Bipolar disorder may be associated with an inherited abnormality of a neural network that incorporates the left prefrontal cortex and bilateral retrosplenial cortex, study findings suggest.

The functional magnetic resonance imaging (fMRI) study showed that when performing a verbal fluency task, bipolar disorder patients showed reduced deactivation the retrosplenial cortex and under-activation of the left prefrontal cortex compared with mentally healthy individuals.

A similar pattern was also seen in their unaffected first-degree relatives, “consistent with an inherited abnormality of functional brain architecture in bipolar patients and their relatives,” say Matthew Allin (King’s College London, UK) and colleagues.

The study participants included 18 remitted individuals with bipolar disorder, 19 of their unaffected first-degree relatives, and 19 mentally healthy controls. There were no significant differences among the groups with regard to age at assessment, gender distribution, or parental socio-economic status.

The participants completed a cued verbal fluency task, in which they generated a word in response to a letter displayed on a screen. The task, which has two levels of difficulty, involves both visual and verbal memory, evaluation of the presented letter along, and the selection of an appropriate word from memory.

The bipolar patients made significantly more errors on the easy level of the verbal task than their relatives and controls, at an average of 5.11 versus 1.95 and 2.10, respectively.

Analysis of fMRI data showed that all three groups showed deactivation in the retrosplenial cortex and adjacent precuneate cortex during task performance relative to a neutral or rest condition.

Both bipolar patients and unaffected relatives showed significantly less deactivation in the retrosplenial/posterior cingulate cortex than controls during both the easy and hard task, however.

The researchers note that the primary group difference was between unaffected relatives and controls, and that, counter-intuitively, activation patterns in bipolar patients seemed to be more similar to controls than to their relatives.

“Since bipolar disorder is likely to be influenced by genetic and epigenetic factors, the lack of a simple linear relationship here is perhaps not surprising,” they say.

Post-hoc group comparisons also revealed relative prefrontal hypo-activation in both bipolar patients and unaffected relatives compared with controls.

Allin and team acknowledge that treatment effects cannot be ruled out, but they report that there was “no evidence for any effect on task performance or on blood-oxygen-level-dependent signal in the posterior cingulate and the results were not altered by entering medication as a confounding variable.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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