Bipolar disorder (BD) patients experiencing an episode of mania show corticolimbic dysregulation characterized by simultaneous resting limbic/paralimbic hypermetabolism and prefrontal hypometabolism, indicate study findings.

John Brooks III (UCLA Semel Institute, Los Angeles, USA) and co-authors say: “These findings support the hypothesis of corticolimbic dysregulation as a crucial contributor to the pathophysiology of BD.”

They add that findings from previous research on the neural substrates of mania have been variable, in part because of heterogeneity of techniques and patients.

“Though some findings have been replicated, the constellation of neuophysiologic changes has not been demonstrated simultaneously.”

To determine the resting state cerebral metabolic changes associated with relatively severe acute mania, Brooks and team performed resting positron emission tomography in eight BD patients with severe mania during the first 3 days of hospitalization, and in eight healthy gender- and age-matched controls.

Average Young Mania Rating Scale scores ranged from 29 to 41 among BD patients. At the time of scanning, BD patients had no more than 3 days of medication (olanzapine [n=5], quetiapine [n=1], or aripiprazole [n=1]), with one medication-naïve patient taking part in the study.

Compared with healthy controls, BD patients showed significant hypometabolism in the dorsolateral prefrontal cortex in Brodmann’s Areas 9, 10, and 46, and in the dorsal anterior cingulated and the precuneus.

In contrast, manic patients showed hypermetabolism in the left hippocampal complex, the rectal gyrus, and bilateral inferior temporal regions compared with controls. A region of hypermetabolism extending from the ventral anterior cingulate to the head of the caudate was also observed in BD patients.

The team concludes in the journal Psychiatry Research: Neuroimaging: “When the present findings are considered in the context of previous work, the metabolic picture of mania that emerges is one of paralimbic hypermetabolism that is not effectively modulated, perhaps because of dorsolateral prefrontal hypometabolism.

“Severe dysregulation of corticolimbic structures may result in more severe neurocognitive deficits and accompanying clinical symptoms.”

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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