Sub-acute default mode network dysfunction predicts post-stroke depression severity

Abstract

Introduction: The aetiology of post-stroke depression (PSD) involves psychosocial and biological mechanisms. The "default-mode" network (DMN) appears to mediate internally-generated thought processes and is inhibited during cognitive tasks. Its structure and functioning have been reported to be modified in patients with mood disorders. We hypothesized that the severity of PSD would be related to a DMN dysfunction. Material and methods: T1-3D MRI and 5-minute resting-state fMRI scan were acquired 10 days after the cerebro-vascular insult in 28 first ever stroke patients, without past medical history of psychiatric illness. Independent component analysis was used to isolate the default mode network in each subject. Hamilton depression rating scale (HDRS-17) was recorded 10 and 90 days after stroke onset. Correlations between severity of depressive symptoms and DMN activations were investigated using SPM5. Significant cluster were determined using height threshold of p <0.001 and extent threshold of 10 voxels. Results: At 10 days, increased HAMDS scores were correlated to increased rest connectivity between bilateral superior and medial frontal cortex, anterior and medial and posterior cingulate cortex and precuneus and other DMN structures. At 90 days, post stroke HAMDS scores were correlated to increased rest connectivity between bilateral medial temporal cortex, right inferior temporal cortex, bilateral medial frontal cortex and left inferior frontal cortex, and the whole DMN. Discussion: Increased connectivity between fronto-cingulate cortex and the DMNin subacute stroke could reflect the involvement of prefrontal and limbic regions in perception and modulation of psychological stress. Conversely, increased connectivity between medial temporal cortex and the whole DMN could be predictive of poststroke depression severity at day 90. Widespread glutamate level changes following the cerebro-vascular insult could contribute to post-stroke DMN dysfunction.