Evidence of impaired neuromuscular responses in the support leg to a destabilizing swing phase perturbation in hemiparetic gait.

The neuromuscular mechanisms that underlie post-stroke impairment in reactive balance control during gait are not fully understood. Previous research has described altered muscle activations in the paretic leg in response to postural perturbations from static positions. Additionally, attenuation of interlimb reflexes after stroke has been reported. Our goal was to characterize post-stroke changes to neuromuscular responses in the stance leg following a swing phase perturbation during gait. We hypothesized that, following a trip, altered timing, sequence, and magnitudes of perturbation-induced activations would emerge in the paretic and nonparetic support legs of stroke survivors compared to healthy control subjects. The swing foot was interrupted, while subjects walked on a treadmill. In healthy subjects, a sequence of perturbation-induced activations emerged in the contralateral stance leg with mean onset latencies of 87-147 ms. The earliest latencies occurred in the hamstrings and hip abductor and adductors. The hamstrings, the adductor magnus, and the gastrocnemius dominated the relative balance of perturbation-induced activations. The sequence and balance of activations were largely preserved after stroke. However, onset latencies were significantly delayed across most muscles in both paretic and nonparetic stance legs. The shortest latencies observed suggest the involvement of interlimb reflexes with supraspinal pathways. The preservation of the sequence and balance of activations may point to a centrally programmed postural response that is preserved after stroke, while post-stroke delays may suggest longer transmission times for interlimb reflexes.

Effect of sensory feedback from the proximal upper limb on voluntary isometric finger flexion and extension in hemiparetic stroke subjects.

This study investigated the potential influence of proximal sensory feedback on voluntary distal motor activity in the paretic upper limb of hemiparetic stroke survivors and the potential effect of voluntary distal motor activity on proximal muscle activity. Ten stroke subjects and 10 neurologically intact control subjects performed maximum voluntary isometric flexion and extension, respectively, at the metacarpophalangeal (MCP) joints of the fingers in two static arm postures and under three conditions of electrical stimulation of the arm. The tasks were quantified in terms of maximum MCP torque [MCP flexion (MCP(flex)) or MCP extension (MCP(ext))] and activity of targeted (flexor digitorum superficialis or extensor digitorum communis) and nontargeted upper limb muscles. From a previous study on the MCP stretch reflex poststroke, we expected stroke subjects to exhibit a modulation of voluntary MCP torque production by arm posture and electrical stimulation and increased nontargeted muscle activity. Posture 1 (flexed elbow, neutral shoulder) led to greater MCP(flex) in stroke subjects than posture 2 (extended elbow, flexed shoulder). Electrical stimulation did not influence MCP(flex) or MCP(ext) in either subject group. In stroke subjects, posture 1 led to greater nontargeted upper limb flexor activity during MCP(flex) and to greater elbow flexor and extensor activity during MCP(ext). Stroke subjects exhibited greater elbow flexor activity during MCP(flex) and greater elbow flexor and extensor activity during MCP(ext) than control subjects. The results suggest that static arm posture can modulate voluntary distal motor activity and accompanying muscle activity in the paretic upper limb poststroke.

Analysis of muscle fiber conduction velocity during finger flexion and extension after stroke.

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 (MFCV) 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 five 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 MFCV was significantly lower in the paretic hand of severely impaired stroke patients compared to moderately impaired patients and healthy control subjects. The relative MFCV 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, MFCV for finger extensors was smaller in the paretic as compared to the nonparetic hand for both groups of stroke survivors. CONCLUSIONS: One explanation for reduced MFCV 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.

Contributions of voluntary activation deficits to hand weakness after stroke.

BACKGROUND: Hemiparetic stroke survivors often exhibit profound weakness in the digits of the paretic hand, but the relative contribution of potential biomechanical and neurological impairment mechanisms is not known. Establishing sources of impairment would help in guiding treatment. OBJECTIVE: The present study sought to quantify the role of diminished capacity to voluntarily active finger flexor and extensor muscles as one possible neurological mechanism. METHODS: Two groups of stroke survivors with "severe" (N = 9) or "moderate" (N = 9) hand impairment and one group of neurologically intact individuals (N = 9) participated. Subjects were asked to create isometric flexion force and extension force, respectively, with the tip of the middle finger. The maximum voluntary force (MVF) and the maximum stimulated force (MSF) produced by an applied train of electrical current pulses (MSF) were recorded for flexion and extension. Percent voluntary activation (PVA) was computed from MVF and MSF. RESULTS: Significant deficits in both MVF and PVA were observed for stroke subjects compared to control subjects. For example, activation deficits were >80% for extensor digitorum communis (EDC) for the "severe" group. Maximum voluntary force and PVA deficits were greater for EDC than for flexor digitorum superficialis (FDS) for stroke subjects with severe impairment. Maximum voluntary force and PVA correlated significantly for stroke subjects but not for control subjects. CONCLUSIONS: 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.

Modulation of stretch reflexes of the finger flexors by sensory feedback from the proximal upper limb poststroke.

Neural coupling of proximal and distal upper limb segments may have functional implications in the recovery of hemiparesis after stroke. The goal of the present study was to investigate whether the stretch reflex response magnitude of spastic finger flexor muscles poststroke is influenced by sensory input from the shoulder and the elbow and whether reflex coupling of muscles throughout the upper limb is altered in spastic stroke survivors. Through imposed extension of the metacarpophalangeal (MCP) joints, stretch of the relaxed finger flexors of the four fingers was imposed in 10 relaxed stroke subjects under different conditions of proximal sensory input, namely static arm posture (3 different shoulder/elbow postures) and electrical stimulation (surface stimulation of biceps brachii or triceps brachii, or none). Fast (300 degrees/s) imposed stretch elicited stretch reflex flexion torque at the MCP joints and reflex electromyographic (EMG) activity in flexor digitorum superficialis. Both measures were greatest in an arm posture of 90 degrees of elbow flexion and neutral shoulder position. Biceps stimulation resulted in greater MCP stretch reflex flexion torque. Fast imposed stretch also elicited reflex EMG activity in nonstretched heteronymous upper limb muscles, both proximal and distal. These results suggest that in the spastic hemiparetic upper limb poststroke, sensorimotor coupling of proximal and distal upper limb segments is involved in both the increased stretch reflex response of the finger flexors and an increased reflex coupling of heteronymous muscles. Both phenomena may be mediated through changes poststroke in the spinal reflex circuits and/or in the descending influence of supraspinal pathways.