Although extrinsic finger muscles could be successfully recruited electrically, voluntary excitation of these muscles was substantially limited in stroke survivors. Thus, finger weakness after stroke results predominantly from the inability to fully activate the muscle voluntarily.

Successful grasp requires that grip forces be properly directed between the fingertips and the held object. Changes in digit posture significantly affect the mapping between muscle force and fingertip force. Joint torques must subsequently be altered to maintain the desired force direction at the fingertips. Our current understanding of the roles of hand muscles in force production remains incomplete, as past studies focused on a limited set of postures or force directions. To thoroughly examine how hand muscles adapt to changing external (force direction) and internal (posture) conditions, activation patterns of six index finger muscles were examined with intramuscular electrodes in 10 healthy subjects. Participants produced submaximal isometric forces in each of six orthogonal directions at 9 different finger postures. Across force directions, participants significantly altered activation patterns to accommodate postural changes in the interphalangeal joint angles, but not changes in the metacarpophalangeal joint angles. Modulation of activation levels of the extrinsic hand muscles, particularly the extensors, were as great as those of intrinsic muscles, suggesting that both extrinsic/intrinsic muscles were involved in creating the desired forces. Despite considerable between-subject variation in the absolute activation patterns, PCA revealed that participants used similar strategies to accommodate the postural changes. The changes in muscle coordination also helped increase joint impedance to stabilize the endpoint force direction, counteracting the increased signal-dependent motor noise that arises with greater magnitude of muscle activation as interphalangeal joints flexed. These results highlight the role of the extrinsic muscles in controlling fingertip force direction across finger postures.

Background Stroke survivors experience greater strength deficits during finger extension than finger flexion. Prior research indicates relatively little observed weakness is directly attributable to muscle atrophy. Changes in other muscle properties, however, may contribute to strength deficits. Objectives This study measured muscle fiber conduction velocity in a finger flexor and extensor muscle to infer changes in muscle fiber type after stroke. Methods Conduction velocity was measured using a linear EMG surface electrode array for both extensor digitorum communis and flexor digitorum superficialis in 12 stroke survivors with chronic hand hemiparesis and 5 control subjects. Measurements were made in both hands for all subjects. Stroke survivors had either severe (n=5) or moderate (n=7) hand impairment. Results Absolute muscle fiber conduction velocity was significantly lower in the paretic hand of severely impaired stroke patients compared to moderately impaired patients and healthy control subjects. The relative conduction velocity between the two hands, however, was quite similar for flexor muscles across all subjects and for extensor muscles for the neurologically intact control subjects. However, muscle fiber conduction velocity for finger extensors was smaller in in the paretic as compared to the non-paretic hand for both groups of stroke survivors. Conclusions One explanation for reduced conduction velocity may be a type II to type I muscle fiber, especially in extrinsic extensors. Clinically, therapists may use this information to develop therapeutic exercises targeting loss of type II fiber in extensor muscles.