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. 2012 Jun;169(6):633-41.
doi: 10.1176/appi.ajp.2012.11081244.

A developmental study of the neural circuitry mediating motor inhibition in bipolar disorder

Affiliations

A developmental study of the neural circuitry mediating motor inhibition in bipolar disorder

Judah D Weathers et al. Am J Psychiatry. 2012 Jun.

Abstract

Objective: Despite increased interest in the developmental trajectory of the pathophysiology mediating bipolar disorder, few studies have compared adults and youths with bipolar disorder. Deficits in motor inhibition are thought to play an important role in the pathophysiology of the illness across the age spectrum. The authors compared the neural circuitry mediating this process in bipolar youths relative to bipolar adults and in healthy volunteers.

Method: Participants were pediatric (N=16) and adult (N=23) patients with bipolar disorder and healthy child (N=21) and adult (N=29) volunteers. Functional MRI (fMRI) data were acquired while participants performed the stop-signal task.

Results: During failed inhibition, an age group-by-diagnosis interaction manifested in the anterior cingulate cortex, with bipolar youths exhibiting hypoactivation relative to both healthy youths and bipolar adults, and bipolar adults exhibiting hyperactivation relative to healthy adults. During successful inhibition, a main effect of diagnosis emerged in the right nucleus accumbens and the left ventral prefrontal cortex, with bipolar patients in both age groups showing less activation than healthy subjects.

Conclusions: Anterior cingulate cortex dysfunction during failed motor inhibition was observed in both bipolar youths and adults, although the nature of this dysfunction differed between the two groups. Adults and youths with bipolar disorder exhibited similar deficits in activation of the nucleus accumbens and the ventral prefrontal cortex during successful inhibition. Therefore, while subcortical and ventral prefrontal cortex hypoactivation was present in bipolar patients across the lifespan, anterior cingulate cortex dysfunction varied developmentally, with reduced activation in youths and increased activation in adults during failed inhibition. Longitudinal fMRI studies of the developmental trajectory of the neural circuitry mediating motor inhibition in bipolar disorder are warranted.

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Conflict of interest statement

Disclosures

The authors have no conflicts to disclose.

Figures

Figure 1
Figure 1. Mean activation in left and right anterior cingulate cortex (ACC) during stop-incorrect vs. go contrast
(A) Anterior cingulate cortex (ACC) activation in stop-incorrect vs. go contrast. (B) Mean activation in right ACC (MNI coordinates x = 4, y = 42, z = 6).(C) Mean activation in left ACC (MNI coordinates x = 4, y = 42, z = 6). HV = healthy volunteers; BD = bipolar disorder
Figure 2
Figure 2. Mean activation in left ventral prefrontal cortex (VPFC) and right nucleus accumbens (NAc) during stop-correct vs. go contrast
(A) Ventral prefrontal cortex (VPFC) and nucleus accumbens (NAc) activation in stop-correct vs. go contrast. (B) Mean activation in left VPFC (MNI coordinates x = −26, y = 26, z = 8). (C) Mean activation in right NAc (MNI coordinates x = 16, y = 4, z = −6). HV= healthy volunteers; BD= bipolar disorder

Comment in

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