Sensorimotor impairments and reaching performance in subjects with poststroke hemiparesis during the first few months of recovery

Background and Purpose Little is known about the relationship between upper-extremity (UE) sensorimotor impairment and reaching performance during the first few months after stroke. The purpose of this study was to examine: (1) how measures of UE sensorimotor impairment are related to the speed, accuracy, and efficiency of reaching in subjects with hemiparesis during the subacute phase after stroke and (2) how impairments measured during the acute phase after stroke may predict the variance in reaching performance a few months later. Subjects and Methods upper-extremity sensorimotor impairments and reaching performance were evaluated in 39 subjects with hemiparesis at 2 time points: during the acute phase (8.7 +/- 3.6 [X +/- SD] days) and the subacute phase (108.7 +/- 16.5 days) after stroke. Ten subjects who were healthy (control subjects) were evaluated once. Regression analyses were used to determine which impairments were the best predictors of variance in reaching performance in the subacute phase after stroke. Results Only a small amount of variance (< 30% in reaching performance was explained at the subacute time point, using either acute or subacute impairments as predictor variables. Of the impairments measured, UE strength deficits were the strongest, most consistent predictors of the variance in reaching performance during the first 3 months after stroke. Discussion and Conclusion Surprisingly, the detailed clinical assessment of UE sensorimotor impairment, measured at the acute or subacute phase after stroke, did not explain much of the variance in reaching performance during the subacute phase after stroke. The findings that UE strength deficits (ie, decreased active range of motion and isometric force production) were the most common predictors of the variance in reaching performance during the first 3 months after stroke are consistent with the current viewpoint that impaired volitional muscle activation, clinically apparent as UE weakness, is a prominent contributing factor to UE dysfunction after stroke.