between two seasonal subtypes.

Adult↗

PubMed1999

Association analysis of the 5-HT(6) receptor polymorphism (C267T) in mood disorders.

The serotonergic system is implicated in the etiology of mood disorders. Among those most recently discovered serotonin receptors, the relative abundance of serotonin type 6 receptor (5-HT(6)) in the limbic area and the high affinity of some antidepressants to 5-HT(6) receptors suggest that this receptor might be involved in the pathogenesis of mood disorders. In a population-based association study, we tested the hypothesis that the allelic variant (C267T) of the human 5-HT(6) gene confers susceptibility to mood disorders. We genotyped the 5-HT(6) receptor in 139 patients with mood disorders and 147 controls. The results demonstrated that there were no significant differences in genotype or allele frequencies between controls and all patients, or between controls and patients with bipolar disorders or major depression, separately. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:601-602, 1999.

Adult↗

PubMed2002

The neuropathology of primary mood disorder.

The biological mechanisms proposed to underlie primary mood disorder do not usually include a neuropathological component. However, a significant MRI literature attests to structural abnormalities in regions and has encouraged neuropathological investigations from which candidate histological correlates have begun to emerge. In particular, there are several reports of cytoarchitectural alterations in anterior cingulate and prefrontal cortices, characterized by a decrease in the number or density of glia. Reductions in the size and density of some neuronal populations have also been described, accompanied by alterations in indices of synaptic terminals and dendrites. This form of pathology putatively reflects aberrant neurodevelopment or impaired cellular plasticity. A separate pathological process is suggested by the excess of subcortical focal lesions seen on MRI, especially in elderly patients; these probably reflect white matter damage of vascular origin. Both types of pathology have been observed, to a greater or lesser extent, in unipolar as well as bipolar mood disorders. None of the findings appear attributable to treatment with antidepressants, mood stabilizers or electroconvulsive therapy (ECT). However, all findings remain preliminary due to a lack of unequivocal replication and the failure to control fully for other potential confounders and co-morbid conditions. There are also basic questions to be answered concerning the clinical correlates, magnitude, progression and heterogeneity of the pathology. Nevertheless, it must now be considered likely that changes in brain structure, both macroscopic and microscopic, are a feature of primary mood disorder, a fact to be taken into account when interpreting functional imaging, neuropsychological and neurochemical data. The neuropathology is postulated to contribute to the pathophysiology and dysfunction of the neural circuits which regulate mood and its associated cognitions, behaviours and somatic symptoms.

Brain↗

PubMed2001

Self-care agency and symptom management in patients treated for mood disorder.

Symptom management of patients with mood disorder, such as depression and bipolar disorder, influences quality of life and relapse. This article describes a study of symptom recognition and management and the ability of self-care agency to predict symptom management. A purposive sample of 45 subjects was studied. Step-wise multiple regression analyses of self-care agency with symptom management resulted in self-care agency explaining 37% of the variance in symptom management at 2 months posthospitalization. Patients with mood disorders have long-term vulnerability for relapse after hospital stabilization. Nurses need to continue to find ways to assess and strengthen symptom management and self-care in these relapse-prone individuals.

Follow-Up Studies↗

PubMed1999

No association between serotonin-2A receptor gene polymorphism and psychotic symptomatology of mood disorders.

Abnormalities of the serotonergic system are involved in the pathophysiology of mood disorders. In the present study, we investigated the possible influence of the T102C polymorphism of the serotonin-2A receptor gene (5-HT2A, 13q14-21) on the symptomatology of mood disorders. Inpatients affected by mood disorders (n = 246, 149 bipolar, 97 major depressive disorder) were assessed with a checklist of operational criteria for psychotic illness (OPCRIT) to score their lifetime psychotic symptomatology. The subjects were also typed for 5-HT2A variants using polymerase chain reaction techniques. No association was found between this polymorphism and psychopathology as defined by the four symptomatologic factors used in phenotype definition (mania, depression, delusion and disorganization). Genetic variation at the 5-HT2A receptor gene does not, therefore, appear to play a major role in the pathogenesis of major mood disorders.

Adult↗

PubMed1999

Cocaine-induced mood disorder: prevalence rates and psychiatric symptoms in an outpatient cocaine-dependent sample.

This paper attempts to examine and compare prevalence rates and symptom patterns of DSM substance-induced and other mood disorders. 243 cocaine-dependent outpatients with cocaine-induced mood disorder (CIMD), other mood disorders, or no mood disorder were compared on measures of psychiatric symptoms. The prevalence rate for CIMD was 12% at baseline. Introduction of the DSM-IV diagnosis of CIMD did not substantially affect rates of the other depressive disorders. Patients with CIMD had symptom severity levels between those of patients with and without a mood disorder. These findings suggest some validity for the new DSM-IV diagnosis of CIMD, but also suggest that it requires further specification and replication.

Adult↗

PubMed2006

Reduced Glucocorticoid Receptor alpha Expression in Mood Disorder Patients and First-Degree Relatives.

BACKGROUND: Individuals with mood disorders exhibit altered function of the hypothalamic-pituitary-adrenal (HPA) axis in response to stress. The glucocorticoid receptor (GR) plays an important role in the negative feedback regulation of the HPA axis. There are two protein isoforms of GR, GRalpha and GRbeta, which have distinct biological activity. It has not been examined whether GRalpha messenger RNA (mRNA) and GRbeta mRNA expressions are altered in peripheral blood cells of mood disorder patients. METHODS: Using quantitative reverse transcription polymerase chain reaction (RT-PCR), GRalpha mRNA and GRbeta mRNA were measured in peripheral blood cells of major depressive disorder patients (depressive n = 18; remissive n = 38), bipolar disorder patients (depressive n = 13; remissive n = 35), normal control subjects (n = 31), and first-degree relatives of major depressive (n = 17) and bipolar (n = 15) disorder patients. RESULTS: Reduced expression of GRalpha mRNA was shown in both bipolar and major depressive disorder patients in a current depressive state as well as in remission. First-degree relatives of bipolar disorder patients also showed GRalpha mRNA reduction. Altered GRbeta mRNA expression was not found in mood disorder patients. CONCLUSIONS: Our results suggest that reduced GRalpha mRNA expression might be trait-dependent and associated with the pathophysiology of mood disorders.

Adult↗

PubMed2004

Inter-episode mood lability in mood disorders: residual symptom or natural course of illness?

Residual depressive symptoms are common in mood disorders. Inter-episode mood lability (IML; i.e. frequent ups and downs of mood) is understudied as a possible residual symptom. The study aim was to find the frequency of IML, and to find if it was more likely to be a residual symptom or if it was instead part of the natural course of mood disorders. Consecutive 89 bipolar-II (BP-II) and 89 major depressive disorder (MDD) outpatients who were not on psychoactive drugs, were interviewed by the Structured Clinical Interview for the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders as modified by Benazzi and Akiskal. Kraepelin's basic definition of IML (i.e. frequent up and down fluctuations of mood between episodes) was followed. IML was present in 48.3% of the patients, significantly more common in BP-II than in MDD (62.9% vs. 33.7%, P= 0.000). The sample of BP-II and MDD plus IML, versus the sample BP-II and MDD without IML, had significantly more BP-II, lower age at onset, longer illness duration, more depressive recurrences, more depressions with atypical features, more depressive mixed states, and more family history of mood disorders. Logistic regression of IML versus recurrences, controlled for duration of illness, found odds ratio = 1.8, z= 1.6, P= 0.103. Forward stepwise multiple logistic regression of IML versus the variables found significant in the univariate analysis, showed that only BP-II (P = 0.002) and duration of illness (P = 0.015) were significant predictors of IML. IML was common in mood disorder outpatients. Its association with BP-II (an unstable disorder by definition) and duration of illness (but not with recurrences when controlled for illness duration), suggest that IML may be more likely to be part of the natural course of illness than the result of kindling induced by recurrences. Its association with depressive mixed state (a depression reported to be more difficult to treat) and the possibility that it may induce/facilitate recurrences (to be shown by prospective studies), support the need to better study IML for its possible important impact on treatment.

Adult↗

PubMedDate not supplied

Influence of 5-HTTLPR and TPH variants on illness time course in mood disorders.

The aim of our study was to investigate gene variants in the long-term outcome of mood disorders. We retrospectively studied a sample of inpatients affected by recurrent and rapid cycling mood disorders. The serotonin transporter gene-linked functional polymorphic region (5-HTTLPR) and the A218C tryptophan hydroxylase (TPH) gene variant were determined using a PCR-based technique. For 5-HTTLPR polymorphism we genotyped 435 inpatients affected by major depressive (n=153), bipolar (n=213) and rapid cycling (n=69) mood disorders and 456 controls; for TPH we genotyped 399 inpatients (MD, n=132; BP, n=203; rapid cycling n=64) and 259 controls. Random Regression Model analysis was used to investigate the longitudinal time course of the illness. 5-HTTLPR and TPH polymorphisms were not associated with mood disorders time course. However we observed an excess of 5-HTTLPR*long alleles among rapid cycling subjects compared to both controls (P=0.018) and remitting mood disorders (P=0.006). TPH frequencies did not differ between mood disorders subtypes. Our results suggest that 5-HTTLPR variants may confer a susceptibility toward rapid cycling mood disorders.

Adult↗

PubMed2003

GABAergic dysfunction in mood disorders.

The authors review the available literature on the preclinical and clinical studies involving GABAergic neurotransmission in mood disorders. Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter present almost exclusively in the central nervous system (CNS), distributed across almost all brain regions, and expressed in interneurons modulating local circuits. The role of GABAergic dysfunction in mood disorders was first proposed 20 years ago. Preclinical studies have suggested that GABA levels may be decreased in animal models of depression, and clinical studies reported low plasma and CSF GABA levels in mood disorder patients. Also, antidepressants, mood stabilizers, electroconvulsive therapy, and GABA agonists have been shown to reverse the depression-like behavior in animal models and to be effective in unipolar and bipolar patients by increasing brain GABAergic activity. The hypothesis of reduced GABAergic activity in mood disorders may complement the monoaminergic and serotonergic theories, proposing that the balance between multiple neurotransmitter systems may be altered in these disorders. However, low GABAergic cortical function may probably be a feature of a subset of mood disorder patients, representing a genetic susceptibility. In this paper, we discuss the status of GABAergic hypothesis of mood disorders and suggest possible directions for future preclinical and clinical research in this area.

Brain Chemistry↗

PubMed2002

Etiology and genetics of early-onset mood disorders.

Most studies dealing with the familiality and genetics of mood disorders have been limited to adults, but several studies suggest that there is continuity between childhood- and adolescence-onset depression and mania and adult illness. More direct estimates of the heritability of depressive symptoms or episodes in children and adolescents indicate that the genetic contributions may be greater than 50%. A number of functional and structural imaging studies have identified particular circuitry as being involved in the generation of emotion and mood disorders. Imaging studies of twins have suggested that regional brain volume and characteristics of brain shape are heritable. A potentially important new avenue of research will be the correlation of the genetics of brain structure or function with the genetics of mood disorders. Preliminary studies of adolescent and young adult twins suggest a significant correspondence between the genetic contributions to some regional brain volumes and early-onset mood disorders.

Adolescent↗