Abstract
A hallmark impairment in a hemiparetic stroke is a loss of independent joint control resulting in abnormal co-activation of shoulder abductor and elbow flexor muscles in their paretic arm, clinically known as the flexion synergy. The flexion synergy appears while generating shoulder abduction (SABD) torques as lifting the paretic arm. This likely be caused by an increased reliance on contralesional indirect motor pathways following damage to direct corticospinal projections. The assessment of functional connectivity between brain and muscle signals, i.e., brain-muscle connectivity (BMC), may provide insight into such changes to the usage of motor pathways. Our previous model simulation shows that multi-synaptic connections along the indirect motor pathway can generate nonlinear connectivity. We hypothesize that increased usage of indirect motor pathways (as increasing SABD load) will lead to an increase of nonlinear BMC. To test this hypothesis, we measured brain activity, muscle activity from shoulder abductors when stroke participants generate 20% and 40% of maximum SABD torque with their paretic arm. We computed both linear and nonlinear BMC between EEG and EMG. We found dominant nonlinear BMC at contralesional/ipsilateral hemisphere for stroke, whose magnitude increased with the SABD load. These results supported our hypothesis and indicated that nonlinear BMC could provide a quantitative indicator for determining the usage of indirect motor pathways following a hemiparetic stroke.
Highlights
THE human motor system is a highly cooperative network comprised of different groups of neurons
Shown in all participants suffering from a hemiparetic stroke, the expression of the flexion synergy enhanced with increased shoulder abduction (SABD) load
By applying our cross-spectral connectivity (CSC) method, we, for the first time, assessed both linear and nonlinear brain-muscle connectivity (BMC) at different SABD levels (20% vs. 40%) in chronic hemiparetic stroke, as compared to the healthy controls
Summary
THE human motor system is a highly cooperative network comprised of different groups of neurons. Damage to the brain increases reliance on indirect motor pathways resulting in motor impairments [2,3,4] and changes in neural connectivity [5]. It is thought to be caused by progressive recruitment of contralesional indirect motor pathways via the brainstem as a function of SABD torque generation following a stroke-induced loss of ipsilesional corticospinal projections [2, 11, 12]. A neural connectivity measure that quantifies the recruitment of these indirect motor pathways would be crucial to evaluate post-stroke motor impairments. This measure allows for the determination of the effect of new therapeutic interventions that aim to reduce such recruitment improving paretic arm function
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