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PubMed2001

Predictions and associations of fatigue syndromes and mood disorders that occur after infectious mononucleosis.

BACKGROUND: Certain infections can trigger chronic fatigue syndromes (CFS) in a minority of people infected, but the reason is unknown. We describe some factors that predict or are associated with prolonged fatigue after infectious mononucleosis and contrast these factors with those that predicted mood disorders after the same infection. METHODS: We prospectively studied a cohort of 250 primary-care patients with infectious mononucleosis or ordinary upper-respiratory-tract infections until 6 months after clinical onset. We sought predictors of both acute and chronic fatigue syndromes and mood disorders from clinical, laboratory, and psychosocial measures. FINDINGS: An empirically defined fatigue syndrome 6 months after onset, which excluded comorbid psychiatric disorders, was most reliably predicted by a positive Monospot test at onset (odds ratio 2.1 [95% CI 1.4-3.3]) and lower physical fitness (0.35 [0.15-0.8]). Cervical lymphadenopathy and initial bed rest were associated with, or predicted, a fatigue syndrome up to 2 months after onset. By contrast, mood disorders were predicted by a premorbid psychiatric history (2.3 [1.4-3.9]), an emotional personality score (1.21 [1.11-1.35]), and social adversity (1.7 [1.0-2.9]). Definitions of CFS that included comorbid mood disorders were predicted by a mixture of those factors that predicted either the empirically defined fatigue syndrome or mood disorders. INTERPRETATION: The predictors of a prolonged fatigue syndrome after an infection differ with both definition and time, depending particularly on the presence or absence of comorbid mood disorders. The particular infection and its consequent immune reaction may have an early role, but physical deconditioning may also be important. By contrast, mood disorders are predicted by factors that predict mood disorders in general.

Chi-Square Distribution↗

PubMed2003

Detection of anti-Borna Disease Virus (BDV) antibodies from patients with schizophrenia and mood disorders in Japan.

The relationship between infection with the Borna Disease Virus (BDV) and the clinical symptoms of schizophrenia and mood disorders (DMS-IV) was investigated. Western blotting techniques were used to examine anti-p10-BDV antibodies in serum from 32 patients with schizophrenia and 33 patients with mood disorders in Japan. The results showed that 1 out of 25 controls (4.0%), 7 out of 32 patients with schizophrenia (21.9%) and 9 out of 33 patients with mood disorders (27.3%) were positive for anti-BDV-p10 antibodies. Compared with levels of anti-BDV-p10 antibodies in controls, the production of anti-BDV-p10 antibodies failed to show a statistically significant relationship with schizophrenia but did show a significant relationship with mood disorder. The subgroup of schizophrenia patients with positive syndromes had a non-significantly higher frequency of anti-BDV-p10 antibodies than the subgroup of patients with negative syndromes. Similarly, the production of anti-BDV-p10 antibodies was non-significantly higher among patients with the unipolar subtype of mood disorder than in those with the bipolar subtype.

Adolescent↗

PubMed2007

Suicide risk in mood disorders.

PURPOSE OF REVIEW: The aim of this review is to highlight the traditional and newly recognized suicide risk factors in patients with mood disorders. RECENT FINDINGS: Current research findings clearly suggest that suicidal behaviour in patients with mood disorder is a 'state-dependent' phenomenon. Recently, there is, however, a growing body of evidence that besides the well accepted clinically explorable suicide risk factors in mood disorders (e.g., severe depression, prior suicide attempt, comorbid anxiety, substance use, personality disorders and so on), mixed state of depression could also be an important precursor of suicidal behaviour. This might be particularly true in unrecognized cases of bipolar depressives, when antidepressant monotherapy (unprotected by mood stabilizers or atypical antipsychotics) can worsen the clinical picture and rarely induce an aggressive or self-destructive behaviour. SUMMARY: In the majority of patients with mood disorders, suicidal behaviour is predictable and preventable, with a good chance. A careful and systematic exploration of suicide risk factors in patients with mood disorder helps clinicians to identify patients at high suicide risk. A successful, acute and long-term treatment of these patients substantially reduces the suicidal behaviour even in this high-risk population.

Adolescent↗

PubMedDate not supplied

The efficacy and use of anticonvulsants in mood disorders.

Carbamazepine and valproate have utility in the acute and prophylactic treatment of mood disorders that appears comparable with that of lithium, but there are emerging differences as well, including responsiveness in some lithium-nonresponsive illness subtypes. Carbamazepine and valproate are generally well tolerated, but each has its own adverse effect profile and proclivity for pharmacokinetic interactions. The high potency (anticonvulsant) benzodiazepines have utility in mood disorders as adjuncts to mood stabilizers and often can obviate the need for neuroleptics. Several small studies suggest that the dihydropyridine L-type calcium channel blockers can be useful mood stabilizers, and several new antiepileptic agents, especially lamotrigine and gabapentin, may have mood-stabilizing properties. The actions of electroconvulsive therapy as they relate to activation of endogenous anticonvulsant processes, and the potential therapeutic effects of nonconvulsive repeated transcranial magnetic stimulation of brain, are promising areas of mood disorder research.

Anticonvulsants↗

PubMed1997

Mood Disorder Due to Human Immunodeficiency Virus: Yes, No, or Maybe?

The potential for secondary (biological or psychological) mood disorders would seem to be heightened in human immunodeficiency virus (HIV) for many reasons. HIV infection is associated with lethal, multisystem illness related to profound immune dysregulation; infection involves the central nervous system (CNS) shortly after infection and leads to substantial neurocognitive impairment even in the absence of other physical evidence of disease. Psychological forces at work include social stigimitization of unparalleled proportion for the modern era, combined with bereavements of epidemic proportions, Nevertheless, it is misleading to attribute to HIV itself-or to its psychological and social consequences-all episodes of mood disorder. Preinfection rates of major depression are high in groups at greatest risk for HIV. Rates of "current" major depression approach 10%, but perhaps 50% of affected individuals have preinfection evidence of mood disorder. Mania is relatively rare, with an overall prevalence less that 1%. "Subsyndromic" mood disorder is understudied, but may effect an important minority of individuals. Given current advances in neuromedical evaluation, neuropsychological assessment, and rigorous psychiatric criteria, it is likely that study of secondary mood disorders in HIV can contribute to important advances in our understanding of brain-behavioral relationships.

Journal Article↗

PubMed2001

Prevalence of mood disorders and relationship to asthma severity in patients at an inner-city asthma clinic.

BACKGROUND: Depressive symptoms are associated with noncompliance and even sudden death in asthma patients. Some studies suggest that low-income, minority, inner-city asthma patients may be at high risk for asthma-related morbidity and mortality in which depression may be a risk factor. Minimal data are available on the prevalence of depression and other mood disorders in asthma patients. OBJECTIVE: In this pilot study, we examined the prevalence of depression and the association between depression and measures of asthma severity in patients at an inner-city asthma clinic. METHODS: Mood disorders were diagnosed using a diagnostic interview given to patients (N = 44) at asthma clinic visits. Inhaled steroid dose, FEV1 percentage, and asthma severity were also obtained. RESULTS: Eighteen patients (41%) had a lifetime mood disorder but only seven of these patients received pharmacotherapy. Patients with a past mood disorder had significantly higher FEV1 percentage predicted values (P = 0.03) than those without a mood disorder. Trends toward less severe asthma (P = 0.13) and lower inhaled steroid dose (P = 0.13) in patients with a mood disorder history were also found. CONCLUSIONS: The data suggest that mood disorders are common, but often unrecognized and untreated in asthma patients. The data also suggest that mood disorders are not necessarily associated with more severe asthma, at least in the population studied.

Asthma↗

PubMed2006

Hippocampal volume and mood disorders after traumatic brain injury.

BACKGROUND: Recent evidence from clinical studies and animal models of traumatic brain injury (TBI) suggest that neuronal and glial loss might progress after the initial insult in selectively vulnerable regions of the brain such as the hippocampus. There is also evidence that hippocampal dysfunction plays a role in the pathogenesis of mood disorders. We examined the relationship between hippocampal damage and mood disorders after TBI and the effect of hippocampal atrophy on the outcome of TBI patients. METHODS: The study group consisted of 37 patients with closed head injury who were evaluated at baseline and at 3, 6, and 12 months after trauma. Psychiatric diagnosis was made with a structured clinical interview and DSM-IV criteria. Quantitative magnetic resonance imaging scans were obtained at 3-months follow-up. RESULTS: Patients with moderate to severe head injury had significantly lower hippocampal volumes than patients with mild TBI. Patients who developed mood disorders had significantly lower hippocampal volumes than patients without mood disturbance. Furthermore, there was a significant interaction between mood disorders diagnosis and severity of TBI, by which patients with moderate to severe TBI who developed mood disorders had significantly smaller hippocampal volumes than patients with equivalent severe TBI who did not develop mood disturbance. Finally, reduced hippocampal volumes were associated with poor vocational outcome at 1-year follow-up. CONCLUSIONS: Our findings are consistent with a "double-hit" mechanism by which neural and glial elements already affected by trauma are further compromised by the functional changes associated with mood disorders (e.g., the neurotoxic effects of increased levels of cortisol or excitotoxic damage resulting from overactivation of glutaminergic pathways). Finally, patients with greater hippocampal damage were less likely to return to a productive life 1 year after trauma.

Adolescent↗

PubMed2007

Stigma and mood disorders.

PURPOSE OF REVIEW: To update the reader on current research on stigmatizing attitudes towards people suffering from mood disorders and to describe recent interventions in this area. RECENT FINDINGS: The public generally feels their own attitudes are more favourable to people with depression than 'most other people's' attitudes are. Among those with depressive symptoms, self-stigma in relation to depression is higher than perceived stigma from others, including professionals, thus hindering help seeking. The main factor that seems to improve the attitudes towards people with any mental illness is personal contact. Moderate improvements in attitudes have been achieved with an online intervention. Caution must be taken when ensuring that improvements in knowledge about mental disorders do not lead to increased social distance. SUMMARY: There exists little research on stigmatizing attitudes towards people with mood disorders. Most of the literature on the stigma towards people with mental illness relates to people with more severe disorders such as schizophrenia. When research has been done on mood disorders, the focus has been on perceived stigma and self-stigma. No up-to-date research exists on discrimination experienced by people with mood disorders, and very little research exists on interventions designed to decrease stigmatizing attitudes towards them.

Humans↗

PubMed1994

Treatment of organic bipolar mood disorders in Parkinson's disease.

Two patients with long-standing idiopathic Parkinson's disease (PD), without individual or family histories of affective disorders, developed bipolar mood disorders. Both were treated with lithium and clozapine, and one responded favorably. These may be the first reported cases in which mania was treated with clozapine in PD patients.

Bipolar Disorder↗

PubMed2002

Association study of the short tandem repeat in the 5' upstream region of the cholecystokinin gene with mood disorders in the Japanese population.

We have recently identified a novel polymorphic short tandem repeat (STR) in the 5' upstream region of the cholecystokinin (CCK) gene and reported its association with panic disorder. A linkage study of affective disorder showed a modest linkage signal on the short arm of chromosome 3, the location of the CCK gene. Furthermore, clinical comorbidity of depression and anxiety disorders have been documented. In the present study, we examined a possible association of the CCK STR with mood disorders. We genotyped 165 subjects with mood disorders consisting of unipolar and bipolar disorders and 253 control samples. However, no significant allelic associations were detected between the STR and either the combined mood disorders (P = 0.885), the unipolar group (P = 0.296), or the bipolar group (P = 0.605). These data suggest that the CCK promoter STR is unlikely to have a major genetic effect on the development of mood disorders in the Japanese population.

Adult↗

PubMed2003

Association study of serotonin transporter gene VNTR polymorphism and mood disorders, onset age and suicide attempts in a Chinese sample.

The human serotonin transporter (5-HTT) gene is an important candidate for the pathogenesis of mood disorders. Associations have been reported between a variable-number tandem-repeat polymorphism in intron 2 of the serotonin transporter gene (5-HTTVNTR) and mood disorders in a number of studies of Western and Chinese populations. However, no such relationships have been determined in other analogous research. To replicate these positive findings in a Chinese population and to determine the association between onset age of bipolar disorder and 5-HTTVNTR, we investigated the prevalence of this polymorphism in an independent Chinese population (83 bipolar disorder patients, 77 major depressive disorder patients and 169 controls), demonstrating no significant association between the 5-HTTVNTR polymorphism and mood disorders or age at onset. Further, no association was demonstrated between this polymorphism and suicidal history in mood disorder patients. These negative findings suggest that 5-HTTVNTR does not play a major role in the pathogenesis of mood disorder in Chinese populations.

Adult↗

PubMed1998

Polymorphism in the promoter region of the alpha 2A adrenergic receptor gene and mood disorders.

Alpha 2 adrenergic receptors are thought to play a crucial role in the etiology or treatment of mood disorders. Polymorphism(s) in the promoter region of the alpha 2 receptor may affect the gene expression and be associated with mood disorders. We studied the previously reported polymorphisms of the alpha 2A receptor gene at position-1291 in 114 healthy controls and 103 mood disorder patients. There was statistically no difference between controls and patients in either the genotype or the allele frequency. There was statistically no difference between the genotype and the clinical characteristics. Our results suggest there is no association between this polymorphism in the promoter region of the alpha 2A receptor gene and mood disorders.

Alleles↗

PubMedDate not supplied

Prednisone mood disorder with associated catatonia.

Since steroid-induced psychoses often appear as mood disorders and since catatonia may be associated with psychotic mood disorders, the possibility exists for a steroid-induced psychotic mood disorder to present with associated catatonia. In a computer review of the medical literature, however, I found no such cases in adult patients. This report is presented as a possible case of steroid-induced catatonia in a 62-year-old woman following treatment with melphalan, prednisone, and cimetidine for multiple myeloma of the IgA class with associated mild hypercalcemia.

Akathisia, Drug-Induced↗

PubMed2002

Relationships between serum magnesium levels and clinical background factors in patients with mood disorders.

We measured serum magnesium (Mg) levels in 71 in-patients and out-patients with mood disorders and in 30 healthy controls and investigated the relationships between serum Mg levels and clinical background factors. Serum Mg levels were found to be significantly higher in patients with mood disorders than in controls. Serum Mg levels showed no significant correlation with patient sex, age, diagnosed subtype and disease phase in the mood disorder group. Serum Mg levels in patients with major depressive disorder who were taking psychotropic drugs were not significantly different from levels seen in patients with major depressive disorder who were not taking psychotropic drugs. These results suggest that the high serum Mg levels noted in patients with mood disorder are related to the underlying disorder itself and are not influenced by clinical background factors.

Adult↗

PubMed2004

Deficiency of theory of mind in patients with remitted mood disorder.

BACKGROUND: Recent researches on theory of mind (ToM) in patients with mood disorders have revealed deficits of ToM ability during episodes. In this study, we aimed to test ToM ability among patients with unipolar or bipolar depression currently in remission. METHODS: ToM ability and IQ obtained by Wechsler Adult Intelligence Scale-Revised (WAIS-R) were evaluated in 50 patients with remitted depression, who met the criteria of mood disorders of DSM-IV, and 50 matched healthy controls. RESULTS: The patients with mood disorders showed statistically significant impairment in a second-order false question (Fisher's Exact Test p < 0.0001). No significant difference was shown in the other three areas of ToM between the patients and the controls. In addition, no correlation of the four areas of ToM with IQ obtained by WAIS-R was found. LIMITATIONS: The relation of ToM deficit to other specific cognitive impairment was not examined. CONCLUSIONS: Our results suggest that depressive patients in symptomatic remission have a lower ability of second-order false belief. The ToM impairment suggests a decline of skillful social relationships. Evaluation of ToM ability in depressive patients in remission may be useful to provide treatment for better social adjustment.

Adolescent↗

PubMed1993

A study of relapses in subjects with mood disorder on lithium treatment.

In a sample of 213 mood disorder subjects on long-term lithium treatment, we analyzed the recurrence indices of relapses during the prophylactic treatment period. The differences found in the recurrence rates were due to the current age and age of onset, duration of illness and polarity of the probands. The patients with personality disorders showed the worst relapse indices and could represent a group of mood disorder subjects with a bad outcome of lithium treatment.

Aging↗

PubMed2001

Treated prevalence, incidence, and pharmacotherapy of child and adolescent mood disorders in an HMO.

This study examined the "treated" prevalence, incidence, and pharmacotherapy of child and adolescent mood disorders in a managed care setting. General prevalence patterns across age and sex were similar to those reported in community epidemiology studies, although, not unexpectedly, the overall rates were somewhat lower. Primary care providers identified a substantial proportion of the youth with a mood disorder. Antidepressant medication was used more often by youth identified with a mood disorder in medical care settings than by those youth identified in specialty mental health care settings. These results are valuable in determining if youth with mood disorders receiving medication prescriptions across settings are treated according to current best practice guidelines (such as the adult depression guidelines [U.S. Department of Health and Human Services, 1993]), that is, primarily with SSRI medications.

Adolescent↗

PubMed2005

Colocalization of corticotropin-releasing hormone and oestrogen receptor-alpha in the paraventricular nucleus of the hypothalamus in mood disorders.

Oestrogens may modulate the activity of the hypothalamic-pituitary-adrenal (HPA) axis. The present study was to investigate whether the activity of the HPA axis in mood disorders might be directly modulated by oestrogens via oestrogen receptors (ORs) in the corticotropin-releasing hormone (CRH) neurons of the human hypothalamic paraventricular nucleus (PVN). Brains of 13 subjects ranging in age between 45 and 79 years suffering from major depression/major depressive disorder (eight cases) or bipolar disorder (five cases) and of 13 controls, matched for sex, age, brain weight, post-mortem delay, fixation time and season and clock time at death, were studied with double-label immunocytochemistry. The total number of CRH-immunoreactive (IR) neurons, CRH neurons that colocalized ORalpha in the neuronal nucleus and the number of only nuclear ORalpha-containing neurons in the PVN were measured using an image analysis system. In addition, the volume of the PVN delineated on the basis of CRH neurons was determined. It was found that the total number of CRH-IR neurons in patients with mood disorders was nearly 1.7 times higher than in controls (P = 0.034). A novel finding was that the total number of CRH-IR neurons and the number of CRH-nuclear ORalpha double-staining neurons in the PVN were strongly correlated both in controls and in patients with mood disorders (P < 0.001 and P = 0.022, respectively). The ratio of the CRH-nuclear-ORalpha double-staining neurons to the total CRH-IR neurons in patients with mood disorders was similar to that in the controls (P = 0.448). The volume of the sub-region of the PVN that was delineated on the basis of CRH neurons was significantly larger in patients with mood disorders than in controls (P = 0.022). Another novel finding was the large population of extra-hypothalamic CRH neurons that was found in the thalamus. In summary, oestrogens may directly influence CRH neurons in the human PVN. The increased numbers of neurons expressing CRH in mood disorders is accompanied by increased ORalpha colocalization in the nucleus of these neurons. These changes seem to be trait- rather than state-related.

Aged↗