Bipolar disorder pick and mix

Smörgåsbord of topics on bipolar disorder

Day three of ECNP 2015 saw an exciting smörgåsbord of topics on bipolar disorder. Here’s a selection of the data, from around the world, that was on offer at the congress today

A Korean study, led by Dr San Heon Jang, investigated the effect of body mass index (BMI) on quality of life in patients with bipolar disorder. It’s well known that people with bipolar disorder are at risk for obesity.1 What this study investigated (and confirmed) was a correlation between increasing BMI and decreasing quality of life: that very heavy patients weren’t very happy ones. But for all patients there was emotional weight too: in an aside to their main conclusions, the authors noted that quality of life in patients with bipolar disorder was consistently below that of the general population, regardless of how heavy they were.

 

Summertime blues

 

Next: to Israel. An interesting presentation, led by Dr Eldar Hochman, which attempted to shed fresh light on a well-documented phenomenon in bipolar I disorder: seasonal patterns of manic episodes.2 Their study investigated what clinical and demographic features differentiated those with seasonal variation from those without. Of the 148 patients investigated, 26% experienced seasonal variation. The authors found this subgroup were more likely to be men and to have comorbid substance abuse (among other factors). The authors postulated whether this subgroup was one that may have poorer outcomes compared with the general bipolar I population.

This study echoes a recent review of 23 studies into seasonal mania, which reported a 15% rate of seasonal mania in bipolar disorder across the aggregated patient populations.2 Spring and summer appear to be the months where mania is more prevalent – the authors of both this review and today’s presentation hypothesising a link between hypersensitivity to increased light levels (and subsequent decreases in central melatonin levels).2

 

Family matters

 

A trio of Turkish studies, led by Professor Aybala Sarıçiçek, used MRI to investigate brain morphology in patients with bipolar disorder to investigate heritability in bipolar disorder.

Delving into greater detail than data already published in their recent study,3 the first study compared the brains of 28 patients with bipolar disorder, 25 healthy first-degree relatives (generally siblings) and 27 unrelated, matched healthy controls. Both patients with bipolar disorder and their relatives had significantly increased inferior frontal gyrus volumes – a brain area believed important in the pathophysiology of bipolar disorder; notably for its role in response inhibition.4

In their second study, major white matter regions were analysed in similar patient groups. Professor Sarıçiçek recorded significant alterations in the bipolar I group of several ‘white matter motorways’ compared with controls. Interestingly, values for many of these areas for the sibling group fell between those of healthy non relatives and the bipolar disorder group.

Tantalisingly low on detail, the authors were cautious to speculate what all this might mean, other than a potential ‘predictive or prognostic value’ in people with a family history of bipolar disorder.

In a final study of the three (in collaboration with a group based in the United Kingdom), the same topic had a slightly different approach – and with results to match. The group again compared patients with bipolar disorder, their first-degree relatives and healthy controls. In contrast to the previous two studies, this study examined cortical thickness. This they found to be reduced in patients with bipolar disorder, as well as correlated with poorer behavioural outcomes.

The conclusions of this study differed slightly from the previous two: the authors speculated on whether these changes were a pre-existing morphology caused by genetics or instead structural changes in the brain caused by repeated episodes – so-called ‘allostatic load.’5  Sadly, the authors did not discuss the role the third (family member) group data may have played in supporting either their genetic or pathophysiology theories.

Until next time, your correspondent.

Our correspondent’s highlights from the symposium are meant as a fair representation of the scientific content presented. The views and opinions expressed on this page do not necessarily reflect those of Lundbeck.

References

1.     Kolotkin RL et al. Obesity (Silver Spring) 2008; 16:749–754.

2.     Wang B, Chan D. J Psychiatr Pract 2014; 19:301–308.

3.     Sarıçiçek A et al. J Affect Disord 2015; 186:110–118.

4.     Aron AR et al. Trends Cogn Sci 2014; 18:177–185.  

5.     Vieta E et al. Eur Psychiatry 2013; 28:21–29.

Country selection
We are registering that you are located in Brazil - if that's correct then please continue to Progress in Mind Brazil
You are leaving Progress in Mind
Hello
Please confirm your email
We have just sent you an email, with a confirmation link.
Before you can gain full access - you need to confirm your email.
The information on this site is exclusively intented for health care professionals.
All the information included in the Website is related to products of the local market and, therefore, directed to health professionals legally authorized to prescribe or dispense medications with professional practice. The technical information of the drugs is provided merely informative, being the responsibility of the professionals authorized to prescribe drugs and decide, in each concrete case, the most appropriate treatment to the needs of the patient.
Congress
Register for access to Progress in Mind in your country