MEMBRANE Na ´ +;-K ´ +; ATPase MEDIATED CASCADE IN BIPOLAR MOOD DISORDER, MAJOR DEPRESSIVE DISORDER, AND SCHIZOPHRENIA RELATIONSHIP TO HEMISPHERIC DOMINANCE

2002 ◽  
Vol 112 (8) ◽  
pp. 965-982 ◽  
Author(s):  
A. RAVI KUMAR KURUP ◽  
P. A. KURUP
2021 ◽  
pp. 1-8
Author(s):  
L. Propper ◽  
A. Sandstrom ◽  
S. Rempel ◽  
E. Howes Vallis ◽  
S. Abidi ◽  
...  

Abstract Background Offspring of parents with major mood disorders (MDDs) are at increased risk for early psychopathology. We aim to compare the rates of neurodevelopmental disorders in offspring of parents with bipolar disorder, major depressive disorder, and controls. Method We established a lifetime diagnosis of neurodevelopmental disorders [attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder, communication disorders, intellectual disabilities, specific learning disorders, and motor disorders] using the Kiddie Schedule for Affective Disorders and Schizophrenia, Present and Lifetime Version in 400 participants (mean age 11.3 + s.d. 3.9 years), including 93 offspring of parents with bipolar disorder, 182 offspring of parents with major depressive disorder, and 125 control offspring of parents with no mood disorder. Results Neurodevelopmental disorders were elevated in offspring of parents with bipolar disorder [odds ratio (OR) 2.34, 95% confidence interval (CI) 1.23–4.47, p = 0.010] and major depressive disorder (OR 1.87, 95% CI 1.03–3.39, p = 0.035) compared to controls. This difference was driven by the rates of ADHD, which were highest among offspring of parents with bipolar disorder (30.1%), intermediate in offspring of parents with major depressive disorder (24.2%), and lowest in controls (14.4%). There were no significant differences in frequencies of other neurodevelopmental disorders between the three groups. Chronic course of mood disorder in parents was associated with higher rates of any neurodevelopmental disorder and higher rates of ADHD in offspring. Conclusions Our findings suggest monitoring for ADHD and other neurodevelopmental disorders in offspring of parents with MDDs may be indicated to improve early diagnosis and treatment.


2010 ◽  
Vol 32 (4) ◽  
pp. 416-423 ◽  
Author(s):  
Odeilton Tadeu Soares ◽  
Doris Hupfeld Moreno ◽  
Eduardo Calmon de Moura ◽  
Jules Angst ◽  
Ricardo Alberto Moreno

OBJECTIVE: Bipolar disorders are often not recognized and undertreated. The diagnosis of current or past episodes of hypomania is of importance in order to increase diagnostic certainty. The Hypomania Checklist-32 is a self-applied questionnaire aimed at recognizing these episodes. As part of the international collaborative effort to develop multi-lingual versions of the Hypomania Checklist-32, we aimed to validate the Brazilian version and to compare its psychometric properties with those of the Mood Disorder Questionnaire. METHOD: Adult outpatients with bipolar disorder I (n = 37), bipolar disorder II (n = 44) and major depressive disorder (n = 42) of a specialized mood disorder unit were diagnosed according to DSM-IV-TR using a modified version of the SCID. We analyzed the internal consistency and discriminative ability of the Hypomania Checklist-32 Brazilian version in relation to the Mood Disorder Questionnaire. RESULTS: The internal consistency of the Brazilian Hypomania Checklist-32, analyzed using Cronbach's alpha coefficient, was 0.86. A score of 18 or higher in the Hypomania Checklist-32 Brazilian version distinguished between bipolar disorder and major depressive disorder, with a sensitivity of 0.75 and a specificity of 0.58, compared to 0.70 and 0.58, respectively, for the Mood Disorder Questionnaire (score > 7). The Hypomania Checklist-32 Brazilian version showed a dual factor structure characterized by "active/elated" and "risk-taking/irritable" items. Hence, the Hypomania Checklist-32 Brazilian version was found to have a higher sensitivity but the same specificity as the Mood Disorder Questionnaire. CONCLUSION: The Brazilian version of the Hypomania Checklist-32 has adequate psychometric properties and helps discriminating bipolar disorder from major depressive disorder (but not bipolar disorder I from bipolar disorder II) with good sensitivity and specificity indices, similar to those of the Mood Disorder Questionnaire.


2007 ◽  
Vol 41 (3-4) ◽  
pp. 214-221 ◽  
Author(s):  
Andrew A. Nierenberg ◽  
Madhukar H. Trivedi ◽  
Maurizio Fava ◽  
Melanie M. Biggs ◽  
Kathy Shores-Wilson ◽  
...  

2016 ◽  
Vol 46 (11) ◽  
pp. 2351-2361 ◽  
Author(s):  
T. Nickson ◽  
S. W. Y. Chan ◽  
M. Papmeyer ◽  
L. Romaniuk ◽  
A. Macdonald ◽  
...  

BackgroundPrevious neuroimaging studies indicate abnormalities in cortico-limbic circuitry in mood disorder. Here we employ prospective longitudinal voxel-based morphometry to examine the trajectory of these abnormalities during early stages of illness development.MethodUnaffected individuals (16–25 years) at high and low familial risk of mood disorder underwent structural brain imaging on two occasions 2 years apart. Further clinical assessment was conducted 2 years after the second scan (time 3). Clinical outcome data at time 3 was used to categorize individuals: (i) healthy controls (‘low risk’, n = 48); (ii) high-risk individuals who remained well (HR well, n = 53); and (iii) high-risk individuals who developed a major depressive disorder (HR MDD, n = 30). Groups were compared using longitudinal voxel-based morphometry. We also examined whether progress to illness was associated with changes in other potential risk markers (personality traits, symptoms scores and baseline measures of childhood trauma), and whether any changes in brain structure could be indexed using these measures.ResultsSignificant decreases in right amygdala grey matter were found in HR MDD v. controls (p = 0.001) and v. HR well (p = 0.005). This structural change was not related to measures of childhood trauma, symptom severity or measures of sub-diagnostic anxiety, neuroticism or extraversion, although cross-sectionally these measures significantly differentiated the groups at baseline.ConclusionsThese longitudinal findings implicate structural amygdala changes in the neurobiology of mood disorder. They also provide a potential biomarker for risk stratification capturing additional information beyond clinically ascertained measures.


Author(s):  
Susan Mineka ◽  
Deepika Anand ◽  
Jennifer A. Sumner

The comorbidity of anxiety and mood disorders has been of great interest to psychopathology researchers for the past 25 years. One topic––the comorbidity of generalized anxiety disorder (GAD) and major depressive disorder (MDD)––has received considerable attention, in part because it has raised fundamental nosological issues regarding whether GAD should continue to be categorized as an anxiety disorder or whether it should be recategorized as a mood disorder. We review the logic for reclassifying GAD with the mood disorders as well as what we believe to be even more compelling reasons for why it should be retained as an anxiety disorder. In doing so, we review three different kinds of comorbidity—cross-sectional, cumulative (lifetime), and sequential. We also discuss overlaps and distinctions in what is known about the etiology of GAD and MDD and how their somewhat different cognitive and affective profiles bear on these issues of classification. Finally, we briefly discuss what some of the treatment implications may be for individuals with comorbid GAD and MDD.


2018 ◽  
Vol 32 (4) ◽  
pp. 385-396 ◽  
Author(s):  
Bruno Romeo ◽  
Lisa Blecha ◽  
Katia Locatelli ◽  
Amine Benyamina ◽  
Catherine Martelli

The objective of this meta-analysis is to assess the efficacy and safety of partial and complete dopamine agonists in the treatment of acute mood disorder episodes. Randomized, double-blind and placebo-controlled trials of dopamine agonists in the treatment of acute mood disorder episodes were identified in the MEDLINE and PsycINFO databases and included in the meta-analysis. In monotherapy of mania, improved remission rates were found for cariprazine (odds ratio (OR): 2.08, P < 0.01) and for high-dose aripiprazole (OR: 3.00; P = 0.05), but not for low-dose aripiprazole. In bipolar depression, no improvement of remission and response rates was found for aripiprazole in monotherapy, whereas improved response rate (OR: 10.27, P < 0.01) was found for pramipexole only as an add-on to another mood stabilizer. In major depressive disorder, relatively similar improvements of remission rates were found for high-dose (OR: 1.96, p < 0.01) and low-dose aripiprazole (OR: 1.68, P = 0.01), as well as brexpiprazole (OR: 1.52, P = 0.05) as an add-on to antidepressant medication. Our meta-analysis shows that partial dopamine agonists at high doses are effective in treating acute mania. In major depressive disorder, which is resistant to classical antidepressants, low doses of partial dopamine agonists as adjunct therapy may represent a relatively safe and effective alternative.


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