Diminished capacity to modulate motor activation patterns according to task contributes to thumb deficits following stroke

Abstract

The objective of this study was to explore motor impairment of the thumb following stroke. More specifically, we quantitatively examined kinetic deficits of the thumb. We anticipated that force deficits would be nonuniformly distributed across the kinetic workspace, due in part to varying levels of difficulty in altering the motor activation pattern to meet the task. Eighteen stroke survivors with chronic hemiparesis participated in the trials, along with nine age-matched controls. Of the stroke-survivor group, nine subjects had moderate hand impairment, and the other nine subjects had severe hand impairment. Subjects were instructed to generate maximal isometric thumb-tip force, as measured with a load cell, in each of six orthogonal directions with respect to the thumb tip. Activity of three representative thumb muscles was monitored through intramuscular and surface electrodes. Univariate split-plot analysis of variance revealed that clinical impairment level had a significant effect on measured force (P < 0.001), with the severely impaired group producing only 13% of the control forces, and the moderately impaired group generating 32% of control forces, on average. Weakness in the moderately impaired group exhibited a dependence on force direction (P = 0.015), with the least-relative weakness in the medial direction. Electromyographic recordings revealed that stroke survivors exhibited limited modulation of thumb-muscle activity with intended force direction. The difference in activation presented by the control group for a given muscle was equal to 40% of its full activation range across force directions, whereas this difference was only 26% for the moderately impaired group and 15% for the severely impaired group. This diminished ability to modify voluntary activation patterns, which we observed previously in index-finger muscles as well, appears to be a primary factor in hand impairment following stroke.