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PubMed2002

Clinical and demographic features of mood disorder subtypes.

The aim of this study was to investigate demographic, clinical and symptomatologic features of the following mood disorder subtypes: bipolar disorder I (BP-I); bipolar disorder II (BP-II); major depressive disorder, recurrent (MDR); and major depressive episode, single episode (MDSE). A total of 1832 patients with mood disorders (BP-I=863, BP-II=141, MDR=708, and MDSE=120) were included in our study. The patients were assessed using structured diagnostic interviews and the operational criteria for psychotic illness checklist (n=885), the Hamilton depression rating scale (n=167), and the social adjustment scale (n=305). The BP-I patients were younger; had more hospital admissions; presented a more severe form of symptomatology in terms of psychotic symptoms, disorganization, and atypical features; and showed less insight into their disorder than patients in the other groups. Compared with the major depressive subgroups, BP-I patients were more likely to have an earlier age at onset, an earlier first lifetime psychiatric treatment, and a greater number of illness episodes. BP-II patients had a higher suicide risk than both BP-I and MDSE patients. MDSE patients presented less severe symptomatology, lower age at observation, and a higher number of males. The retrospective approach and the selection constraints due to the inclusion criteria are the main limitations of the study. Our data support the view that BP-I disorder is quite different from the remaining mood disorders from a demographic and clinical perspective, with BP-II disorder having an intermediate position to MDR and MDSE, that is, as a less severe disorder. This finding may help in the search for the biological basis of mood disorders.

Adult↗

PubMed2005

Temperamental commonalities and differences in euthymic mood disorder patients, creative controls, and healthy controls.

OBJECTIVE: Understanding of mood disorders can be enhanced through assessment of temperamental traits. We explored temperamental commonalities and differences among euthymic bipolar (BP) and unipolar (MDD) mood disorder patients, creative discipline graduate student controls (CC), and healthy controls (HC). METHODS: Forty-nine BP, 25 MDD, 32 CC, and 47 HC completed self-report temperament/personality measures including: The Affective Temperament Evaluation of Memphis, Pisa, Paris and San Diego (TEMPS-A); the Revised NEO Personality Inventory (NEO-PI-R); and the Temperament and Character Inventory (TCI). RESULTS: Euthymic BP, MDD, and CC, compared to HC, had significantly increased cyclothymia, dysthymia and irritability scores on TEMPS-A; increased neuroticism and decreased conscientiousness on NEO-PI-R; and increased harm avoidance and novelty seeking as well as decreased self-directedness on TCI. TEMPS-A cyclothymia scores were significantly higher in BP than in MDD. NEO-PI-R openness was increased in BP and CC, compared to HC, and in CC compared to MDD. TCI self-transcendence scores in BP were significantly higher than in MDD, CC, and HC. LIMITATIONS: Most of the subjects were not professional artists, and represented many fields; temperament might be different in different art fields. CONCLUSIONS: Euthymic BP, MDD, and CC compared to HC, had prominent temperamental commonalities. However, BP and CC had the additional commonality of increased openness compared to HC. BP had particularly high Cyclothymia scores that were significantly higher then those of MDD. The prominent BP-CC overlap suggests underlying neurobiological commonalities between people with mood disorders and individuals involved in creative disciplines, consistent with the notion of a temperamental contribution to enhanced creativity in individuals with bipolar disorders.

Adult↗

PubMed2006

Telomere shortening and mood disorders: preliminary support for a chronic stress model of accelerated aging.

BACKGROUND: Little is known about the biological mechanisms underlying the excess medical morbidity and mortality associated with mood disorders. Substantial evidence supports abnormalities in stress-related biological systems in depression. Accelerated telomere shortening may reflect stress-related oxidative damage to cells and accelerated aging, and severe psychosocial stress has been linked to telomere shortening. We propose that chronic stress associated with mood disorders may contribute to excess vulnerability for diseases of aging such as cardiovascular disease and possibly some cancers through accelerated organismal aging. METHODS: Telomere length was measured by Southern Analysis in 44 individuals with chronic mood disorders and 44 nonpsychiatrically ill age-matched control subjects. RESULTS: Telomere length was significantly shorter in those with mood disorders, representing as much as 10 years of accelerated aging. CONCLUSIONS: These results provide preliminary evidence that mood disorders are associated with accelerated aging and may suggest a novel mechanism for mood disorder-associated morbidity and mortality.

Adult↗

PubMed2005

Sleep and perinatal mood disorders: a critical review.

Pregnancy and the postpartum period are recognized as times of vulnerability to mood disorders, including postpartum depression and psychosis. Recently, changes in sleep physiology and sleep deprivation have been proposed as having roles in perinatal psychiatric disorders. In this article we review what is known about changes in sleep physiology and behaviour during the perinatal period, with a focus on the relations between sleep and postpartum "blues," depression and psychosis and on sleep-based interventions for the treatment and prevention of perinatal mood disorders. The interaction between sleep and perinatal mood disorders is significant, but evidence-based research in this field is limited. Studies that measure both sleep and mood during the perinatal period, particularly those that employ objective measurement tools such as polysomnography and actigraphy, will provide important information about the causes, prevention and treatment of perinatal mood disorders.

Depression, Postpartum↗

PubMed1998

GABA function in mood disorders: an update and critical review.

Over the past twenty years, several lines of evidence from preclinical and clinical studies has accumulated suggesting that a GABA deficit may be involved in mood disorders, particularly in depression, and that increasing GABAergic neurotransmission may exert an antidepressant effect and perhaps a mood stabilizing effect. Given that GABA has an inhibitory effect on biogenic amine neurotransmitters such as norepinephrine and serotonin and this inhibition may be involved in local circuits and interneurons, it has been suggested that the hypothesis of a GABA deficit in mood disorders does not compete with but complements the well-established hypotheses of alterations in noradrenergic and serotonergic function in mood disorders. In this paper, we systematically reviewed the results from preclinical and clinical studies of GABA function in the pathophysiology of mood disorders and in the mechanism of action of mood stabilizers, antidepressants and electroconvulsive therapy. We also discussed the unifying theory of the neurochemistry of mood disorders, which integrates the GABA hypothesis into the biogenic amine hypotheses, and indicated future directions for research.

Animals↗

PubMed2006

Targeting glycogen synthase kinase-3 in the CNS: implications for the development of new treatments for mood disorders.

There exists an immediate need to develop novel medications for the treatment of mood disorders such as bipolar disorder and depression. Initial interest in glycogen synthase kinase-3 (GSK-3) as a target for the treatment of mood disorders arose from the finding that the mood stabilizing drug lithium directly inhibited the enzyme. More recent preclinical evidence implicates the modulation of GSK-3 in either the direct or downstream mechanism of action of many other mood stabilizer and antidepressant medications currently in use. One of the cellular targets of GSK-3, which may mediate some of the effects of lithium and other drugs, is beta-catenin, a transcription factor that is rapidly degraded when GSK-3 is active. Recent rodent behavioral data (both genetic and pharmacological) supports GSK-3 representing a therapeutically relevant target of lithium. This includes antidepressant-like behavior in the forced swim test and antimanic-like response to amphetamine following administration of the GSK-3 inhibitor AR-A014418, a findings that is concomitant with an increase in brain beta-catenin. The evidence described in this review suggests that regulating GSK-3 may represent a target for novel medications to treat mood disorders.

Animals↗

PubMed2000

Mood disorders in multiple sclerosis: diagnosis and treatment.

Emotional disturbances are common in MS and consist of disturbances of mood and disturbances of affect. The important mood disorders are major depressive disorder, dysthymic disorder, bipolar disorder, panic disorder, and generalized anxiety disorder. Their relationship to MS is multi-factorial and complex, and the extent to which they are direct consequences of the disease process or psychological reactions to it remains unclear. Whatever their cause, however, the symptoms of mood disorders in people with MS are no different from the symptoms of mood disorders in people without MS, and respond just as well to standard treatments. The disorders of affect are euphoria, pathological laughing and weeping, and other frontal lobe syndromes. These disorders result from demyelination, are some of the most characteristic symptoms of MS, and have the same implications for treatment as do other aspects of the disease. Mood and affective disturbances can cause enormous pain and suffering and lead to significant disruption of family, work, and social life. Physicians who can identify, diagnose, treat, and manage mood and affective disturbances effectively and who can help their patients and family members acknowledge these difficulties, talk about them, and accept psychiatric consultation and treatment can have a dramatic impact on the quality of their lives. This paper outlines the symptoms and diagnostic criteria for mood disorders and affective disturbances, reviews current treatment options, summarizes data from epidemiologic and pathophysiological studies, and suggests areas for future research.

Humans↗

PubMed1987

Bipolar mood disorder and endometriosis: preliminary findings.

A consecutive sample of 16 women with laparoscopy-diagnosed endometriosis were evaluated for mood disorders. Twelve women met DSM-III criteria for a mood disorder: seven for bipolar disorder, mixed, three for bipolar disorder, manic, and two for major depression. Two women had equivocal diagnoses and two showed no evidence of mood disorder. Nine subjects had first-degree relatives with histories of severe mood disorders.

Adult↗

PubMed2004

Autism and familial major mood disorder: are they related?

Family history studies of autism consistently reveal a large subgroup with a high incidence of major mood disorder in family members, suggesting the two entities are related clinically and genetically. This review examines this concept, comparing current clinlical and biological knowledge of autism and major mood disorder, and advances the hypothesis that this subgroup of autism represents an early-life phenotype of major mood disorder. If confirmed, this hypothesis would suggest that the basic biological defects determining major mood disorders may have prominent neurodevelopmental and cognitive dimensions. Testing of the hypothesis will depend on genetic studies.

Autistic Disorder↗

PubMed2000

Absence of cognitive impairment at long-term follow-up in adolescents treated with ECT for severe mood disorder.

OBJECTIVE: Cognitive functions of adolescents treated with ECT for mood disorder were evaluated at long-term follow-up. METHOD: At an average of 3.5 years (SD=1.7) after the last ECT, 10 subjects treated during adolescence with bilateral ECT for severe mood disorder completed a clinical and cognitive evaluation, including the California Verbal Learning Test and Squire's Subjective Memory Questionnaire. The same assessments were given to 10 psychiatric comparison subjects matched for sex, age, and diagnosis. RESULTS: All cognitive test scores of the patients treated with ECT were similar to those of the comparison subjects and did not differ from norms from the community. Six of the 10 ECT-treated patients reported having had memory losses immediately after the ECT course, but only one complained of subjective memory impairment at follow-up. CONCLUSIONS: The results suggest that adolescents given ECT for severe mood disorder do not suffer measurable cognitive impairment at long-term follow-up.

Adolescent↗

PubMed2003

Depression and Bipolar Support Alliance consensus statement on the unmet needs in diagnosis and treatment of mood disorders in late life.

OBJECTIVES: To review progress made during the past decade in late-life mood disorders and to identify areas of unmet need in health care delivery and research. PARTICIPANTS: The Consensus Development Panel consisted of experts in late-life mood disorders, geriatrics, primary care, mental health and aging policy research, and advocacy. EVIDENCE: (1) Literature reviews addressing risk factors, prevention, diagnosis, treatment, and delivery of services and (2) opinions and experiences of primary care and mental health care providers, policy analysts, and advocates. CONSENSUS PROCESS: The Consensus Development Panel listened to presentations and participated in discussions. Workgroups considered the evidence and prepared preliminary statements. Workgroup leaders presented drafts for discussion by the Consensus Development Panel. The final document was reviewed and edited to incorporate input from the entire Consensus Development Panel. CONCLUSIONS: Despite the availability of safe and efficacious treatments, mood disorders remain a significant health care issue for the elderly and are associated with disability, functional decline, diminished quality of life, mortality from comorbid medical conditions or suicide, demands on caregivers, and increased service utilization. Discriminatory coverage and reimbursement policies for mental health care are a challenge for the elderly, especially those with modest incomes, and for clinicians. Minorities are particularly underserved. Access to mental health care services for most elderly individuals is inadequate, and coordination of services is lacking. There is an immediate need for collaboration among patients, families, researchers, clinicians, governmental agencies, and third-party payers to improve diagnosis, treatment, and delivery of services for elderly persons with mood disorders.

Age Factors↗

PubMed2002

National Depressive and Manic-Depressive Association consensus statement on the use of placebo in clinical trials of mood disorders.

A consensus conference on the use of placebo in mood disorder studies consisted of expert presentations on bioethics, biostatistics, unipolar depression, and bipolar disorder. Work groups considered evidence and presented statements to the group. Although it was not possible to write a document for which there was complete agreement on all issues, the final document incorporated input from all authors. There was consensus that placebo has a definite role in mood disorder studies. Findings of equivalence between a new drug and standard treatment in active control studies is not evidence of efficacy unless the new drug is also significantly more effective than placebo. Add-on studies in which patients are randomized to standard therapy plus the investigational drug or standard therapy plus placebo are especially indicated for high-risk patients. Mood disorders in elderly and pediatric patients are understudied, and properly designed trials are urgently needed. Research is needed on the ethical conduct of studies to limit risks of medication-free intervals and facilitate poststudy treatment. Patients must fully understand the risks and lack of individualized treatment involved in research.

Bipolar Disorder↗

PubMed1995

The gene encoding the 5-HT1A receptor is intact in mood disorders.

We studied the 5-HT1A receptor gene in 50 mood disorders and 50 normal volunteers. The 5-HT1A receptor gene was amplified by polymerase chain reaction and sequenced by the dideoxy method. The sequence of the 5-HT1A receptor encodes a protein of 422 amino acids, that is, one amino acid longer than the reported sequence (Kobilka et al. 1987). The DNA sequence at positions 454 to 459 is CGC GCC GCT, not CCG CGT, and the amino acids sequence at these positions is changing from proline arginine to arginine alanine alanine. These differences, however, were observed in both mood disorders and controls. One silent polymorphism, CTG to GTA at position 294, was found. These results suggest that the 5-HT1A receptor gene is intact in mood disorders.

Adult↗

PubMed2000

A placebo-controlled study of lamotrigine and gabapentin monotherapy in refractory mood disorders.

There is a pressing need for additional treatment options for refractory mood disorders. This controlled comparative study evaluated the efficacy of lamotrigine (LTG) and gabapentin (GBP) monotherapy versus placebo (PLC). Thirty-one patients with refractory bipolar and unipolar mood disorders participated in a double-blind, randomized, crossover series of three 6-week monotherapy evaluations including LTG, GBP, and PLC. There was a standardized blinded titration to assess clinical efficacy or to determine the maximum tolerated daily dose (LTG 500 mg or GBP 4,800 mg). The primary outcome measure was the Clinical Global Impressions Scale (CGI) for Bipolar Illness as supplemented by other standard rating instruments. The mean doses at week 6 were 274 +/- 128 mg for LTG and 3,987 +/- 856 mg for GBP. Response rates (CGI ratings of much or very much improved) were the following: LTG, 52% (16/31); GBP, 26% (8/31); and PLC, 23% (7/31) (Cochran's Q = 6.952, df = 2, N = 31, p = 0.031). Post hoc Q differences (df = 1, N = 31) were the following: LTG versus GBP (Qdiff = 5.33, p = 0.011); LTG versus PLC (Qdiff = 4.76, p = 0.022); and GBP versus PLC (Qdiff = 0.08, p = 0.70). With respect to anticonvulsant dose and gender, there was no difference between the responders and the nonresponders. The agents were generally well tolerated. This controlled investigation preliminarily suggests the efficacy of LTG in treatment-refractory affectively ill patients. Further definition of responsive subtypes and the role of these medications in the treatment of mood disorders requires additional study.

Acetates↗

PubMed1997

The anatomy of mood disorders--review of structural neuroimaging studies.

The structural neuroimaging findings in mood disorders were reviewed, to evaluate evidence for a neuroanatomic model of pathophysiology, involving the prefrontal cortex, the basal ganglia, the amygdala-hippocampus complex, thalamus, and connections among these structures. Global atrophy is not consistently found. The best replicated finding is an increased rate of white matter and periventricular hyperintensities. A smaller frontal lobe, cerebellum, caudate, and putamen appear present in unipolar depression. A larger third ventricle, and smaller cerebellum and perhaps temporal lobe appear present in bipolar disorder. These localized structural changes involve regions that may be critical in the pathogenesis of mood disorders. Generalized and localized anatomic alterations may be related to age or vascular disease. The clinical and biological correlates of these changes need to be investigated to allow development of a more complete model of pathophysiology of mood disorders.

Atrophy↗

PubMed1996

Increased neural cell adhesion molecule in the CSF of patients with mood disorder.

Neural cell adhesion molecule (N-CAM) is involved in cell-cell interactions during synaptogenesis, morphogenesis, and plasticity of the nervous system. Disturbances in synaptic restructuring and neural plasticity may be related to the pathogenesis of several neuropsychiatric diseases, including mood disorders and schizophrenia. Disturbances in brain cellular function may alter concentrations of N-CAM in the CSF. Soluble human N-CAM proteins are detectable in the CSF but are minor constituents of serum. We have recently found an increase in N-CAM content in the CSF of patients with schizophrenia. Although the pathogenesis of both schizophrenia and mood disorders is unknown, ventriculomegaly, decreased temporal lobe volume, and subcortical structural abnormalities have been reported for both disorders. We have therefore measured N-CAM concentrations in the CSF of patients with mood disorder. There were significant increases in amounts of N-CAM immunoreactive proteins, primarily the 120-kDa band, in the CSF of psychiatric inpatients with bipolar mood disorder type I and recurrent unipolar major depression. There were no differences in bipolar mood disorder type II patients as compared with normals. There were no significant effects of medication treatment on N-CAM concentrations. It is possible that the 120-kDa N-CAM band present in the CSF is derived from CNS cells as a secreted soluble N-CAM isoform. Our results suggest the possibility of latent state-related disturbances in N-CAM cellular function, i.e., residue from a previous episode, or abnormal N-CAM turnover in the CNS of patients with mood disorder.

Adult↗

PubMed1992

D1 dopamine receptor binding in mood disorders measured by positron emission tomography.

D1 dopamine receptor binding in mood disorders was studied by positron emission tomography (PET) using 11C-SCH23390. Ten patients with bipolar mood disorders and 21 normal controls were studied in the drug-free state. The patients were in euthymic (N = 6), depressed (N = 3) and manic (N = 1) states. Regional radioactivity in the brain was followed for 40 min by PET. A two-compartment model was used to obtain the binding potential (k3/k4) for the striatum and frontal cortex. The binding potentials for the frontal cortex for the patients were significantly lower than those for normal controls, whereas those for striatum were not significantly different. These findings suggest that D1 dopamine receptors in the frontal cortex may be in a different state in patients with bipolar mood disorders.

Adult↗

PubMedDate not supplied

Mood disorders and the reproductive cycle.

Women have a significantly higher risk for developing mood disorders than men. Although reasons for this gender difference are not fully understood, it is clear that changing levels of reproductive hormones throughout women's life cycles can have direct or indirect effects on mood. Fluctuations in reproductive hormones may interactively affect neuroendocrine, neurotransmitter, and circadian systems. Reproductive hormones also may affect response to some antidepressant drugs and alter the course of rapid-cycling mood disorders. Nonpharmacologic interventions, such as light therapy and sleep deprivation, may be beneficial for mood disorders linked to the reproductive cycle. These interventions may have fewer side effects and a greater potential for patient compliance than some antidepressant drugs.

Female↗