scholarly journals 28.3 NEURAL TARGETS OF A MINDFULNESS INTERVENTION IN YOUTH WITH MOOD LABILITY AND FAMILIAL RISK FOR BIPOLAR DISORDER

Author(s):  
Danella Hafeman ◽  
A. Noelle Ostroff ◽  
Jamie Feldman ◽  
Mary L. Phillips ◽  
Boris Birmaher ◽  
...  
2014 ◽  
Vol 20 (14) ◽  
pp. 1881-1891 ◽  
Author(s):  
Viktoria Johansson ◽  
Cecilia Lundholm ◽  
Jan Hillert ◽  
Thomas Masterman ◽  
Paul Lichtenstein ◽  
...  

Background: Psychiatric disorders are known to be prevalent in multiple sclerosis (MS). Objective: The objective of this paper is to study comorbidity between MS and bipolar disorder, schizophrenia and depression in a nationwide cohort and to determine whether shared genetic liability underlies the putative association. Methods: We identified ICD-diagnosed patients with MS ( n = 16,467), bipolar disorder ( n = 30,761), schizophrenia ( n = 22,781) and depression ( n = 172,479) in the Swedish National Patient Register and identified their siblings in the Multi-Generation Register. The risk of MS was compared in psychiatric patients and in matched unexposed individuals. Shared familial risk between MS and psychiatric disorders was estimated by sibling comparison. Results: The risk of MS was increased in patients with bipolar disorder (hazard ratio (HR) 1.8, 95% confidence interval (CI) 1.6–2.2, p < 0.0001) and depression (HR 1.9, 95% CI 1.7–2.0, p < 0.0001). MS risk in schizophrenia was decreased (HR 0.6, 95% CI 0.4–0.9, p = 0.005). The association between having a sibling with a psychiatric disorder and developing MS was not significant. Conclusion: We found a strong positive association between MS and bipolar disorder and depression that could not be explained by genetic liability. The unexpected negative association between MS and schizophrenia might be spurious or indicate possible protective mechanisms that warrant further exploration.


2017 ◽  
Vol 41 (S1) ◽  
pp. S683-S683
Author(s):  
B. Francis ◽  
S.T. Jambunathan ◽  
J.S. Gill

Trichotillomania has been found to be associated with mood disorders, particularly bipolar disorder. Trichotillomania has shared similarities with bipolar disorder by virtue of phenomenology, co-morbidity, and psychopharmacologic observations. In the past, trichotillomania with comorbid bipolar disorder was treated with lithium and sodium valproate. There has been little, if any, literature on using asenapine to augment treatment in patients with trichotillomania with comorbid bipolar disorder. A patient presented with hair-pulling episodes for a year, resulting in bald scalp patches. She had no mood symptoms prior to this. She developed low mood, anhedonia, poor sleep and poor appetite subsequently as she could not stop pulling her hair. She was started on escitalopram 10 mg daily for he depressive symptoms. Three years later, she developed hypomanic symptoms such as irritability and spending sprees. Her hair pulling behaviour worsened at this time. At this point, a diagnosis of bipolar disorder type 2 was considered and she was started on lithium 300 mg daily. Her escitalopram was discontinued. As her mood was still labile 10 months later, asenapine was added to augment lithium in the treatment of the bipolar disorder. With asenapine, her hair pulling frequency started to decrease rapidly. Asenapine was increased to 10 mg daily and her hair pulling ceased. Her mood also stabilized and she no longer had erratic periods of mood lability. In conclusion, asenapine augmentation of lithium has potential to be used in patients who have trichotillomania with comorbid bipolar disorder due to its unique receptor profile.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2018 ◽  
Vol 83 (9) ◽  
pp. S84 ◽  
Author(s):  
David Pagliaccio ◽  
Jillian Wiggins ◽  
Nancy Adleman ◽  
Elizabeth Harkins ◽  
Alexa Curhan ◽  
...  

2019 ◽  
Vol 86 (7) ◽  
pp. 545-556 ◽  
Author(s):  
Sonja M.C. de Zwarte ◽  
Rachel M. Brouwer ◽  
Ingrid Agartz ◽  
Martin Alda ◽  
André Aleman ◽  
...  

2020 ◽  
Vol 59 (10) ◽  
pp. S197-S198
Author(s):  
Ewelina A. Migut ◽  
Rose-Marie T. Larios ◽  
Blake Novy ◽  
Crystal Franklin ◽  
Amy S. Garrett ◽  
...  

2019 ◽  
Vol 29 ◽  
pp. S192
Author(s):  
Sonia Hesam-Shariati ◽  
Bronwyn Overs ◽  
Claudio Toma ◽  
Oliver Watkeys ◽  
Melissa Green ◽  
...  

2017 ◽  
Vol 4 (5) ◽  
pp. 400-408 ◽  
Author(s):  
Birgitte Klee Burton ◽  
Anne A E Thorup ◽  
Jens Richardt Jepsen ◽  
Gry Poulsen ◽  
Ditte Ellersgaard ◽  
...  

2007 ◽  
Vol 17 ◽  
pp. S404-S405 ◽  
Author(s):  
V. Mondelli ◽  
C. McDonald ◽  
A. Gabilondo ◽  
K. Tournikioti ◽  
M. Walshe ◽  
...  

2014 ◽  
Vol 204 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Anne Duffy ◽  
Julie Horrocks ◽  
Sarah Doucette ◽  
Charles Keown-Stoneman ◽  
Shannon McCloskey ◽  
...  

BackgroundBipolar disorder is highly heritable and therefore longitudinal observation of children of affected parents is important to mapping the early natural history.AimsTo model the developmental trajectory of bipolar disorder based on the latest findings from an ongoing prospective study of the offspring of parents with well-characterised bipolar disorder.MethodA total of 229 offspring from families in which 1 parent had confirmed bipolar disorder and 86 control offspring were prospectively studied for up to 16 years. High-risk offspring were divided into subgroups based on the parental long-term response to lithium. Offspring were clinically assessed and DSM-IV diagnoses determined on masked consensus review using best estimate procedure. Adjusted survival analysis and generalised estimating equations were used to calculate differences in lifetime psychopathology. Multistate models were used to examine the progression through proposed clinical stages.ResultsHigh-risk offspring had an increased lifetime risk of a broad spectrum of disorders including bipolar disorder (hazard ratio (HR) = 20.89; P = 0.04), major depressive disorder (HR = 17.16; P = 0.004), anxiety (HR = 2.20; P = 0.03), sleep (HR = 28.21; P = 0.02) and substance use disorders (HR = 2.60; P = 0.05) compared with controls. However, only offspring from lithium non-responsive parents developed psychotic disorders. Childhood anxiety disorder predicted an increased risk of major mood disorder and evidence supported a progressive transition through clinical stages, from non-specific psychopathology to depressive and then manic or psychotic episodes.ConclusionsFindings underscore the importance of a developmental approach in conjunction with an appreciation of familial risk to facilitate earlier accurate diagnosis in symptomatic youth.


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