Ipsilesional motor deficits following stroke reflect hemispheric specializations for movement control.

Recent reports of functional impairment in the 'unaffected' limb of stroke patients have suggested that these deficits vary with the side of lesion. This not only supports the idea that the ipsilateral hemisphere contributes to arm movements, but also implies that such contributions are lateralized. We have previously suggested that the left and right hemispheres are specialized for controlling different features of movement. In reaching movements, the non-dominant arm appears better adapted for achieving accurate final positions and the dominant arm for specifying initial trajectory features, such as movement direction and peak acceleration. The purpose of this study was to determine whether different features of control could characterize ipsilesional motor deficits following stroke. Healthy control subjects and patients with either left- or right-hemisphere damage performed targeted single-joint elbow movements of different amplitudes in their ipsilateral hemispace. We predicted that left-hemisphere damage would produce deficits in specification of initial trajectory features, while right-hemisphere damage would produce deficits in final position accuracy. Consistent with our predictions, patients with left, but not right, hemisphere damage showed reduced modulation of acceleration amplitude. However, patients with right, but not left, hemisphere damage showed significantly larger errors in final position, which corresponded to reduced modulation of acceleration duration. Neither patient group differed from controls in terms of movement speed. Instead, the mechanisms by which speed was specified, through modulation of acceleration amplitude and modulation of acceleration duration, appeared to be differentially affected by left- and right-hemisphere damage. These findings support the idea that each hemisphere contributes differentially to the control of initial trajectory and final position, and that ipsilesional deficits following stroke reflect this lateralization in control.