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Mood Dysregulation (mood + dysregulation)

Distribution by Scientific Domains

Medical Sciences	60%

Selected Abstracts

Molecular genetics of bipolar disorder

GENES, BRAIN AND BEHAVIOR, Issue 1 2006
E. P. Hayden
Bipolar disorder (BPD) is an often devastating illness characterized by extreme mood dysregulation. Although family, twin and adoption studies consistently indicate a strong genetic component, specific genes that contribute to the illness remain unclear. This study gives an overview of linkage studies of BPD, concluding that the regions with the best evidence for linkage include areas on chromosomes 2p, 4p, 4q, 6q, 8q, 11p, 12q, 13q, 16p, 16q, 18p, 18q, 21q, 22q and Xq. Association studies are summarized, which support a possible role for numerous candidate genes in BPD including COMT, DAT, HTR4, DRD4, DRD2, HTR2A, 5-HTT, the G72/G30 complex, DISC1, P2RX7, MAOA and BDNF. Animal models related to bipolar illness are also reviewed, with special attention paid to those with clear genetic implications. We conclude with suggestions for strategies that may help clarify the genetic bases of this complex illness. [source]

Dynamic mapping of cortical development before and after the onset of pediatric bipolar illness

THE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 9 2007
Nitin Gogtay
Background:, There are, to date, no pre-post onset longitudinal imaging studies of bipolar disorder at any age. We report the first prospective study of cortical brain development in pediatric bipolar illness for 9 male children, visualized before and after illness onset. Method:, We contrast this pattern with that observed in a matched group of healthy children as well as in a matched group of 8 children with ,atypical psychosis' who had similar initial presentation marked by mood dysregulation and transient psychosis (labeled as ,multi-dimensionally impaired' (MDI)) as in the bipolar group, but have not, to date, developed bipolar illness. Results:, Dynamic maps, reconstructed by applying novel cortical pattern matching algorithms, for the children who became bipolar I showed subtle, regionally specific, bilaterally asymmetrical cortical changes. Cortical GM increased over the left temporal cortex and decreased bilaterally in the anterior (and sub genual) cingulate cortex. This was seen most strikingly after the illness onset, and showed a pattern distinct from that seen in childhood onset schizophrenia. The bipolar neurodevelopmental trajectory was generally shared by the children who remained with MDI diagnosis without converting to bipolar I, suggesting that this pattern of cortical development may reflect affective dysregulation (lability) in general. Conclusions:, These dynamic trajectories of cortical development may explain age-related disparate findings from cross-sectional studies of bipolar illness, and suggest the importance of mood disordered non-bipolar control group in future studies. [source]

Psychotic features in borderline patients: is there a connection to mood dysregulation?

BIPOLAR DISORDERS, Issue 4 2005
Benvenuti A
Objective:, To investigate the relationship between lifetime mood and psychotic spectrum features in patients with borderline personality disorder (BPD). Method:, The study sample consisted of BPD patients with (n = 39, BPD-M) or without (n = 21, BPD-noM) lifetime mood disorders. The diagnostic assessment was conducted with the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I). The diagnosis of BPD was made clinically and then confirmed by Gunderson's diagnostic interview for borderlines. Subjects were also administered the Structured Clinical Interview for Psychotic Spectrum (SCI-PSY) and the Mood Spectrum self-report questionnaire (MOODS-SR). Results:, BPD-M had significantly higher scores than BPD-noM on the ,lifetime' mood spectrum subdomains ,depressive mood' and ,depressive cognition'. The two groups did not differ on the scores of psychotic spectrum except for higher ,hypertrophic self-esteem' scores in BPD-noM. In BPD-noM both the depressive and the manic-hypomanic component of mood spectrum were significantly correlated with the ,delusion' subdomain of the psychotic spectrum. The depressive component was correlated with ,depersonalization/derealization' and the manic-hypomanic component was correlated with ,hypertrophic self-esteem'. In BPD-M, the manic-hypomanic component of mood spectrum was correlated with different subdomains of the psychotic spectrum: ,hypertrophic self-esteem', ,self-reference', ,interpretive attitude', ,anger/overreactivity, ,unusual and odd thoughts', ,illusions', ,delusions', ,hallucinations' and ,catatonia'. The depressive component of mood spectrum was ,uncorrelated' with the subdomains of the psychotic spectrum. Conclusions:, Our data support the hypothesis that ,lifetime' manic-hypomanic mood dysregulations are correlated with psychotic spectrum features in borderline patients. The assessment of these spectrum features in borderline patients may be useful to inform treatment choices. [source]

Interferon, tryptophan and depression

ACTA NEUROPSYCHIATRICA, Issue 1 2003
D. Fekkes
Depression is a frequent comorbid disorder of many inflammatory diseases and it is suggested that brain inflammatory processes have a pathogenic role in mood dysregulation. Several immunocompromised patients have been treated with cytokines and long-term treatments have resulted in a variety of neuropsychiatric side-effects. The objective of the study was to present evidence for an association between the induction of neuropsychiatric side-effects during treatment with interferon-, (IFN-,) and changes in serotonergic and immunological parameters. Moreover, the use of IFN-,-induced depression as a paradigm for research into the pathophysiology of depressive disorders in general will be discussed. This literature review focused on the relationships between tryptophan, serotonin, cytokines and depression associated with interferon treatment. Immunotherapy with IFN-, influences several immunological and serotonergic parameters, and induces in most patients neurovegetative, somatic and depressive symptoms. Literature findings indicate that the development of depressive symptoms in patients undergoing cytokine therapy are secondary to cytokine induction and could be mediated by a reduced availability of tryptophan to the brain, resulting ultimately in decreased serotonergic activity. Changes in the metabolism of tryptophan and consequently of serotonin may play a role in the pathophysiology of interferon-induced depression. Studies on interferon-induced neuropsychiatric side-effects may be a promising research paradigm and shed light on the role of immunological and serotonergic factors in the pathogenesis of depressive disorders in general. However, first the appropriate symptomatology of the interferon-induced depressive states has to be documented. [source]