Absence of stretch reflex gain enhancement in voluntarily activated spastic muscle

Static and dynamic stiffnesses of voluntarily activated elbow muscles were compared in spastic and contralateral arms of 15 subjects with spastic hemiparesis. Stiffnesses were estimated from the positional deflections induced by applying load perturbations to each forearm. In 11/15 subjects (73%), stiffness were comparable on the two sides. In the remaining 4/15 subjects (27%), stiffness were consistently greater on the spastic side, however, EMG recordings from these spastic muscles were of much smaller amplitude than those of the contralateral muscles, indicating that this increase was probably caused by changes in the mechanical properties of elbow muscles, rather than by stretch reflex enhancement. We conclude that for voluntarily activated muscles of spastic hemiparetic subjects, reflex stiffness (and presumably stretch reflex gain), of spastic and contralateral limbs is not significantly different. These findings impose important constraints upon theories attempting to explain spastic hypertonia, and they also provide guidelines for clinical quantification of spasticity.     

Reliability of dynamic muscle performance in the hemiparetic upper limb

We established reliability of upper-limb muscle performance in adults with post-stroke hemiparesis. Ten adults with post-stroke hemiparesis (51.5 +/- 34.5 months) performed isokinetic concentric shoulder flexion, elbow flexion, and extension at 3 criterion speeds (30 degrees/s, 75 degrees/s, and 120 degrees/s) on 3 separate occasions (Days 1, 7, and 49). As several participants were unable to reach criterion speeds, actual speed and power were also analyzed. Relative reliability (intraclass correlation coefficient-ICC) was excellent for torque and power (0.82 to 0.98) but less consistent for speed (0.63 to 0.99). Absolute reliability (standard error of measurement-%SEM) ranged between 0% to 34%. No systematic errors were observed across sessions. Smallest real differences (SRD) ranged between 4-11Nm for torque and 3-24W for power. Shoulder flexion, elbow flexion, and elbow extension torque, speed, and power can be measured reliably following stroke. Given that many of these individuals demonstrate inability to generate torque at preselected speeds, power may be a more valid indicator of muscle performance.     

Effects of changing wrist positions on finger flexor hypertonia in stroke survivors

We sought to establish whether spastic hypertonia results from changes in intrinsic muscle properties or from altered stretch reflex properties. We hypothesized that finger flexor spastic hypertonia is primarily of neural origin, and that the dynamics of spastic muscle responses to stretch should therefore reflect the dynamics of muscle spindle receptor responses. In 12 stroke survivors, we recorded torque and electromyographic (EMG) responses of extrinsic finger flexors to constant-velocity rotation of the metacarpophalangeal (MCP) joints of the affected hand, over a range of initial muscle lengths. Stretch velocity was set to 6 degrees, 50 degrees, 150 degrees, or 300 degrees per second. Muscle length changes were imposed by changing wrist angle between 0 degree, 25 degrees, and 50 degrees of flexion. We found that reflex torque and EMG responses exhibited both velocity and length dependence, and there were significant interactions between velocity and length, replicating known characteristics of muscle spindle receptors. Our results support the hypothesis that finger flexor hypertonia is primarily of neural origin, and that it accurately reflects spindle receptor firing properties.     

Reflex activity and muscle tone during elbow movements in patients with spastic paresis.

Reflex behavior and tension development in upper limb muscles were analyzed and comparisons made between the unaffected and spastic sides of patients with spastic hemiparesis. During sinusoidal (0.3-Hz) isometric or isotonic elbow tracking, with a control either of joint position or of torque, randomly timed displacements were induced (at one of three velocities) stretching either the activated flexor or the extensor muscles. On the spastic side, exaggerated short-latency reflexes were apparent, but in contrast, the amplitude of long-latency electromyography (EMG) responses was reduced. The latter responses were differentially modulated on the unaffected side, predominantly by the acceleration signal during control of position and more by the velocity signal during control of torque, while the mode of muscle contraction (isometric or isotonic) had little influence on this behavior. This difference in reflex modulation was lost on the spastic side. The functional consequence of this reduced EMG modulation could be difficulty in performing finely controlled arm movements. The ratio of torque to EMG activity during displacements was higher for both background and reflex-induced EMG on the spastic limb than on the unaffected side. This effect was more pronounced for the flexor than for the extensor muscles. Consequently, the development of spastic muscle hypertonia cannot be attributed to an increase in EMG activity. It is suggested that secondary to a supraspinal lesion, mechanical muscle properties change in such a way that the activated spastic muscle develops more tension when it is stretched.     

Activation impairment alters muscle torque-velocity in the knee extensors of persons with post-stroke hemiparesis.

OBJECTIVE: To elucidate mechanisms of impaired force production in post-stroke hemiparesis. METHODS: Knee extensor torque-velocity and activation-velocity relationships were examined in seventeen persons with post-stroke hemiparesis (age 57.5, +/-6.9) and thirteen non-disabled (age 63.0 +/-10.4) persons. RESULTS: Velocity-dependent concentric torque impairment was exaggerated in subjects with hemiparesis relative to control subjects (p<.001). Muscle power was also less in the group with hemiparesis (p<.001), and plateaued at velocities > or =90deg/s (p>.05). In the control group agonist EMG during concentric actions exhibited a positive linear relationship as velocity increased (R(2)=.93, p<.05). The group with hemiparesis produced 34-60% less agonist EMG than controls (p<.02) and modulation was absent (p>.05). Antagonist EMG was either greater in the control (biceps femoris, p<.006) or similar between groups (semimembranosus, p=.95). Under eccentric testing conditions, torque normalized to peak isometric torque (p=.44) and rectus femoris activation (p=.33) were similar between groups, indicating a relative preservation of eccentric torque producing capacity post-stroke. CONCLUSIONS: Certain clinical perspectives assert that weakness following central nervous system injury stems from spastic antagonist restraint. Instead, absence of an antagonist restraint strongly suggests that impaired agonist activation is the principal determinant of hemiparetic weakness. SIGNIFICANCE: These findings have important implications for promoting optimal recovery of motor function in neuro-rehabilitation.     

Stretch reflex dynamics in spastic elbow flexor muscles

Previous studies of stretch reflexes in patients with spastic hypertonia have emphasized the dynamic character of stretch reflex output. In contrast, our own studies of stretch reflex dynamics in spastic elbow flexor muscles of 14 hemiparetic human subjects have shown that stretch-evoked torque displays a relatively weak dependence on stretch velocity, and there is generally no preferential enhancement of dynamic as compared with static reflex output. Moreover, stretch reflex dynamics are broadly similar in voluntarily activated spastic and normal elbow flexor muscles. These findings support our hypothesis that spastic hypertonia results primarily from a decrease in stretch reflex threshold. The strong velocity dependence of stretch-evoked electromyographic activity in initially inactive spastic muscles could be due to a decrease in reflex threshold with increasing stretch velocity, rather than an abnormal velocity-dependent increase in stretch reflex responsiveness.     

Regulation of stretch reflex threshold in elbow flexors in children with cerebral palsy: a new measure of spasticity

The tonic stretch reflex threshold in children with cerebral palsy (CP) was measured to determine its test-retest reliability and its concurrent validity as a potential measure of spasticity. Fourteen children with spastic CP aged 6 to 18 years were tested on three separate occasions for clinical spasticity and stretch reflex thresholds of affected elbow flexors. Electromyographic (EMG) recordings were obtained by surface electrodes for elbow flexors and extensors during mechanical displacements of the passive joint towards extension. Displacements were produced by a torque motor at seven velocities which randomly varied from trial to trial. EMG activity was measured in the stretched flexor muscles to determine threshold angles and velocities for each velocity of stretch. These were plotted on a velocity-angle-phase diagram and regression analysis was used to determine the static stretch reflex threshold for each participant. The measure showed good test-retest reliability for the group (ICC 0.73, p<0.001) whereas a significant correlation between the measure and the clinical spasticity scale was not found. This technique is a potential outcome variable for measuring the efficacy of treatments aimed at decreasing spasticity in children with CP.     

A comprehensive model of spastic hypertonia derived from the pendulum test of the leg.

We propose a comprehensive model of spastic hypertonia based on clinical neurophysiology and validated using experimental data obtained from the pendulum test of the leg in 8 healthy volunteers and 15 spastic patients. This nonlinear computational model includes mechanical parameters and a stretch reflex representation involving three neural parameters: a threshold coefficient, the gain of the stretch reflex, and a time lag accounting for the reflex loop latency and the electromechanical coupling delay. Variation of the threshold coefficient alone allowed an overall reproduction of experimental data obtained from spastic and healthy subjects. We propose that this parameter could represent the supraspinal drive, supposed to be preserved in control subjects and decreased in spastic patients. No subsequent variation of the reflex gain was required to simulate spastic traces. Adjustment of the time lag influenced the duration of the swinging phase and oscillatory phenomena possibly occurring during the pendulum test. It could be related to the involvement of either short- or long-latency stretch reflex loops. With respect to current neurophysiological concepts of motor control, this modeling approach may help in understanding mechanisms underlying spastic hypertonia, and in predicting the clinical effect of antispasticity agents.     

Muscle inhibition following tendon stimulation is reduced in chronic stroke

ObjectiveElectrical tendon stimulation elicits reflex inhibition in the homonymous muscle that is thought to be mediated by group III afferents. The study goals were to: evaluate group III-mediated reflex inhibition in people with post-stroke hemiparesis; determine the presence of heteronymous group III pathways; investigate the relevance of reflex inhibition to arm function.MethodsReflex responses were recorded in wrist, elbow, and shoulder muscles following stimulation of the extensor carpi radialis (ECR) tendon in 16 people with post-stroke hemiparesis and 16 control subjects. In control subjects, reflex inhibition also was compared between static and dynamic muscle activation.ResultsReflex inhibition following ECR tendon stimulation was present in heteronymous muscles of most, but not all, stroke and control subjects. The level of reflex inhibition was significantly reduced in stroke subjects. In the controls, reflex inhibition was greater during dynamic activation of elbow muscles compared to static activation.ConclusionsEvidence that reflex inhibition projects to heteronymous muscles and is modulated during movement suggests a role for the reflex in multi-joint coordination. The reflex is impaired in post-stroke hemiparesis.SignificanceAbnormalities in the regulation of group III-mediated muscle inhibition in the stroke population may contribute to impaired muscle activation patterns during movement.     

Quantitative measures of spasticity in post-stroke patients.

OBJECTIVE: Quantitative evaluation of muscle tone in post-stroke patients; correlation of biomechanical indices with conventional clinical scales and neurophysiological measures; characterization of passive and neural components of muscle tone. METHODS: Mechanical stretches of the wrist flexor muscles of 53 post-stroke patients were imposed by means of a torque motor at constant speed. Patients were clinically studied using the Ashworth scale for spasticity and the Medical Research Council score for residual muscle strength. The neurophysiological measures were Hoffmann reflex latency, Hmax/Mmax ratio, stretch reflex threshold speed (SRTS), stretch reflex (SR) latency and area, passive (ISI) and total (TSI) stiffness indices. RESULTS: Hmax/Mmax ratio, SR area, ISI and TSI values were significantly higher in patients, while SRTS was significantly lower. TSI, SRTS and SR area were highly correlated to the Ashworth score. CONCLUSIONS: This EMG-biomechanical technique allows an objective evaluation of changes in muscle tone in post-stroke patients, providing easily measurable, quantitative indices of muscle stiffness. The linear distribution of these measures is particularly indicated for monitoring changes induced by treatment. The apparatus seems suitable to characterize neural stiffness, while difficulties were found in isolating the passive components, because of the occurrence of tonic EMG activity in most spastic patients.     

Gait recovery is not associated with changes in the temporal patterning of muscle activity during treadmill walking in patients with post-stroke hemiparesis.

OBJECTIVE: To establish whether functional recovery of gait in patients with post-stroke hemiparesis coincides with changes in the temporal patterning of lower extremity muscle activity and coactivity during treadmill walking. METHODS: Electromyographic (EMG) data from both legs, maximum walking speed, the amount of swing phase asymmetry and clinical measures were obtained from a group of post-acute patients with hemiparesis, as early as possible after admission in a rehabilitation centre (mean time post-stroke 35 days) and 1, 3, 6, and 10 weeks later, while all patients participated in a regular rehabilitation program. EMG data from the first assessment were compared to those obtained from a group of healthy controls to identify abnormalities in the temporal patterning of muscle activity. Within subject comparisons of patient data were made over time to investigate whether functional gait recovery was accompanied by changes in the temporal patterns muscle (co-)activity. RESULTS: EMG patterns during the first assessment showed a number of abnormalities on the paretic side, namely abnormally long durations of activity in biceps femoris (BF) during the single support (SS) phase and in gastrocnemius medialis (GM) during the first double support phase (DS1). Furthermore, in both legs a prolongation of the activity was seen in the rectus femoris (RF) during the SS phase. In addition, the duration of BF-RF coactivation was longer on the paretic side than it was in controls. Over time, the level of ambulatory independence, body mobility, and maximum walking speed increased significantly, indicating that substantial improvements in gait ability occurred. Despite these improvements, durations of muscle (co-) activity and the level of swing phase asymmetry did not change during rehabilitation. More specifically, timing abnormalities in muscle (co-)activity that were found during the first assessment did not change significantly, indicating that these aberrations were not an impediment for functional gait improvements. CONCLUSIONS: Normalization of the temporal patterning of gait related muscle activity in the lower extremities is not a prerequisite for functional recovery of gait in patients with post-stroke hemiparesis. Apparently, physiological processes other than improved temporal muscular coordination must be important determinants of the restoration of ambulatory capacity after stroke. SIGNIFICANCE: Recovery of walking ability in post-stroke hemiparesis is not necessarily associated with, or dependent on, reorganization in the temporal control of gait related muscle activity. Normalization of the temporal coordination of muscle activity during gait may not be an important clinical goal during post-acute rehabilitation.     

Spasticity measurement based on tonic stretch reflex threshold in stroke using a portable device

OBJECTIVES: We investigated intra- and inter-evaluator reliability to quantify spasticity based on the tonic stretch reflex threshold (TSRT) and the correlation between TSRT and resistance to stretch. METHODS: Spasticity was evaluated in 20 subjects with chronic stroke-related spasticity using a portable device and the Modified Ashworth Scale (MAS). Evaluations were done on 2 days, by three evaluators. Biceps brachii EMG signals and elbow displacement were recorded during 20 elbow stretches applied at different velocities for each evaluation. Velocity-dependent dynamic stretch reflex thresholds (angle where EMG signal increased in the biceps for a given velocity of stretch) were recorded. These values were used to compute TSRT (excitability of motoneurons at 0 degrees /s). Spasticity was also measured with MAS. RESULTS: Reliability was moderately good for subjects with moderate to high spasticity (intra-evaluator: 0.46-0.68, and inter-evaluator: 0.53-0.68). The TSRT measure of spasticity did not correlate with resistance to stretch (MAS). CONCLUSIONS: TSRT may be a more representative measure for subjects with moderate to high spasticity. Further improvements are suggested for the portable device in order to quantify all the levels of spasticity. SIGNIFICANCE: TSRT may be an alternative clinical measure to current clinical scales.     

Electromyographic Studies on Flexor Hypertonia of the Extremities of Newborn Infants

In order to investigate flexor hypertonia of the extremities in newborns, a neurological examination and superficial electromyogram (EMG) recordings were carried out on 50 full-term infants both before and after the first 48 hours of life (the 'birth-shock period). EMG amplituds on the flexor side of the upper arm in the traction response were low during the first 48 hours despite flexion of the elbow (hypertonia); after the first 48 hours EMG amplitudes increased in a large percentage of the infants although elbow flexion decreased (hypotonia). This finding suggests that the frflex response to passive movement (traction) is weaker during the first two days of life than after this time. Flexor tone of the upper arm in recoil of the forearm increased during the first 48 hours in spite of low EMG amplitudes; after the first 48 hours the amplitudes increased although flexor tone of the upper arm decreased. The popliteal angle was more than 90 degrees in 27 infants and less than 90 degrees in 23 infants during the first 48 hours; after this period the angle was more than 90 degrees in 11 infants and less than 90 degrees in 39 infants. EMG amplitudes on the flexor side of the thigh in most cases increased after the first 48 hours for both groups of infants, i.e. those with an angle more than 90 degrees and those with an angle less than 90 degrees. It is suggested that flexor hypertonia of the extremities in newborn infants is not a result of muscle contraction (i.e. real muscle strength) but rather is residual from the infant's position in utero.     

A comparative study of methods for estimation of presynaptic inhibition

Summary The influence of vibration on the H-reflex and on the tendon reflex amplitudes was compared and the efficacy of both methods for the assessment of the presynaptic inhibition was studied. One hundred and twenty patients with post-stroke spastic hemiparesis were investigated. Muscle tone, muscle force and tendon reflexes were assessed. The H-reflex and the Achilles tendon reflex (TA) were recorded under identical experimental conditions. Vibration at a frequency of 100 Hz and an amplitude of 2 mm was applied to the TA. Just after vibration the maximal amplitudes of both reflexes were measured. The ratios of reflex amplitudes after vibration to normal maximal reflex amplitudes (H_vibr/H_max and TA_vibr/TA_max) were evaluated. In all patients with hemiparesis the healthy side was used as a control. Our results revealed significantly increased amplitude ratios on the spastic side. Hence it is concluded that presynaptic inhibition is decreased in spasticity. The amplitude ratios on the healthy and the spastic side were consistent. There was good positive correlation between H_vibr/H_max and TA_vibr/TA_max ratios, suggesting that they provide similar and reliable estimates of presynaptic inhibition.     

Ballistic elbow flexion movements in patients with amyotrophic lateral sclerosis.

Patients with amyotrophic lateral sclerosis made stereotyped 20 degrees elbow flexion movements as rapidly as possible while surface EMG was recorded from biceps and triceps. The characteristic ballistic movement EMG pattern could be recognised in almost all the patients. The first agonist burst and the first antagonist burst, which are normally limited in duration, were prolonged in patients with clinical signs of pyramidal tract disease or alpha motor neurone disease or both. Prolongation of these components permits the muscles to generate sufficient forces to accomplish the movements.     

Spastic dystonia in stroke subjects: prevalence and features of the neglected phenomenon of the upper motor neuron syndrome

ObjectiveSpastic dystonia is one of the positive phenomena of the upper motor neuron syndrome (UMNS). It is characterised by the inability to relax a muscle leading to a spontaneous, although stretch-sensitive, tonic contraction. Although spastic dystonia is a recognized cause of muscle hypertonia, its prevalence among hypertonic muscles of stroke subjects has never been investigated. Differently from spasticity, which is an exaggerated stretch reflex, spastic dystonia is viewed as an efferent phenomenon, due to an abnormal central drive to motoneurons.MethodsIn 23 hemiparetic stroke subjects showing increased muscle tone of wrist flexors, surface EMG was used to investigate the presence of spontaneous, stretch-sensitive EMG activity in flexor carpi radialis.ResultsSpontaneous, stretch-sensitive EMG activity was found in 17 subjects. In the remaining 6 subjects, no spontaneous EMG activity was found.ConclusionsThe majority of stroke subjects is affected by spastic dystonia in their hypertonic wrist flexor muscles. Only a minority of subjects is affected by spasticity.SignificanceTo stop spastic dystonia from being the neglected aspect of UMNS, it is essential to link its definition to increased muscle tone, as occurred for spasticity. Recognizing the real phenomena underling muscle hypertonia could improve its management.     

Pathophysiology of gait in children with cerebral palsy

The surface electromyogram (EMG) of leg muscles was recorded together with the changes of the angle at the ankle joint during slow gait in 10 normal children and 10 with cerebral palsy. The characteristic pattern of muscle activity recorded from the spastic legs mainly consisted of a co-activation of antagonistic leg muscles during the stance phase of a gait cycle and a general reduction in amplitude of EMG activity. The tension of the Achilles tendon, measured in 2 hemiparetic children during gait, increased much more steeply in the spastic leg than in the normal one at the beginning of the stance phase, when the electrically almost silent triceps surae was stretched. It is suggested that muscle hypertonia during gait in spastic children is mainly due to changed muscle fibre mechanical properties, as recently discussed also for spastic adults. While in the latter the reciprocal EMG activity of antagonistic leg muscles was preserved it is proposed that muscle co-activation recorded in spastic children is due to an impaired maturation of the locomotor pattern with an early neuronal adaptation to altered muscle fibre mechanical characteristics.     

Spastic paresis: impaired spinal reflexes and intact motor programs.

Leg muscle EMG responses evoked by short treadmill acceleration impulses applied during stance were analysed in patients with spastic hemiparesis. The compensatory reactions on the unaffected side consisted of a diphasic pattern of leg muscle activation. The first response could best be described as a polysynaptic spinal stretch reflex response. This response was absent on the spastic side, except for its later, declining component. This remainder of the first response and the following activation of the antagonistic muscle was identical on both the unaffected and the spastic side. This part of the pattern is assumed to be centrally programmed (at the spinal level) and triggered by the termination of the acceleration impulse.     

Inter-rater and test/retest reliabilities of the isokinetic measurements: assessing strength and endurance of the trunk muscles in two different protocols for able-bodied and post-stroke hemiparesis

Background Stroke represents the largest cause of chronic disability resulting in muscle weakness and instability in the trunk muscles. Despite the reliable measures from isokinetic devices for upper/lower limb muscles, there is a lack of measures for trunk muscles in post-stroke hemiparesis.

Objectives To investigate the reliability of the strength and endurance measures from an isokinetic dynamometer for able-bodied and post-stroke hemiparesis people.

Methods The measures were taken from both groups (control/hemiparesis) performing antagonistic movements (flexion/extension) during different protocols (seated-compressed and semi-standing) to assess strength (60º/s) and endurance (120º/s). The intra-class correlation coefficient (ICC) and limits of agreement (LOA) defined the quality and magnitude of reliability on the measurements plotted with 95% confidence interval (95% CI) by Bland–Altman method.

Results ICC ranged from 0.58 to 0.99, with few ICC values classified as moderate when repeated by raters during test and a single value during retest. The total work was the only variable to present LOA higher than the limits.

Conclusion Results indicate acceptable reliability, in two different protocols, confirming the repeatability of the isokinetic measures for trunk muscles in able-bodied and post-stroke hemiparesis.