Abstract
Psychiatric disorders are commonly characterized by sleep abnormalities. Conversely, disrupted sleep may contribute to the development of psychiatric conditions. This bidirectional causal relationship suggests common pathophysiological mechanisms in primary sleep and psychiatric disorders that could serve as clinical biomarkers or targets for novel therapeutics. Thirteen individuals with primary insomnia were age and sex matched to 13 good sleeping controls and 12 persons with generalized anxiety disorder (GAD). Each completed a 10-min, resting state scan in a 3-T fMRI scanner and completed inventories of state anxiety and neuroticism. Controls and primary insomniacs also recorded sleep for 2 weeks using diaries and actigraphy. Resting state data were preprocessed using standard methods and whole-brain connectivity of 6 fear and extinction-related seeds were compared between the 3 groups. Significant between-group differences in resting-state functional connectivity were seen between a left amygdala seed and a bilateral cluster in the rostral anterior cingulate cortex. This connectivity was significantly greater in controls than in both primary insomnia and GAD and this difference was greatest in GAD. No other seed regions revealed significant results. Across subjects, mean connectivity for left amygdala to rostral ACC decreased with poorer sleep, greater neuroticism and greater pre-scan state anxiety. For resting state connectivity in an emotion regulatory circuit, primary insomnia is intermediate between healthy controls and patients with GAD. These differences in connectivity correlate with measures of poor sleep and anxiety. This pattern may contribute to a greater risk of developing an anxiety disorder with preexisting primary insomnia. R21MH101567; 2015–2016 Harvard Mind/Brain/Behavior Interfaculty Initiative.
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