Reorganization of flexion reflexes in the upper extremity of hemiparetic subjects.

We examined spatiotemporal abnormalities in the flexor reflex response in the impaired upper extremity of hemiparetic subjects. Electrical stimulation was used to elicit flexion reflexes in both upper extremities of 8 hemiparetic brain-injured and 6 control subjects. Electromyograms (EMGs) were recorded from 12 arm muscles, and reflex forces and moments were recorded at the wrist with a load cell, and converted to shoulder and elbow torques. We found that the onset of reflex torque and EMG was delayed in the impaired arm and delays were greater at the shoulder than at the elbow. The normal reflex torque response consisted of elbow flexion, shoulder extension, and shoulder adduction. In contrast, in the impaired limb shoulder, flexion torque was observed in 7 subjects and shoulder abduction in 3. The delays in reflex onset and altered torque patterns in the impaired arm may be related to the abnormal movement synergies observed following stroke. © 1999 John Wiley & Sons, Inc.

Task-dependent weakness at the elbow in patients with hemiparesis.

OBJECTIVE: To investigate the task dependence of elbow weakness in patients with hemiparesis. DESIGN: Descriptive study based on interlimb comparisons of maximum voluntary torques (MVTs) generated isometrically in elbow flexion and extension under four task conditions: without explicit control of the torques at adjacent joints and in combination with each of three submaximal shoulder abduction/adduction torque levels. SETTING: Rehabilitation center research laboratory. PATIENTS: Volunteer samples of six patients with chronic hemiparesis and four controls. MAIN OUTCOME MEASURE: Residual strength (RS), defined as the ratio of MVTs for the paretic and nonparetic limbs of patients and nondominant and dominant limbs of controls. RESULTS: For the patient group a significant effect of task condition on RS was found (analysis of variance, p = .0003 and p = .002 for elbow flexion and extension, respectively). With increasing shoulder abduction torque level, elbow flexion RS increased and elbow extension RS decreased. In contrast, for the control group, the effect of task condition on RS was not significant. CONCLUSION: In hemiparetic patients, weakness of the paretic elbow musculature shows a strong task dependence. This task dependence likely reflects the existence of abnormal synergies between elbow and shoulder muscles of the paretic limb and has important implications for the rehabilitation of motor function following hemiparesis.

Long-lasting reductions of spasticity induced by skin electrical stimulation.

We studied the effects of electrical stimulation of the skin on upper extremity spasticity in nine hemiparetic stroke subjects. The effects were quantified by comparing reflex torque responses elicited during ramp and hold angular perturbations of the elbow recorded before and after low-intensity skin stimulation. Electrical stimulation was applied to skin over the biceps muscle for a period of ten minutes at a 20 Hz frequency, pulse duration 0.1 ms, with an intensity level below motor threshold but above sensory threshold. In seven of the nine subjects, stimulation of skin over spastic muscle reduced peak torque responses in both flexors and extensors for at least 30 min. In these seven subjects there were significant increases in mean threshold angle for the onset of reflex torque so that a greater angular rotation was required to initiate the stretch reflex response. This shift occurred without change in reflex impedance. The origins of these long-term changes in reflex torque are unclear, but may reflect synaptic plasticity of spinal circuitry outside the stretch reflex loop.

Joint dependent passive stiffness in paretic and contralateral limbs of spastic patients with hemiparetic stroke.

Torque-angle relations at the elbow and ankle joints of relaxed normal controls and patients with hemiparetic stroke were compared. Low velocity flexion/hold/extension angular perturbations were applied to the joint under examination. The resulting torque-angle profiles described a hysteresis loop with similar slopes during the extension and flexion stages but separated by a vertical torque offset. Torque-angle responses obtained in the absence of significant muscle activation, as recorded by surface electromyographic activity, were designated as passive. Elbow passive stiffness estimates were calculated from the slope of the torque-angle response during the flexion stage of the perturbation. The elbow torque-angle plots exhibited linear passive stiffness with magnitude significantly lower than the passive stiffness of the ankle in both normal subjects and spastic patients. Changing ramp velocity had no significant effect on the passive torque-angle hysteresis loop at the elbow. A comparison of the torque-angle relations between hemiparetic spastic and normal control arms showed no significant differences in passive stiffness. Furthermore, no significant differences were found between paretic and contralateral upper limbs of a given hemiparetic subject. By contrast, significant differences in the torque-angle hysteresis loop were present between the paretic and contralateral ankles in all hemiparetic patients tested. These differences were more significant during dorsiflexion, and therefore seem to be related to preferential changes in mechanical properties of plantar flexor muscles. It is hypothesised that the differences in the torque-angle hysteresis loop between elbow and angle joints are related primarily to the larger amount of connective tissue in the calf muscles, as well as to a larger total physiological cross sectional area of calf muscles compared with elbow muscles. It is further hypothesized that the preferential increases in passive stiffness at the ankle in spastic legs result from immobilisation induced changes in muscle connective tissue, which are most prominent in muscles with predominantly slow-twitch fibres (such as soleus). Connective tissue surrounding such slow twitch muscle fibres have been shown to be more sensitive to immobilisation than those in fast twitch muscle. The functional, pathophysiological, and clinical implications of our findings are reviewed.

Abnormal muscle coactivation patterns during isometric torque generation at the elbow and shoulder in hemiparetic subjects.

To study abnormal spatial patterns of muscle activation in hemiparetic stroke, we compared EMG activity in paretic and contralateral elbow and shoulder muscles of 10 hemiparetic subjects during 1.5-s voluntary isometric contractions, against five to eight different loads. Isometric forces were generated in eight directions, referenced to a plane orthogonal to the long axis of the forearm, and were recorded by a three degrees of freedom load cell, mounted at the wrist. Surface and intramuscular EMGs of six elbow and six shoulder muscles were recorded from both impaired and contralateral upper extremities of each subject. The spatial characteristics of EMG activation of individual muscles were summarized using two measures. The first, called the 'net resultant EMG vector' is a new measure which calculated the vector sum of EMG magnitudes for each of the eight directions, and the second, index of EMG focus, is a measure of the range of EMG activation recorded for each load level. Use of these measures permitted us to describe spatial EMG characteristics quantitatively, which has not been done previously. We observed consistent and statistically significant shifts in the resultant EMG vector directions in the impaired limb, especially in shoulder and other proximal muscles. Significant increases in the angular range of EMG activity were also identified and were most evident at the elbow. Correlation analysis techniques were used to assess the degree of coactivation of different muscle pairs. There were consistent EMG coactivation patterns observed across all subjects (both normal and hemiparetic). However, in spasticparetic limbs, additional novel coactivational relationships were also recorded, especially between elbow flexors/shoulder abductors and elbow extensors/shoulder adductors. These novel coactivation patterns represent a reduction in the number of possible muscle combinations, or in the number of possible 'synergies' in the paretic limb of the stroke subject. This reduction in number of 'synergies' could result from a loss of descending command options; from an increased reliance on residual, descending brainstem pathways (such as the reticulospinal and vestibulospinal projections); from changes in spinal interneuronal excitability; or from a combination of several of these factors. The relative merits of these hypotheses are addressed.