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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability to objectively measure spasticity, related to cerebral stroke, is important in the rehabilitation therapies since many therapeutic modalities have been developed over the years to reduce spasticity. The unproven clinical expectation is that function would be improved were spasticity to be reduced. Unfortunately, the ability to measure spasticity to conduct efficacy studies of spasticity-reducing therapies is not possible. This relates to the multi-variable nature of the spastic syndrome with the result that no clinical measurement technique has been proven to be sensitive, valid and reliable. Therefore, it is important to develop a research-oriented spasticity measurement system to meet this need. We describe the current development of such a system. Details of our pilot study of a reflex excitability technique, designed to measure certain components of cerebral spasticity, are presented. The technique combined biomechanical and electrophysiological measures to investigate a homogenous stroke sample (n = 6); it incorporated the H-reflex in soleus, during passive ankle movements, as a measure of faulty neural inhibition. This component significantly (p < .05) differentiated the stroke sample from a matched, healthy control group (n = 6). Evocation of a cutaneous reflex in soleus was a condition that was problematic and it had to be dropped from the protocol. Joint stiffness, which is thought to affect measures of spasticity during passive movement, did not contaminate the measures. Further research in this direction is required to delineate and measure other neural components of spasticity while taking into account related non-neural variables. The final objective in this line of research is to develop a valid, reliable and sensitive spasticity measurement system that could be used to judge the efficacy of physical neurorehabilitation treatments currently employed to reduce spasticity following stroke.
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PMID:Spasticity measurement in stroke: a pilot study. 146 49

The purpose of this study was to evaluate the feasibility of reflex excitability measurement techniques in the partial measurement of spasticity related to cerebral stroke. Techniques involved the testing of the soleus H-reflex at specific ankle positions during passive dorsiflexing movements with and without background plantarflexing contractions; conditions attempted to simulate the terminal stance phase of gait. Testing of 12 stroke subjects, having cerebrovascular lesions related only to occlusion of the middle cerebral artery, demonstrated significantly (p < 0.01) less inhibition of the H-reflex during passive ankle dorsiflexion compared to 12 matched, healthy controls. However, evocation of the H-reflex during a low-level, voluntary plantarflexing contraction concomitant with passive dorsiflexion, did not reflect a statistical difference between the two groups. The two conditions were thought to each represent measures of faulty presynaptic inhibition as indicators of cerebral spasticity. A Chi-square calculation of sensitivity for the passive ankle movement without background plantarflexing contraction condition, was shown to significantly differentiate (p < 0.05) between the stroke and normal groups. A positive, but weak, correlation was found for stroke subjects between this reflex measure and the Ashworth clinical measure of spasticity (r = 0.49). Although stroke subjects exhibited increased joint stiffness when the full range of passive ankle dorsiflexion movement was considered, in comparison to the matched healthy control subjects, no significant increase in passive stiffness was found at the joint position of the reflex evocation. Size of the cerebral lesion, as determined from CT or MRI scan, was not related to the spasticity measures. Therefore, in a homogeneous stroke sample, a component of cerebral spasticity i.e., faculty Ia presynaptic inhibition, has been measured during a simulated functional movement in the lower extremity and was shown to differentiate this group from a matched, healthy, control sample. Joint stiffness did not contaminate the measures.
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PMID:A reflex technique to measure presynaptic inhibition in cerebral stroke. 764 61

The operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (TSR). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. From recent studies it is clear that increased passive joint resistance in resting limbs following stroke is highly correlated with the induced TSR, but this evidence is lacking in spinal injury. The contribution of the TSR to hypertonia in spinal cord injury (SCI) is unclear and it is possible that hypertonia has a different origin in SCI. The contribution of resting and activated TSR activity to joint stiffness was compared in SCI and normal subjects. The magnitude of the TSR in ankle dorsiflexors (DF) and plantarflexors (PF) and mechanical ankle resistive torque were measured at rest and over a range of contraction levels in normal subjects. Similar measures were made in 13 subjects with SCI to the limits of their range of voluntary contraction. Normals and SCI received a pseudo-sinusoidal stretch perturbation of maximum amplitude +/- 20 degrees and frequency band 0.1-3.5 Hz that was comparable to that used in manual clinical testing of muscle tone. Elastic resistance and resonant frequency of the ankle joint, after normalization for limb volume, were significantly lower in complete and incomplete SCI than normal subjects. No reflex response related to stretch velocity was observed. Resting DF and PF TSR gain, when averaged over the tested band of frequencies, were significantly lower in complete SCI than in resting normal subjects (<0.5 microV/deg). Linear regression analysis found no significant relationship between TSR gain and resting joint stiffness in SCI. Mean TSR gain of DFs and PFs at rest was not correlated with the subject variables: age, time since SCI, level of injury, Frankel score, number of spasms per day, Ashworth score or anti-spastic medication. DF and PF reflex gain were linearly related to voluntary contraction level and regression analysis produced similar slopes in incomplete SCI and normal subjects. Hence TSR loop gain was not significantly increased in SCI at any equivalent contraction level. Extrapolation of the regression lines to zero contraction level predicted that reflex threshold was not reduced in SCI. Low frequency passive stretches did not induce significant TSR activity in the resting limbs of any member of this SCI group. The TSR thus did not contribute to their clinical hypertonia. Other reflex mechanisms must contribute to hypertonia as assessed clinically. This result contrasts with our similar study of cerebral spasticity after stroke, where a comparable low frequency stretch perturbation produced clear evidence of increased TSR gain that was correlated with the hypertonia at rest. We conclude that a low frequency stretch perturbation clearly distinguished between spasticity after stroke and SCI. Spasticity in the two conditions is not equivalent and care should be taken in generalizing results between them.
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PMID:The tonic stretch reflex and spastic hypertonia after spinal cord injury. 1668 Apr 28

Spasticity is often seen in patients with central nervous system lesion, such as stroke. It hinders functional movement and may induce pain. Current measures for assessing Spasticity are either quantitative but not convenient to use or convenient to use in clinics but lack of objective quantification. We developed a manual spasticity evaluator (MSE) to evaluate the spasticity quantitatively and potentially suitable for a clinical setting. Joint position and torque from 10 subjects with right hemiplegia and 9 healthy subjects were measured conveniently and used to evaluate spasticity and determine the catch angle. EMG signal was obtained from the biceps brachii and triceps brachii to corroborate the mechanical measurement of the MSE. Results showed that the MSE provided a convenient and quantitative measurement of spasticity, including presence of catch angle, increase in joint stiffness, and decrease in joint range of motion in the stroke patients, as compared with healthy subjects. EMG signals corroborated MSE assessment of the catch angle.
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PMID:Measurement of elbow spasticity in stroke patients using a manual spasticity evaluator. 1794 63

In addition to muscle weakness caused by injury to supraspinal centers, several mechanisms may contribute to motor impairment in the paretic lower limb following a stroke. Physiological changes in the paretic muscles and their motor units, passive or active restraint of agonist activation, and abnormal muscle activation patterns have been shown to occur after a stroke and to reduce muscle force generation. Other factors such as increased passive tone may impede agonist and antagonist muscle torque generation, while abnormal motor activation and altered motor control of muscles can produce abnormal gait patterns. Co-activation of opposing lower limb muscles contributes to joint stiffness and postural stability; abnormal co-activation in paretic lower limbs can lead to deficits in postural stabilization. Abnormal timing of muscle activation can also yield reduced muscle work output and, in turn, reduced limb function. When sensory deficits accompany muscle weakness, impaired processing of afferent signals may contribute to abnormal muscle activation, abnormal gait patterns, and abnormal responses to perturbation during gait and stance. This article reviews the impact of these various factors, individually and in combination, on impaired motor function in the paretic lower limb after a stroke.
Top Stroke Rehabil
PMID:Understanding motor impairment in the paretic lower limb after a stroke: a review of the literature. 1990 53

Quantitative measurement of ankle joint stiffness following stroke could prove useful in monitoring the progress of a rehabilitation programme. The objective of this study was to design a manual device for use in the clinical setting. Manual measurement of spastic ankle joint stiffness has historically been conducted using hand-held dynamometers or alternative devices, but some difficulties have been reported in controlling the velocity applied to the ankle during the measurement. In this study, a manually operated device was constructed with a footplate, a torquemeter and a potentiometer. It was mechanically designed to rotate around an approximated axis of the ankle joint and to measure ankle joint angular position and its corresponding resistive torque. Two stroke hemiplegic subjects pariticapted in a pilot study. The results suggested that difficulty in controlling the applied velocity might be complemented by presenting torque data as a function of peak angular velocity in each stretching cycle. Moreover, the results demonstrated that the device could potentially apply a wide range of angular velocities and provide potentially useful clinical information. Quantitative data successfully acquired using this method included the approximate ankle angular position, where the velocity-dependent characteristics of stiffness was notably initiated and its corresponding torque and velocity.
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PMID:Quantitative measurement of spastic ankle joint stiffness using a manual device: a preliminary study. 2018 76

Lower-limb multi-joint (knee and ankle) stiffness may play an important role in functional activities such as walking, and may be significantly altered post stroke. Thus, determination of lower-limb multi joint stiffness matrix is important for better understanding of gait and of pathological changes post stroke. In this study, using novel dynamics decomposition, the knee and ankle joint stiffness matrix including cross-coupled stiffness terms between the two joints were determined and reported ever first. The determined stiffness matrix may be useful for gait studies, and can be served as a baseline for studying pathophysiological changes post stroke.
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PMID:Lower-limb multi-joint stiffness of knee and ankle. 2557 Aug 71

It is unclear whether muscle contraction is necessary to increase quasi-joint stiffness (QJS) of the ankle joint during gait in patients with hemiparesis. The purpose of the present study was to investigate the relationship between QJS and muscle activation at the ankle joint in the stance phase during gait in patients with hemiparesis. Spatiotemporal and kinetic gait parameters and activation of the medial head of the gastrocnemius (MG), soleus (SOL), and tibialis anterior (TA) muscles were measured using a 3-dimensional motion analysis system and surface electromyography, in 21 patients with hemiparesis due to stroke and 10 healthy individuals. In the early stance, the QJS on the paretic side (PS) of patients was greater than that on the non-PS (p<0.05) and not significantly correlated with activation of the three muscles. In the middle stance, the QJS on the PS was lower than that on the non-PS (p<0.05) and that on the right side of controls (p<0.001), which was positively correlated with activation of the MG (r=0.51, p<0.05) and SOL (r=0.49, p<0.05). In the patients with hemiparesis, plantarflexor activation may not contribute to QJS in the early stance. On the other hand, QJS in the middle stance may be attributed to activation of the MG and SOL. Our findings suggest that activation of the MG and SOL in the middle stance on the PS may require to be enhanced to increase QJS during gait in patients with hemiparesis.
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PMID:Relationship between activation of ankle muscles and quasi-joint stiffness in early and middle stances during gait in patients with hemiparesis. 2621 41

Stroke affects multiple joints in the arm with stereotypical patterns of arm deformity involving the shoulder, elbow, wrist, and hand and with disrupted coordination of multiple joints in active movements. However, there is a lack of systematic methods to evaluate multi-joints and multi-degree of freedoms (DOF) neuro-mechanical changes, especially for complex systems with three or more joints/DOFs involved. This paper used a novel systematic method to characterize dynamics and control of the shoulder, elbow, and wrist of the human arm individually and simultaneously, including the couplings across the multiple joints during controlled movements. A novel method was developed to decompose the complex system into manageable single-joint level for more reliable characterizations. The method was used in clinical studies to characterize the multi-joint changes associated with spastic impaired arm of 11 patients post stroke and 12 healthy controls. It was found that stroke survivors showed not only increased stiffness at the individual joints locally but also significantly higher couplings across the joints. The relative increases in couplings are often higher than that of the local joint stiffness. The multi-joint characterization provided a tool to characterize impairment of individual patients, which would allow more focused impairment-specific treatment. In general, the decomposition method can be used for even more complex systems, making characterization of intractable system dynamics of three or more joints/DOFs manageable.
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PMID:Changes of Shoulder, Elbow, and Wrist Stiffness Matrix Post Stroke. 2854 1

Exaggerated sensory activity has been assumed to contribute to functional impairment following lesion of the central motor pathway. However, recent studies have suggested that sensory contribution to muscle activity during gait is reduced in stroke patients and children with cerebral palsy (CP). We investigated whether this also occurs in CP adults and whether daily treadmill training is accompanied by alterations in sensory contribution to muscle activity. Seventeen adults with CP and 12 uninjured individuals participated. The participants walked on a treadmill while a robotized ankle-foot orthosis applied unload perturbations at the ankle, thereby removing sensory feedback naturally activated during push-off. Reduction of electromyographic (EMG) activity in the soleus muscle caused by unloads was compared and related to kinematics and ankle joint stiffness measurements. Similar measures were obtained after 6 wk of gait training. We found that sensory contribution to soleus EMG activation was reduced in CP adults compared with uninjured adults. The lowest contribution of sensory feedback was found in participants with lowest maximal gait speed. This was related to increased ankle plantar flexor stiffness. Six weeks of gait training did not alter the contribution of sensory feedback. We conclude that exaggerated sensory activity is unlikely to contribute to impaired gait in CP adults, because sensory contribution to muscle activity during gait was reduced compared with in uninjured individuals. Increased passive stiffness around the ankle joint is likely to diminish sensory feedback during gait so that a larger part of plantar flexor muscle activity must be generated by descending motor commands.NEW & NOTEWORTHY Findings suggest that adults with cerebral palsy have less contribution of sensory feedback to ongoing soleus muscle activation during push-off than uninjured individuals. Increased passive stiffness around the ankle joint is likely to diminish sensory feedback during gait, and/or sensory feedback is less integrated with central motor commands in the activation of spinal motor neurons. Consequently, muscle activation must to a larger extent rely on descending drive, which is already decreased because of the cerebral lesion.
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PMID:Contribution of sensory feedback to plantar flexor muscle activation during push-off in adults with cerebral palsy. 2890 5


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