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Query: UMLS:C0026838 (spasticity)
 6,471 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

Spasticity was quantified in nine children with spastic diplegia, using a sinusoidal displacement of the foot at frequencies from 3 to 12Hz. Ankle-joint stiffness was separated into elastic (energy-storing) and viscous (energy-dissipating) components. 'Path length' was used to represent the variation in stiffness over this frequency range. Compared with 11 unaffected children, a significant difference in path lengths was demonstrated for the children with spasticity. An age-dependent effect was demonstrated when path lengths of unaffected children were compared with those of 10 unaffected adults. A modified path-length measure is proposed which minimizes age dependency, yet enables detection of spasticity. Passive stiffness properties of unaffected adults showed higher elastic stiffness, viscosity and friction than unaffected children. A method was developed to evade the need for temporary nerve blocks to calculate inerital properties of the foot in persons with spasticity.
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PMID:Quantitative measurement of spasticity in children with cerebral palsy. 187 22

The relative contributions of variations in stretch reflex threshold and total joint stiffness to changes in stretch-evoked torque were assessed in the spastic elbow muscles of 14 hemiparetic spastic subjects. For a given subject, variations in torque, measured after a constant angular deflection, were mediated largely by changes in stretch reflex threshold, rather than by changes in reflex stiffness. Between-subject comparisons were sensitive to stiffness differences between limbs, but reflex thresholds were still broadly correlated with torque magnitude, suggesting that reductions in stretch reflex threshold are uniformly present in spastic muscles. These findings, coupled with the apparent similarity of reflex stiffness estimates in voluntarily activated spastic and normal muscles, suggest that the central disturbance in spasticity is a reduction in the threshold of the stretch reflex, without a significant enhancement of reflex gain.
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PMID:Quantitative relations between hypertonia and stretch reflex threshold in spastic hemiparesis. 337 34

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

Muscle spasm can be reduced by heat as well as by therapeutic cold. However, in upper motor neuron lesions, cold is more effective in reducing the spasticity. This effect lasts long enough to be of therapeutic value. Water immersion supports the reduction of muscle tone. Pain may be reduced by both thermal stimuli. The pain threshold seems to be elevated by the direct effect of both heat and cold on the free nerve endings and the pain-killing fibers. The tendency to bleed is increased with heat application and decreased with cold therapy. Edema resulting from trauma is increased with heat, and decreased in its development by cold application. Joint stiffness is decreased with heat application and increased with cold application. Water immersion removes weight from the joints and facilitates mobility.
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PMID:[Thermo- and hydrotherapy]. 787 3

Flexor and extensor spasms associated with severe spasticity frequently cause pain and suffering in neurologically impaired patients, and greatly interfere with comfort and activities. When high doses of oral medications are necessary to keep the symptoms under control and are poorly tolerated, the long-term spinal-selective intrathecal infusion of baclofen by means of implanted drug pump and catheter is a safe, efficient and reversible alternative to destructive surgical procedures. Between September 1991 and March 1995, intrathecal baclofen was infused in 18 selected patients out of a series of 42 severely disabled spastic cases. We report here our preliminary experience with the criteria of selection, the initial intrathecal bolus test and the long-term benefit of the selected patients. Our results confirm the dramatic immediate and long-term benefit reported in other series. After a period of treatment of 1 to 42 months, 13 patients had a complete disappearance of their spastic symptoms without any oral treatment, one patient kept unchanged clonus despite the use of low-dose oral treatment and another one a severe, not improved dysuria although in both of them hypertonia and spasms were abolished. Finally, 2 patients had important joint stiffness slightly impairing the benefit from the treatment. None of the 18 patients had central side-effects related to baclofen. With time, a slight increase in daily dose (inferior to 10%) was necessary in most patients.
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PMID:Chronic intrathecal baclofen in severely disabling spasticity: selection, clinical assessment and long-term benefit. 900 75

Placode untethering in myelomeningocele patients can result in improvement and/or stabilization of neurological function, spinal curvature and pain. This paper reviews the outcome of untethering procedures in 24 patients to determine the frequency of subsequent functional deterioration. Decreased range of movement, joint stiffness and changes in muscle tone were the commonest indications for surgical intervention, occurring in 15 patients. Untethering resulted in improvement in 8 patients, stabilization of progression in 6 and continued deterioration in 1 patient. Two patients previously untroubled with spasticity became symptomatic within 3 months of the procedure. Changes in ambulation were present preoperatively in 9 patients. Stabilization was observed in 4 and improvement in 5. One of the patients, who had improved, deteriorated during the 1st year of follow-up. Alterations in bladder capacity and continence occurred in 7 patients. Improvement was seen in 2 patients, deterioration in 2 and no change in 3. Of the patients who improved, 1 subsequently deteriorated again within the 2nd postoperative year. Of those patients who had stable bladder function preoperatively, 6 subsequently deteriorated despite untethering. Pain was a less frequent symptom, occurring in 6 patients. Six patients became pain-free within 3 months of untethering. Two patients who did not have pain preoperatively had pain at the operative site persisting for up to 3 months postoperatively. Of the 20 patients having a single untethering procedure to date, 11 have further symptoms that can be attributed to retethering.
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PMID:Functional deterioration following placode untethering in myelomeningocele. 969 32

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

This study was made to elucidate the changes in the periarticular connective tissue that can underlie the contracture after spasticity development. Sixteen Wistar rats underwent a spinal cord injury and 16 rats were either sham- or nonoperated. The periarticular connective tissue of the knee joint was assessed with histological, histomorphometric, immunohistochemical, and biochemical analyses. Histological results showed a smaller synovial intima, a dense subintimal and posterior joint capsule without fibrosis, and a disarranged posterior capsule in the spinal cord-injured knees with the flexion contracture. The synovial intima length was shortened only at the posterior capsule. Neither the distribution nor expression of type I and III collagen was affected. Contractures after spinal cord injuries are characterized by synovial intima adhesions. A dense and disarranged capsule may lead to joint stiffness. The alteration of periarticular connective tissues exhibits properties characteristic of the contracture after spasticity development.
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PMID:Alteration of knee joint connective tissues during contracture formation in spastic rats after an experimentally induced spinal cord injury. 1765 74

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


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