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Diverse pathophysiological processes converge on network disruption in mania.

Abstract：

BACKGROUND:Neuroimaging of psychiatric disease is challenged by the difficulty of establishing the causal role of neuroimaging abnormalities. Lesions that cause mania present a unique opportunity to understand how brain network disruption may cause mania in both lesions and in bipolar disorder. METHODS:A literature search revealed 23 case reports with imaged lesions that caused mania in patients without history of bipolar disorder. We traced these lesions and examined resting-state functional Magnetic Resonance Imaging (rsfMRI) connectivity to these lesions and control lesions to find networks that would be disrupted specifically by mania-causing lesions. The results were then used as regions-of-interest to examine rsfMRI connectivity in patients with bipolar disorder (n = 16) who underwent imaging longitudinally across states of both mania and euthymia alongside a cohort of healthy participants scanned longitudinally. We then sought to replicate these results in independent cohorts of manic (n = 26) and euthymic (n = 21) participants with bipolar disorder. RESULTS:Mania-inducing lesions overlap significantly in network connectivity. Mania-causing lesions selectively disrupt networks that include orbitofrontal cortex, dorsolateral prefrontal cortex, and temporal lobes. In bipolar disorder, the manic state was reflected in strong, significant, and specific disruption in network communication between these regions and regions implicated in bipolar pathophysiology: the amygdala and ventro-lateral prefrontal cortex. LIMITATIONS:There was heterogeneity in the clinical characterization of mania causing lesions. CONCLUSIONS:Lesions causing mania demonstrate shared and specific network disruptions. These disruptions are also observed in bipolar mania and suggest a convergence of multiple disorders on shared circuit dysfunction to cause mania.

journal_name

J Affect Disord

journal_title

Journal of affective disorders

authors

Lee I,Nielsen K,Nawaz U,Hall MH,Öngür D,Keshavan M,Brady R Jr

doi

10.1016/j.jad.2018.10.087

subject

Has Abstract

pub_date

2019-02-01 00:00:00

pages

115-123

eissn

0165-0327

issn

1573-2517

pii

S0165-0327(18)31702-6

journal_volume

244

pub_type

杂志文章

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