Measuring poststroke spasticity

2000 ◽  
Vol 10 (1) ◽  
pp. 69-74 ◽  
Author(s):  
J. M. Gregson ◽  
A. K. Sharma

What is spasticity?Spasticity is a well-recognized and potentially important clinical syndrome comprising inappropriate and involuntary high muscle tone. It has been variably defined, with debate still ongoing. Currently, the most widely accepted definition is that of Lance, stating that spasticity is ‘a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex.’ Unfortunately, even this description does not fully encompass the multifactorial nature of spasticity, since resistance to movement, even in the normal state, is subject to varied contributors. These include patient volition, inertia, visco-elastic muscle forces and range of joint movement, as well as true muscle activation secondary to reflex action. In the real clinical world, it is often not possible to distinguish which of these features is/are dominant. Furthermore, spastic muscle undergoes physiopathological, rheologic change with stiffness, atrophy, fibrosis and finally contracture.

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Sho Ito ◽  
Hiroaki Gomi

Fast signaling from vision and proprioception to muscle activation plays essential roles in quickly correcting movement. Though many studies have demonstrated modulation of the quick sensorimotor responses as depending on context in each modality, the contribution of multimodal information has not been established. Here, we examined whether state estimates contributing to stretch reflexes are represented solely by proprioceptive information or by multimodal information. Unlike previous studies, we newly found a significant stretch-reflex attenuation by the distortion and elimination of visual-feedback without any change in motor tasks. Furthermore, the stretch-reflex amplitude reduced with increasing elimination durations which would degrade state estimates. By contrast, even though a distortion was introduced in the target-motor-mapping, the stretch reflex was not simultaneously attenuated with visuomotor reflex. Our results therefore indicate that the observed stretch-reflex attenuation is specifically ascribed to uncertainty increase in estimating hand states, suggesting multimodal contributions to the generation of stretch reflexes.


2010 ◽  
Vol 104 (6) ◽  
pp. 3612-3624 ◽  
Author(s):  
Randy D. Trumbower ◽  
Vengateswaran J. Ravichandran ◽  
Matthew A. Krutky ◽  
Eric J. Perreault

Patterns of stereotyped muscle coactivation, clinically referred to as synergies, emerge following stroke and impair arm function. Although researchers have focused on cortical contributions, there is growing evidence that altered stretch reflex pathways may also contribute to impairment. However, most previous reflex studies have focused on passive, single-joint movements without regard to their coordination during volitional actions. The purpose of this study was to examine the effects of stroke on coordinated activity of stretch reflexes elicited in multiple arm muscles following multijoint perturbations. We hypothesized that cortical injury results in increased stretch reflexes of muscles characteristic of the abnormal flexor synergy during active arm conditions. To test this hypothesis, we used a robot to apply position perturbations to impaired arms of 10 stroke survivors and dominant arms of 8 healthy age-matched controls. Corresponding reflexes were assessed during volitional contractions simulating different levels of gravitational support, as well as during voluntary flexion and extension of the elbow and shoulder. Reflexes were quantified by average rectified surface electromyogram, recorded from eight muscles spanning the elbow and shoulder. Reflex coordination was quantified using an independent components analysis. We found stretch reflexes elicited in the stroke group were significantly less sensitive to changes in background muscle activation compared with those in the control group ( P < 0.05). We also observed significantly increased reflex coupling between elbow flexor and shoulder abductor–extensor muscles in stroke subjects relative to that in control subjects. This increased coupling was present only during volitional tasks that required elbow flexion ( P < 0.001), shoulder extension ( P < 0.01), and gravity opposition ( P < 0.01), but not during the “no load” condition. During volitional contractions, reflex amplitudes scaled with the level of impairment, as assessed by Fugl-Meyer scores ( r2 = 0.63; P < 0.05). We conclude that altered reflex coordination is indicative of motor impairment level and may contribute to impaired arm function following stroke.


Motor Control ◽  
2015 ◽  
Vol 19 (4) ◽  
pp. 253-270 ◽  
Author(s):  
Asger Roer Pedersen ◽  
Peter William Stubbs ◽  
Jørgen Feldbæk Nielsen

The aim was to investigate trial-by-trial response characteristics in the short-latency stretch reflex (SSR). Fourteen dorsiflexion stretches were applied to the ankle joint with a precontracted soleus muscle on 2 days. The magnitude and variability of trial-by-trial responses of the SSR were assessed. The SSR was log-normally distributed and variance heterogeneous between subjects. For some subjects, the magnitude and variance differed between days and stretches. As velocity increased, variance heterogeneity tended to decrease and response magnitude increased. The current study demonstrates the need to assess trial-by-trial response characteristics and not averaged curves. Moreover, it provides an analysis of SSR characteristics accounting for log-normally distributed and variance heterogeneous trial-by-trial responses.


1993 ◽  
Vol 69 (3) ◽  
pp. 943-952 ◽  
Author(s):  
R. R. Carter ◽  
P. E. Crago ◽  
P. H. Gorman

1. We investigated the role of stretch reflexes in controlling two antagonist muscles acting at the interphalangeal joint in the normal human thumb. Reflex action was compared when either muscle contracted alone and during cocontraction. 2. The total torque of the flexor pollicis longus (FPL) and extensor pollicis longus (EPL) muscles was measured in response to an externally imposed extension of the interphalangeal joint. The initial joint angle and the amplitude of the extension were constant in all experiments, and the preload of the active muscle(s) was varied. Joint torque was measured at the peak of short-latency stretch reflex action during contraction of the FPL alone, contraction of the EPL alone, and during cocontraction. Incremental joint stiffness was calculated as the change in torque divided by the change in angle. 3. Incremental stiffness increased in proportion to the preload torque during single muscle contractions of either the FPL (lengthening disturbances) or the EPL (shortening disturbances). Thus stiffness was not regulated to a constant value in the face of varying loads for either single muscle stretch or release. 4. Incremental stiffness varied across the range of cocontraction levels while the net torque was maintained at approximately 0. Thus net torque alone did not determine the stiffness during cocontraction. 5. The contributions of each muscle to the net intrinsic torque during cocontraction were estimated by scaling the individual muscles' responses so that their sum gave the best fit (in a least-squares sense) to the cocontraction torque before reflex action. The solution is unique because the individual torques have opposite signs, but the stiffnesses add. This gave estimates of the initial torques of both muscles during cocontraction. 6. The contributions of the two muscles during cocontraction were used to estimate the active joint stiffness that would be expected if the two muscles were activated independently to the same levels as in the cocontraction trials. The stiffness measured at the peak of stretch reflex action during cocontraction trials differed from the sum of the stiffnesses of the two muscles when they were contracting alone. At low cocontraction levels, the measured stiffness was less than expected on the basis of summation of the action of the two muscles, whereas at high cocontraction levels, the measured stiffness was greater than expected. This demonstrates that there is nonlinear stretch reflex interaction. That is, reflex action for a pair of antagonists is not simply the linear sum of the reflex actions of the two muscles acting independently.(ABSTRACT TRUNCATED AT 400 WORDS)


Author(s):  
Daniel N. Bassett ◽  
Joseph D. Gardinier ◽  
Kurt T. Manal ◽  
Thomas S. Buchanan

This chapter describes a biomechanical model of the forces about the ankle joint applicable to both unimpaired and neurologically impaired subjects. EMGs and joint kinematics are used as inputs and muscle forces are the outputs. A hybrid modeling approach that uses both forward and inverse dynamics is employed and physiological parameters for the model are tuned for each subject using optimization procedures. The forward dynamics part of the model takes muscle activation and uses Hill-type models of muscle contraction dynamics to estimate muscle forces and the corresponding joint moments. Inverse dynamics is used to calibrate the forward dynamics model predictions of joint moments. In this chapter we will describe how to implement an EMG-driven hybrid forward and inverse dynamics model of the ankle that can be used in healthy and neurologically impaired people.


2001 ◽  
Vol 94 (2) ◽  
pp. 309-314 ◽  
Author(s):  
Robert B. King ◽  
Christine Fuller ◽  
George H. Collins

✓ The authors report the case of a young man who suffered multiple injuries in a motor vehicle accident, the most significant of which arose in the brain, creating an unusual clinical syndrome. After experiencing an initial coma for several days, the patient was found to have a right-sided homonymous hemianopsia and a right hemiparesis, which was more marked at the shoulder and was accompanied by preservation of finger movement. Dystonic movements appeared 2 months later and progressed, along with increased spasticity on volition, to severe uncontrolled arm movements at 2 years postinjury. This motor disorder continued to worsen during the following 6 years prior to the patient's death. At autopsy, the left side of the brain was observed to have marked atrophy of the optic tract, a partial lesion of the posterior portion of the medial segment of the globus pallidus (GP), and a reduction in the size of the internal capsule at the level of the GP, suggesting impaired circulation to these areas at the time of injury. The isolated lesion of the internal segment of the GP was the presumed cause of the dystonia, acting through an alteration in thalamic inhibition. The atrophic subthalamic nucleus was the probable cause of the hemiballismus. The authors speculate that this and other delayed and progressive features of this case were the result of an active, but disordered, adaptive process that failed to compensate and, instead, caused even greater problems than the original injury.


1991 ◽  
Vol 66 (4) ◽  
pp. 1139-1155 ◽  
Author(s):  
T. R. Nichols ◽  
D. Koffler-Smulevitz

1. The role of proprioceptive pathways linking the direct antagonists soleus (S) and tibialis anterior (TA) muscles in governing the mechanical properties of the ankle joint were studied in the decerebrate cat. Actions of these heterogenic pathways were compared with those between S and extensor digitorum longus (EDL), a muscle that also acts at the metatarsophalangeal joint. These neurally mediated interactions between S and either TA or EDL were studied by applying controlled length changes to the isolated tendons of pairs of these muscles and recording the resulting changes in force. The muscles were activated with the use of electrically evoked crossed-extension reflexes, flexion reflexes, and brain stem stimulation. 2. Heterogenic inhibition from TA or EDL onto S was well developed whether S was initially quiescent or activated by a crossed-extension reflex. The inhibition persisted for the duration of the stretch of TA or EDL. During a crossed-extension reflex, TA did not generate background force, but brief stretch reflexes could be obtained. During flexion reflexes, stretch reflexes in S were usually abolished, and heterogenic inhibition from S to TA was weak or absent. 3. The strength of the heterogenic inhibition onto S was dependent on the initial length and activation level of TA and EDL. Changes in flexor length or activation level per se did not alter the background force or strength of the stretch reflex in S. Even taking into account the variation of strength of inhibition with the initial state of the muscle of origin, the strength of the inhibition was stronger from TA to S than the other way around. 4. The contributions of heterogenic inhibition from TA and EDL to S were independent in the sense that these components summed linearly with each other and with the autogenic reflex in S. In addition, the magnitude of the inhibition from TA to S was proportional to the amplitude of stretch for low to intermediate levels of initial force in S. The inhibition appeared to affect the mechanical responses of S essentially as rapidly as the stretch reflex in this muscle. 5. The heterogenic inhibition from TA to S was reduced or abolished by intravenous injections of strychnine but unaffected by injections of picrotoxin or bicuculline. These results, together with the observation that the inhibition sums linearly with the stretch reflex, suggest that the mechanism of this heterogenic inhibition is glycinergic and postsynaptic and, therefore, may include Ia-disynaptic reciprocal inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)


2013 ◽  
Vol 93 (10) ◽  
pp. 1331-1341 ◽  
Author(s):  
Judith M. Burnfield ◽  
Bernadette McCrory ◽  
Yu Shu ◽  
Thad W. Buster ◽  
Adam P. Taylor ◽  
...  

Background Workplace injuries from patient handling are prevalent. With the adoption of no-lift policies, sit-to-stand transfer devices have emerged as one tool to combat injuries. However, the therapeutic value associated with sit-to-stand transfers with the use of an assistive apparatus cannot be determined due to a lack of evidence-based data. Objective The aim of this study was to compare clinician-assisted, device-assisted, and the combination of clinician- and device-assisted sit-to-stand transfers in individuals who recently had a stroke. Design This cross-sectional, controlled laboratory study used a repeated-measures design. Methods The duration, joint kinematics, and muscle activity of 4 sit-to-stand transfer conditions were compared for 10 patients with stroke. Each patient performed 4 randomized sit-to-stand transfer conditions: clinician-assisted, device-assisted with no patient effort, device-assisted with the patient’s best effort, and device- and clinician-assisted. Results Device-assisted transfers took nearly twice as long as clinician-assisted transfers. Hip and knee joint movement patterns were similar across all conditions. Forward trunk flexion was lacking and ankle motion was restrained during device-assisted transfers. Encouragement and guidance from the clinician during device-assisted transfers led to increased lower extremity muscle activation levels. Limitations One lifting device and one clinician were evaluated. Clinician effort could not be controlled. Conclusions Lack of forward trunk flexion and restrained ankle movement during device-assisted transfers may dissuade clinicians from selecting this device for use as a dedicated rehabilitation tool. However, with clinician encouragement, muscle activation increased, which suggests that it is possible to safely practice transfers while challenging key leg muscles essential for standing. Future sit-to-stand devices should promote safety for the patient and clinician and encourage a movement pattern that more closely mimics normal sit-to-stand biomechanics.


2008 ◽  
Vol 105 (1) ◽  
pp. 226-232 ◽  
Author(s):  
Neil J. Cronin ◽  
Jussi Peltonen ◽  
Masaki Ishikawa ◽  
Paavo V. Komi ◽  
Janne Avela ◽  
...  

The aims of this study were to examine changes in the distribution of a stretch to the muscle fascicles with changes in contraction intensity in the human triceps surae and to relate fascicle stretch responses to short-latency stretch reflex behavior. Thirteen healthy subjects were seated in an ankle ergometer, and dorsiflexion stretches (8°; 250°/s) were applied to the triceps surae at different moment levels (0–100% of maximal voluntary contraction). Surface EMG was recorded in the medial gastrocnemius, soleus, and tibialis anterior muscles, and ultrasound was used to measure medial gastrocnemius and soleus fascicle lengths. At low forces, reflex amplitudes increased despite a lack of change or even a decrease in fascicle stretch velocities. At high forces, lower fascicle stretch velocities coincided with smaller stretch reflexes. The results revealed a decline in fascicle stretch velocity of over 50% between passive conditions and maximal force levels in the major muscles of the triceps surae. This is likely to be an important factor related to the decline in stretch reflex amplitudes at high forces. Because short-latency stretch reflexes contribute to force production and stiffness regulation of human muscle fibers, a reduction in afferent feedback from muscle spindles could decrease the efficacy of human movements involving the triceps surae, particularly where high force production is required.


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