Altered dynamics of brain segregation and integration in poststroke aphasia. Issue 11 (23rd April 2019) - Guo, Jing
Abstract: Poststroke aphasia (PSA) results from direct effect of focal lesions and dysfunction of distributed language networks. However, how flexible the activity at specific nodes control global dynamics is currently unknown. In this study, we demonstrate that alterations in the regional activity may cause imbalances between segregation and integration in temporo‐spatial pattern, and the transient dynamics are disrupted in PSA patients. Specifically, we applied dynamic framework to eyes‐closed resting‐state functional MRI data from PSA patients ( n = 17), and age‐, gender‐, and education‐matched healthy controls (HCs, n = 20). Subsequently, we calculated two basis brain organizational principles: "dynamic segregation, " obtained from dynamic amplitude of low‐frequency fluctuations (dALFF), which represent the specialized processing within interconnected brain regions; and "dynamic integration, " obtained from dynamic functional connectivity, which measures the efficient communication between interconnected brain regions. We found that both measures were decreased in the PSA patients within the left frontal and temporal subregions compared to the HCs. PSA patients displayed increased flexibility of interaction between left temporo‐frontal subregions and right temporo‐parieto‐frontal subnetworks. Furthermore, we found that dALFF in the pars triangularis of left inferior frontal gyrus was associated with aphasia quotient. These findings suggest that the reduced temporal flexibility of regional activity in language‐relevant cortical regions in PSA is related to the disrupted organization of intrahemispheric networks, leading to a loss of the corresponding functions. By using dynamic framework, our results offer valuable information about the alterations in segregation and integration of spatiotemporal information across networks and illuminate how dysfunction in flexible activity may underlie language deficits in PSA.