Abstract

Persistent motor deficits in the paretic arm present a major barrier to the recovery of the ability to perform bimanual tasks even in individuals who have recovered well after a stroke. Impaired performance may be related to deficits in bimanual temporal coordination due to stroke-related damage of specific brain motor structures as well as changed biomechanics of the paretic arm. To determine the extent of the deficit in bilateral temporal coordination after the stroke, we investigated how bilateral reciprocal coordination was regained after external perturbations of the arm in individuals with hemiparesis due to stroke. We used a bilateral task that would be minimally affected by the unilateral arm motor deficit. Nine non-disabled control subjects and 12 individuals with chronic hemiparesis performed reciprocal (anti-phase) arm swinging in the standing position for 15 s per trial. In each trial, movement of one arm was unexpectedly and transiently (approximately 150-350 ms) arrested at the level of the wrist once in the forward and once in the backward phase of swinging. Perturbation was applied to the left and right arms in control subjects and to the paretic and non-paretic arms of individuals with hemiparesis. Kinematic data from endpoint markers on both hands and electromyographic activity of anterior and posterior deltoid muscles from both arms were recorded. The oscillatory period, the phase differences between arms and the mean EMG activity before, during and after perturbation were analyzed. In both groups the perturbation altered the period of the perturbed cycle in both the arrested and non-arrested arms and resulted in a change from anti-phase to in-phase coordination, following which anti-phase coordination was regained. Recovery of anti-phase swinging took significantly longer in patients with hemiparesis compared to control subjects. Stable pre-perturbed (anti-phase) reciprocal coordination was regained within one cycle following perturbation for the control subjects and within two cycles following perturbation for the patients with hemiparesis. Analysis of EMG activation levels showed that, compared to control subjects, there was significantly less activation of the shoulder muscles in response to perturbation in the patient group and the pattern of muscle activation in the paretic arm was opposite to that in the non-paretic and control arms. The finding that patients had a reduced capacity for maintaining and restoring the required reciprocal coordination when perturbation occurred suggests that stroke-related brain damage in our patients led to instability of bilateral temporal coordination for this rhythmical task.

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