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Bupropion in the long-term treatment of cyclic mood disorders: mood stabilizing effects.

The effects of bupropion HCl in treating 11 patients with bipolar or schizoaffective disorder were examined in an open trial. Most patients had been intolerant of or showed minimal to moderate improvement on lithium, neuroleptics, antidepressants, or a combination of these drugs. All patients were maintained on bupropion alone or bupropion in combination with low-dose neuroleptics or anxiolytics for 1 year or more, with little or no relapse and few side effects.

Adult↗

Sleep and mood disorders.

Mood disorders are found in one-third to one-half of patients with chronic sleep problems. Likewise, most patients with mood disorders experience insomnia, but a minority obtain significantly increased amounts of sleep. Although mood disorders cause significant morbidity and mortality, they often go undiagnosed. Attention to sleep complaints could lead to better identification of mood disorders. Management of sleep problems in patients with mood disorders should focus on treating underlying mood disorders with attention to the nature of the sleep complaint. Patients with depression show characteristic abnormalities in sleep continuity, slow-wave sleep and REM sleep patterns. Differences in sleep patterns cannot reliably distinguish patients with depression from those with other psychiatric disorders, but sleep changes may provide a window on neurobiologieal abnormalities in depression.

Journal Article↗

Family study of the aggregation of eating disorders and mood disorders.

BACKGROUND: Family studies have suggested that eating disorders and mood disorders may coaggregate in families. To study further this question, data from a family interview study of probands with and without major depressive disorder was examined. METHOD: A bivariate proband predictive logistic regression model was applied to data from a family interview study, conducted in Innsbruck, Austria, of probands with (N = 64) and without (N = 58) major depressive disorder, together with 330 of their first-degree relatives. RESULTS: The estimated odds ratio (OR) for the familial aggregation of eating disorders (anorexia nervosa, bulimia nervosa and binge-eating disorder) was 7.0 (95 % CI 1.4, 28; P = 0.006); the OR for the familial aggregation of mood disorders (major depression and bipolar disorder) was 2.2 (0.92, 5.4; P = 0.076); and for the familial coaggregation of eating disorders with mood disorders the OR was 2.2 (1.1, 4.6; P = 0.035). CONCLUSIONS: The familial coaggregation of eating disorders with mood disorders was significant and of the same magnitude as the aggregation of mood disorders alone--suggesting that eating disorders and mood disorders have common familial causal factors.

Adult↗

Social adjustment and self-esteem in remitted patients with mood disorders.

Mood disorders are characterized by manic and depressive episodes alternating with normal mood. While social function is heavily impaired during episodes of illness, there are conflicting opinions about inter-episode function. The present paper focuses on self-esteem and social adjustment in remitted mood disorders patients. Patients with mood disorders (99 bipolar and 86 major depressive subjects, in remission) were compared with a group of 100 control subjects. The self-esteem scale (SES) and the social adjustment scale (SAS) were used to measure self-esteem and social adjustment, respectively, in both groups of subjects. Patients with mood disorder exhibited worse social adjustment and lower self-esteem than control subjects. These results strongly confirm previous observations of poor inter-episode function in patients with mooddisorder.

Adult↗

[Molecular genetics of mood disorders].

Mood disorders are common diseases and cause a big burden on society, including suicide. Because there are many treatment resistant cases in mood disorders, it is very important to elucidate the pathophysiology of this condition to establish its prevention and its treatment. Genetic epidemiological studies have shown that genetic factors have an important role in the pathophysiology of mood disorders; therefore the molecular genetics studies of this condition have been extensively performed, such as positional approach (i.e., linkage study) and candidate gene approach (i.e., association study). Linkage studies have shown some candidate locations that have been reproduced in two or more studies, such as 1q21-42, 4p16, 10q21-26, 11p15, 12q23-24, 13q11-32, 18p11, 18q21-22, 22q11-13, Xp11, and Xq24-28. Most association studies have until now focused on the neurotransmitter system as a candidate molecule including serotonin transporter, serotonin receptors, dopamine receptors, tyrosine hydroxylase, MAO-A, COMT, and tryptophan hydroxylase. Moreover, phamacogenetic studies also have been carried out in this field to develop new drugs as well as personalized medicine. Future molecular genetic studies will find out the mood-disorder susceptible genes and open the gate to true treatment and prevention of this disorder as the Human Genome Project attains its goal.

Drug Design↗

The functional neuroanatomy of mood disorders.

Mood disorders may be associated with global and regional changes in cerebral blood flow and metabolism. The accumulated functional neuroimaging findings in mood disorders were reviewed in order to examine a proposed neuroanatomic model of pathophysiology. Global cerebral blood flow and glucose metabolism appear normal, but may be decreased in late-life depression. Regional cerebral blood flow and glucose metabolism deficits are present, and may be indicators of brain regions participating in neuroanatomic circuits involved in mood disorders. Decreased pre-frontal cortex blood flow and metabolism in depressed unipolar and bipolar patients are the most consistently replicated findings, and correlate with severity of illness. Basal ganglia abnormalities have been found in depressed unipolar and bipolar patients, involving decreased blood flow and metabolism. Temporal lobe abnormalities are present in bipolar disorder patients, and perhaps unipolar depression. There is conflicting evidence of abnormalities in other limbic regions. Cognitive impairment may correlate with decreased metabolism in frontal and cerebellar areas. The relationship between functional neuroimaging findings and clinical course, and therefore state and trait characteristics, has not been systematically investigated. Antidepressant medications, but not ECT, seem to reverse some of the identified functional brain changes in the depressed state. The structural, neurotransmitter and neuropathological correlates of these functional abnormalities are yet to be determined. Functional abnormalities in frontal, subcortical and limbic structures appear to be part of the pathophysiology of mood disorders.

Adult↗

Anxiety disorders comorbidity in mood disorder subgroups: data from a mood disorders clinic.

BACKGROUND: Previous research has identified a high rate of anxiety disorders comorbidity in patients with a primary mood disorder diagnosis. Discrepancies between studies in the comorbidity prevalence of specific anxiety disorders in mood disorders, and of anxiety disorders comorbidity between unipolar depression and bipolar mood disorder are in part due to differences in sampling and diagnostic assessment methodology. METHOD: The authors reviewed the charts of 138 patients who received the SCID-P for DSM-III on enrollment in a Mood Disorders Clinic during the period 1982 through 1988. The comorbidity of specific DSM-III Anxiety Disorders with specific mood disorders was determined and comparatively examined using non-parametric statistics. RESULTS: There was high overall comorbidity of anxiety disorders that did not differ between bipolar and unipolar subjects. There were no differences in the comorbidity of individual anxiety disorder diagnoses in the unipolar vs. bipolar groups. However, in unipolar patients with, compared to those without an additional diagnosis of dysthymia, there was greater overall anxiety disorders comorbidity, with a particularly high prevalence of generalized anxiety disorder. LIMITATION: The subgroup of patients with bipolar I disorder was relatively small (N=8). CONCLUSION: Mood and anxiety disorders comorbidity is complex and presents a continuing challenge for both clinicians and researchers.

Adult↗

Glial reduction in the subgenual prefrontal cortex in mood disorders.

Mood disorders are among the most common neuropsychiatric illnesses, yet little is known about their neurobiology. Recent neuroimaging studies have found that the volume of the subgenual part of Brodmann's area 24 (sg24) is reduced in familial forms of major depressive disorder (MDD) and bipolar disorder (BD). In this histological study, we used unbiased stereological techniques to examine the cellular composition of area sg24 in two different sets of brains. There was no change in the number or size of neurons in area sg24 in mood disorders. In contrast, the numbers of glia were reduced markedly in both MDD and BD. The reduction in glial number was most prominent in subgroups of subjects with familial MDD (24%, P = 0.01) or BD (41%, P = 0.01). The glial reduction in subjects without a clear family history was lower in magnitude and not statistically significant. Consistent with neuroimaging findings, cortical volume was reduced in area sg24 in subjects with familial mood disorders. Schizophrenic brains studied as psychiatric controls had normal neuronal and glial numbers and cortical volume. Glial and neuronal numbers also were counted in area 3b of the somatosensory cortex in the same group of brains and were normal in all psychiatric groups. Glia affect several processes, including regulation of extracellular potassium, glucose storage and metabolism, and glutamate uptake, all of which are crucial for normal neuronal activity. We thus have identified a biological marker associated with familial mood disorders that may provide important clues regarding the pathogenesis of these common psychiatric conditions.

Adult↗

[Comorbidity between eating disorders and mood disorders: review].

OBJECTIVE: Comorbidity between eating disorders (ED) and mood disorders is a major issue when evaluating and treating patients with anorexia nervosa (AN) or bulimia nervosa (BN). In the literature, estimated comorbidity rates of mood disorders in subjects with ED differ widely across studies. Obviously, it is difficult to compare results from various sources because of differences in methods of assessment of depressive symptoms and in diagnostic criteria for both ED and mood disorders. Furthermore, few studies have included control groups, and, since mood disorders are among the most frequent psychiatric disorders in women--with an average estimated lifetime prevalence of 23.9 % (Kessleret al., 1994)--, it is not clear, yet, whether mood disorders are more common among women with an ED (AN or BN) than among women from the community. The only review articles we found on the relationships between ED and mood disorders survey different types of arguments in favour of a link between both categories of disorders, including symptoms, personal and family comorbidity, overlap in biological findings, and treatment results, but do not review in detail available comorbidity data. The aim of this paper is to conduct a critical literature review on studies assessing the prevalence of mood disorders in subjects with an ED (AN or BN). In the first part, we will discuss methodological issues relevant to comorbidity studies between ED and mood disorders, and select the most reliable studies. In the second part, taking into account these methodological considerations raised, we summarize the findings of these studies. METHOD: We performed a manual and computerized search (Medline) for all published studies on comorbidity between ED and AD, limiting our search to the 1985-2002 period, in order to get sufficiently homogeneous diagnostic criteria for both categories of disorders. RESULTS: Too few studies include control groups and few studies have compared diagnostic subgroups of ED subjects, with scarce or conflicting results. DISCUSSION: We reviewed numerous studies here and conclude simply that there are many arguments in favor of elevated rates of MD in ED subjects, but there is no convincing evidence yet. Many questions are left unanswered or have conflicting responses. Our review highlights the need for further studies, which should address several requisites: comorbidity studies should be designed with this as a specific goal, rather than as a secondary aim within other types of studies (such as treatment studies, follow-up studies, etc.). Kendler et al. (1991) state that individuals with two disorders are more likely to present for treatment than individuals with one, therefore, comorbidity rates (which are not in agreement with a special etiologic relationship between BN and depression) may be exaggerated in clinical population results. New studies should include control subjects, matched (at least) for sex and age with ED subjects. Studies should evaluate prevalence of all types of MD in order to yield comparable estimates of MD in general. Comorbidity studies should be conducted on both current and recovered patients, compared to subjects from the community. It is still necessary to demonstrate specificity of findings, i.e. that early onset MD are of specific etiological importance to ED and do not simply increase the risk of later psychopathology in general. Studies should be conducted on larger samples, and all diagnostic subgroups should be considered (restrictive and bulimic anorexics, bulimics with and without history of AN, with or without purging). Multivariate comparisons should be performed, taking into account subject age, sex (if men are included), in- and outpatient status, course of illness, and other possibly relevant variables. Thus, more reliable estimates of the frequency of MD in subjects with ED could provide us with valuable etiologic, therapeutic and prognostic information.

Comorbidity↗

Hippocampal remodeling and damage by corticosteroids: implications for mood disorders.

Mood disorders are common, recurrent and disabling illnesses which are frequently associated with hypothalamic-pituitary-adrenal (HPA) axis dysregulation and memory loss. The hippocampus provides negative feedback to the HPA axis and has an important role in key aspects of spatial and declarative memory. Thus, hippocampal dysfunction could account for both the memory impairment and neuroendocrine abnormalities found in mood disorders. The critical role of the hippocampus in declarative memory, emotional processing, and vulnerability to stress has been demonstrated in both animal and human studies. Cellular processes in the hippocampus including long-term potentiation, neurogenesis, and dendritic remodeling are currently areas of intense study. Human studies report cognitive impairment consistent with hippocampal dysfunction in depression, bipolar disorder, Cushing's disease, and in those individuals receiving exogenous corticosteroids. This review examines data on the role of corticosteroids in hippocampal remodeling and atrophy in patients with mood disorders. Interventions to prevent or reverse the damaging effects of corticosteroids on the hippocampus are discussed.

Adrenal Cortex Hormones↗

Development and validation of a screening instrument for bipolar spectrum disorder: the Mood Disorder Questionnaire.

OBJECTIVE: Bipolar spectrum disorders, which include bipolar I, bipolar II, and bipolar disorder not otherwise specified, frequently go unrecognized, undiagnosed, and untreated. This report describes the validation of a new brief self-report screening instrument for bipolar spectrum disorders called the Mood Disorder Questionnaire. METHOD: A total of 198 patients attending five outpatient clinics that primarily treat patients with mood disorders completed the Mood Disorder Questionnaire. A research professional, blind to the Mood Disorder Questionnaire results, conducted a telephone research diagnostic interview by means of the bipolar module of the Structured Clinical Interview for DSM-IV. RESULTS: A Mood Disorder Questionnaire screening score of 7 or more items yielded good sensitivity (0.73) and very good specificity (0.90). CONCLUSIONS: The Mood Disorder Questionnaire is a useful screening instrument for bipolar spectrum disorder in a psychiatric outpatient population.

Adolescent↗

[Modern aspects of mood disorders].

Mood disorders, particularly depression, now represent a major world health problem which will most likely continue increasing. From a clinical standpoint, the synthesis of new antidepressant agents of various chemical structures and the advent of the thymoregulators (lithium salts) has allowed a more flexible, better individualized, therapeutic approach to the affective disorders. However, the widespread use by general practitioners of the antidepressants, alone or in combination with other psychotropic drugs, often with mitigated success, brings to psychiatric consultation patients whose symptomatology has become less characteristics, is more difficult to identify rapidly, requiring thus greater diagnositc refinement. Moreover, greater attention is currently given to depressive affects that can occur during organic illnesses or at various periods of life, particularly at senescence. Besides sustained concerns concerning suicide, the attitude of man confronted with his death arouses great interest and a depressive phase constitutes one of the steps towards this ending. Finally, during the last two decades, some psychoanalysts have reexamined the psychodynamic concepts of mood disorders, whereas from behavioral and cognitive theories new techniques of treatment of depression have emerged. In brief, if no revolution has occurred, there has been evolution. Mood disorders and their approach have known modifications and some concepts pertinent to this are considered here from various angles, particularly from the clinical (association with organic illnesses, with respect to death), therapeutic (psychopharmacological, behavioral and cognitive therapies), sociological (including suicide) and psychoanalytic viewpoints.

Antidepressive Agents, Tricyclic↗

Treatment of insomnia in patients with mood disorders.

Mood disorders and chronic insomnia share complex theoretical and clinical relationships. This article reviews the subjective symptoms and polysomnographic findings of subjects with mood and insomnia syndromes. The polysomnographic findings reviewed include macro-architectural and micro-architectural data. Various treatments of patients with insomnia and mood disorders will be presented, including both behavioral and pharmacological interventions.

Antidepressive Agents↗

Mood Disorders Secondary to Demyelinating and Movement Disorders.

Mood disorders are recognized in several neurologic diseases. This chapter reviews three specific disorders, Parkinson's disease, Huntington's disease, and multiple sclerosis. The demographics of mood disorders and unique clinical characteristics are discussed for each disease. The possible causes for neurobiologically based affective symptoms are explored.

Journal Article↗

Dental implications of mood disorders.

Mood disorders refers to a heterogenous group of mental conditions characterized by extreme exaggeration and disturbance of mood and affect. This article examines major depression and bipolar disorders and how these disorders can affect a patient's dental care. The drugs used to treat these conditions have significant side effects that dentists should be aware of. In addition, important drug interactions can occur as a result of agents used by the dentist. The dentist should refer patients found with signs and symptoms of mood disorders for medical evaluation and treatment. Depressed patients often have poor oral hygiene due to a lack of interest in self-care. Xerostomia occurs due to depression and the drugs used to treat it. The dentist needs to provide an aggressive preventive dental education program for these patients, including the use of artificial salivary products, mouthwashes, and topical fluoride applications, in addition to the treatment of candidiasis when present.

Antidepressive Agents↗

Obsessive compulsive disorder and mood disorders: a family study.

Obsessive compulsive disorder (OCD) often coexists with major depression (MD), with rates varying from 35 to 75%. The nature of the depressive symptomatology can be investigated by familial aggregation analysis, assuming that the disorder which occurs first is the one showing greater genetic liability and should have higher familial concentration. Therefore, the aim of our study was to assess the familial loading for OCD and mood disorders in the families of OCD patients with different chronology of onset for the mood disorder, to evaluate how the familial pattern of the diseases differs with different temporal sequences in which the two syndromes occur. A total of 172 OCD patients entered the study; 112 were pure OCD probands, 12 were unable to separate the onset of the two syndromes, 11 had prior mood disorder, and 37 of them had experienced their first depressive episodes after the onset of OCD. Information about the family history was collected by means of the Family History-Research Diagnostic Criteria (FH-RDC) and by directly interviewing at least 2 relatives per family. Morbidity risks for OCD indicate a familial concentration of the disorder in all groups, except the MD/OCD group. We found the highest rate of relatives affected by mood disorders in the families of patients with first onset of MD (28.8%), whereas in the other 3 groups MRs were much lower. These results suggest the affective nature of OCD patients who experienced first onset of MD. Thus, the chronology of onset seems to identify 2 different typologies of familial distribution.

Adult↗

Bupropion SR for the treatment of substance-abusing outpatient adolescents with attention-deficit/hyperactivity disorder and mood disorders.

OBJECTIVE: Few studies exist on pharmacological interventions for adolescents with substance use disorders (SUD). To this end, we evaluated the response of bupropion hydrochloride sustained release (SR) in SUD adolescents with comorbid psychopathology (both attention-deficit/ hyperactivity disorder (ADHD) and a mood disorder). METHODS: Fourteen adolescent outpatients were treated naturalistically and followed openly for 6 months. Adolescents were rated using the Drug Use Screening Inventory--Revised (DUSI-R), ADHD Symptom Checklist, and the Hamilton Rating Scale for Depression (HAM-D). Clinical Global Impression (CGI) Scale scores were obtained for Substance Abuse, ADHD, Anxiety, and Depression. The ratings were completed at baseline, at month 3, and at the 6-month endpoint. Bupropion SR was initiated at 100 mg once-daily and titrated naturalistically to a maximum dose of 400 mg/day. RESULTS: Of the 14 subjects followed, 13 subjects completed 6 months of treatment. At the 6- month endpoint compared to baseline, treatment with bupropion was associated with clinical and significant reductions in DUSI scores (-39%; p < 0.05), ADHD symptom checklist (-43%; p < 0.001), HAM-D (-76%; p < or = 0.001); and reductions in the CGIs for ADHD (p < or = 0.001), depression (p < or = 0.001), and substance abuse (p < 0.05). The mean daily dose of bupropion SR was 315 mg (in divided doses). No significant adverse events were noted during the follow-up period. CONCLUSIONS: These naturalistic data suggest that bupropion is well tolerated and may be an effective medication for the treatment of substance abusing adolescents with comorbid mood disorders and ADHD.

Adolescent↗

Functional gastrointestinal disorders and mood disorders in patients with inactive inflammatory bowel disease: prevalence and impact on health.

BACKGROUND: Symptoms of functional gastrointestinal disorders (FGID) associated with mood disorders (MD), such as depression and anxiety, occur in some patients with quiescent inflammatory bowel disease (IBD) and could be caused by changes in gut motility, visceral hypersensitivity, or psychological dysfunction. We assessed the prevalence of FGID symptoms and mood disorders in ambulatory patients with quiescent IBD and examined their impact on health-related quality of life (HRQOL) and use of health resources. METHODS: Consecutive ambulatory patients with IBD completed a survey of Rome II criteria for FGID, the Hospital Anxiety and Depression Survey, HRQOL indices, and health resource utilization. Logistic and linear regression analyses tested for predictors of FGID and HRQOL. RESULTS: Of 361 patients surveyed, 149 (44 ulcerative colitis [UC] and 105 Crohn's disease [CD]) had inactive IBD during the previous 12 months. Symptoms of at least 1 FGID occurred in 81.9%. Functional anorectal disorders were the most prevalent (53.7%) followed by functional bowel disorders (51.7%), and both were of greater prevalence than in the Canadian population (41.6% and 22.6%, respectively). Irritable bowel syndrome symptoms were more common in inactive CD than in UC (26% versus 9.1%, P = .01) and functional constipation was more common in inactive UC than in CD (26.2% versus 5.8%, P < .01). MD occurred in 27.3% of UC and 31.3% of CD patients. Age > or =40 years and anxiety independently predicted an FGID. Both FGID symptoms and MD were associated with impaired HRQOL and increased use of health services. CONCLUSIONS: Many patients with inactive IBD have symptoms compatible with FGID. Both FGID-like symptoms and MD are associated with impaired HRQOL and increased health resource utilization. Recognition and treatment of FGID and MD could potentially improve daily functioning of IBD patients.

Adult↗