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Publication Detail
Reduced Functional Connectivity of the Motor Network in Chronic Stroke
Background: Reorganization of functional brain networks after stroke has mainly focused on the activation of ipsi- and contralesional primary motor cortex (M1). However, the contribution of other areas of the brain remains unclear. To help clarifying this, we investigated whole-brain functional connectivity in a cohort of chronic stroke patients while they performed a motor task in the magnetic resonance scanner. Methods: Twenty-four healthy control subjects and 17 chronic stroke patients participated in a functional magnetic resonance imaging (fMRI) study that required the performance of a series of isometric handgrips with their dominant hand (control subjects) or affected hand (stroke patients). The data were analyzed using Constrained Principal Component Analysis for fMRI (fMRI-CPCA), a task-based analysis method that enables derivation of distinct, simultaneously active, functional brain networks that vary as a function of task-timing. Results: Our analysis revealed three distinct functional brain networks. The first one involved activation of the dorsal attention network, in which brain activity did not differ between groups. The second network was largely dominated by activations in motor regions (e.g., premotor cortex and M1), in which stroke patients demonstrated reduced activation relative to healthy controls. The third network included deactivations in premotor cortex as well as in regions that comprise the default-mode network, in which stroke patients exhibited less deactivation relative to control subjects. Interestingly, the motor and premotor/default-mode networks had temporally staggered peaks, whereby motor network activations occurred earlier in the trial than premotor/default-mode network deactivations. Conclusions: Our results suggest that performance of isometric handgrips in stroke patients, relative to control subjects, involves decreased activity in the motor network early in the trial, which is followed by an inability to suppress the premotor cortex later in the trial. This may indicate that chronic stroke patients activate premotor regions as a compensatory mechanism.
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