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.
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.
Original language | English |
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Pages (from-to) | 633-641 |
Number of pages | 9 |
Journal | The American Journal of Psychiatry |
Volume | 169 |
Issue number | 6 |
DOIs | |
Publication status | Published - 1 Jun 2012 |