ORIGINS OF EXAGGERATED FINGER FLEXION IN STROKE

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Following stroke-induced paresis of the upper extremity, spontaneous finger flexion often appears with weeks, and then increases progressively. This flexion hinders rehabilitation by interfering with voluntary control of finger motion. The primary goal of the proposed research is to characterize the tonic nature and the possible causation of the flexion posture through imposed perturbations, in the hope of directing future research for remedies. The proposed experiments seek to examine the relative contributions of contracture, static hypertonicity, and spasticity to spontaneous finger flexion, and to test the effects of cutaneous afferents on this posture. Static as well as constant-velocity stretches would be imposed on the extrinsic finger flexors by rotation of the metacarpophalangeal joints, as produced by a servomotor coupled to the fingers. Subject response would be quantified in terms of torque, angular position, and EMG data. The position dependence of tone seen in the hand contralateral to the brain lesion would be compared with that of the ipsilateral hand by examining torque values recorded in the voluntarily relaxed state. Velocity dependence would be analyzed through quantification of stretch reflex responses for a series of constant-velocity displacements. To examine the effects of the cutaneous afferents, a topical anesthetic would be applied to the fingers and the stretch protocol repeated. These studies should provide insight into the role of the cutaneous afferents in the development of flexor tone and extensor weakness in the fingers following stroke.