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PubMed2006

Clinical assessment of spasticity in children with cerebral palsy: a critical review of available instruments.

This study reviews the instruments used for the clinical assessment of spasticity in children with cerebral palsy, and evaluates their compliance with the concept of spasticity, defined as a velocity-dependent increase in muscle tone to passive stretch. Searches were performed in Medline, Embase, and Cinahl, including the keywords 'spasticity', 'child', and 'cerebral palsy', to identify articles in which a clinical method to measure spasticity was reported. Thirteen clinical spasticity assessment instruments were identified and evaluated using predetermined criteria. This review consists of reports on the standardization applied for assessment at different velocities, testing posture, and quantification of spasticity. Results show that most instruments do not comply with the concept of spasticity; standardization of assessment method is often lacking, and scoring systems of most instruments are ambiguous. Only the Tardieu Scale complies with the concept of spasticity, but this instrument has a comprehensive and time-consuming clinical scoring system.

Cerebral Palsy↗
PubMed2002

Surgical treatment of painful spasticity after spinal cord injury.

STUDY DESIGN: There are several conservative methods of painful spasticity treatment. However, conservative methods do not always provide long-term and complete antispastic effects in cases of spinal cord injury with severe painful spasticity. OBJECTIVES: The aim of the present study was to analyse and compare the effectiveness of myelotomy by Bischof II and Pourpre in patients with paraplegia and severe painful spasticity in the late period after spinal cord trauma. SETTING: Spinal Care Unit, Meir General Hospital, Israel. METHODS: Twenty patients had longitudinal T-myelotomy by the Bischof II technique and 20 longitudinal myelotomy en croix (Pourpre). The spasticity was determined by evaluated muscle tone and muscle spasm according to the Ashworth and spasm-frequency scales. The pain was determined by McGill short questionnaire. The results were calculated by the Wilcoxon signed rank test, by Mann-Whitney U-test and Students t-test. Clinical outcomes after myelotomy in-patients with chronic spinal cord injury and painful spasticity were evaluated after 6 months, 5 and 10 year follow-up period. RESULTS: Pain was relieved in all cases. The best motor antispastic effect was achieved after Pourpre myelotomy in 18 of the patients (90%) were evaluated after a follow-up of 6 months, 15 patients (75%) after 5 years, and 11 patients (64.7%) after 10 years. Following Bischof II myelotomy results were classified as good: in 13 patients-(65%) at 6 months; in nine patients (45%) at 5 years and in six patients-(40%) at 10 years. Statistical analysis showed no reliable relationship between the level of Spinal cord lesion (T4-T10) and the type of operation. No instability occurred as a result of antispastic operation in any patient. CONCLUSION: A higher rate of beneficial outcome was achieved after Pourpre myelotomy. We recommend this operation for patients with paraplegia and painful spasticity, who do not have hope of regaining voluntary motor function. However, transections of basic pathways of spasticity are not always sufficient for complete antispastic effects. Good results after the operation may deteriorate in time. Therefore further investigations into the mechanism of the spasticity syndrome in the spinal cord injured patient are required.

Adult↗
PubMed1984

Interlimb coordination of posture in patients with spastic paresis. Impaired function of spinal reflexes.

Activation of leg musculature on both sides following a unilateral displacement was studied during stance on separate see-saws, or on stable force-measuring platforms, in patients with spastic hemiparesis and paraparesis. During balancing the movements on the spastic side were damped and the degree of muscle activation reduced. Whereas in healthy subjects the tibialis anterior muscles of both sides were activated, following a unilateral displacement, with the same strength and latency (see-saws 55 ms, platforms 85 ms), in hemispastic patients the EMG responses were delayed (by about 20 to 30 ms) and of reduced strength on the spastic leg, irrespective of whether the unaffected or the spastic side was displaced. In addition, the compensatory movements on the spastic side were damped in both conditions, although the amplitude of displacement was the same bilaterally. Although there was no correlation between the delay and the reduction in EMG response, the latter was correlated with the severity of paresis. In patients with spastic paraparesis quite similar results were obtained with delayed and reduced EMG responses on both sides. It is concluded that in spasticity the impaired regulation of quick compensatory movements is due to a dysfunction of a spinal interneuronal system by which the early EMG responses are mediated. This could be explained by loss of supraspinal control. In addition to the impaired neural activation of leg muscles, changes in the mechanical properties of muscle can be assumed to contribute to the damped movements on the spastic side.

Adult↗
PubMed2004

Reciprocal inhibition and corticospinal transmission in the arm and leg in patients with autosomal dominant pure spastic paraparesis (ADPSP).

The pathophysiological mechanisms underlying the development of spasticity are not clear, but the excitability of the disynaptic reciprocal inhibitory pathway is affected in many patients with spasticity of different origin. Patients with genetically identified autosomal dominant pure spastic paraparesis (ADPSP) develop spasticity and paresis in the legs, but usually have no symptoms in the arms. Comparison of the spinal and supraspinal control of the legs and arms in these patients may therefore provide valuable information about the pathophysiology of spasticity. In the present study, we tested the hypothesis that one of the pathophysiological mechanisms of spasticity in these patients is abnormal corticospinal transmission and that this may lead to decreased reciprocal inhibition. Ten patients and 15 healthy age-matched control subjects were investigated. The patients were all spastic in the legs (with hyperactive tendon reflexes, increased muscle tone and Babinski sign), but had no neurological symptoms in the arms (except for one patient). Disynaptic reciprocal Ia inhibition of flexor carpi radialis (FCR) and soleus (SOL) motoneurons was measured (as the depression of the background FCR and SOL EMG activity and as the short latency inhibition of the FCR and SOL H-reflex evoked by radial and peroneal nerve stimulation). In addition, the latency of motor evoked potentials (MEPs) in the FCR muscle and the tibialis anterior (TA) muscle was measured. In the patients, the mean reciprocal inhibition was normal in the arms, while it was significantly decreased in the leg compared with the healthy subjects. In the patients, the average latency of MEPs in the FCR muscle was normal, while the latency to the MEP in TA muscle was significantly longer than that found in healthy subjects. Four patients, however, differed from the other patients by having significant reciprocal inhibition in the leg and a significantly shorter latency of TA MEPs than found in the other patients. The six patients without reciprocal inhibition in the leg instead had significant short latency facilitation of the SOL H-reflex and a longer TA MEP latency than seen in the healthy subjects and in the four patients with retained reciprocal inhibition. These findings support the hypothesis that disynaptic reciprocal inhibition and short latency facilitation are involved in the development of spasticity and, furthermore, they suggest a positive correlation between impairment of corticospinal transmission and decrease of reciprocal inhibition/appearance of reciprocal facilitation.

Adult↗
PubMed1991

An objective comparison of intrathecal lidocaine versus fentanyl for the treatment of lower extremity spasticity.

The reduction of spasticity after administration of intrathecal fentanyl, 35 micrograms, and intrathecal lidocaine, 50 mg, was compared with preinjection spasticity levels in ten subjects with central nervous system disease or injury. Spasticity was objectively assessed by an electronic instrument that simultaneously measures degrees of extension and force during passive knee extension. Duration of spasticity relief and adverse effects were recorded. Both drugs equally reduced spasticity and increased the range of motion. There were no supraspinal side effects from the fentanyl, whereas three subjects became hypotensive after receiving lidocaine. The reduction of spasticity with intrathecal fentanyl lasted at least 3 h. The authors postulate that fentanyl reduced spasticity by an effect on spinal pathways. Intrathecal fentanyl should be considered as an alternative to lidocaine for diagnostic blocks in patients with spasticity.

Adult↗
PubMedDate not supplied

Gabapentin for relief of spasticity associated with multiple sclerosis.

The use of a recently released anticonvulsant, gabapentin, in the treatment of spasticity in two patients with multiple sclerosis is reported. Gabapentin was chosen because of its GABA-ergic effect and because previously reported studies have shown that it is well tolerated compared with other GABA-mimetic medication. Satisfactory release of spasticity with significant improvement of functional outcome was noted in both cases. Both patients were first treated with gabapentin for one month at 300 mg per day and then, with no reported side-effects, at 400 mg per day. Before treatment, spasticity (graded with modified Ashworth Scale) in one patient was 3 for left lower and 2 for right lower limbs, and Expanded Disability Status Scale (EDSS) was 7; ambulation was limited to a few steps with a standard walker. After two weeks of treatment, spasticity was 2 and 1 for the left and right lower limbs, respectively. At three-month intervals, spasticity was +1 for left and 1 for right lower limbs, and EDSS was 6; the patient could ambulate 75 to 100 m with a standard walker. In the second patient, spasticity before treatment was 2 for both lower and left upper limbs. EDSS was 5.5, and ambulation was confined to 100 m with a cane. Spasticity improved to +1 in lower and 1 in left upper limbs after two weeks and to 1 and normal after three months. At three months, EDSS was 3 and the patient could ambulate for long distances without an assistive device. We suggest that gabapentin can be used effectively to decrease spasticity without significant side effects in patients with multiple sclerosis.

Acetates↗
PubMedDate not supplied

Treatment of spasticity with botulinum toxin.

Spasticity is an abnormal increase in muscle contraction often caused by damage to central motor pathways that control voluntary movement. During clinical examination, spasticity manifests as an increase in stretch reflexes, producing tendon jerks and resistance appearing as muscle tone. There are many causes of spasticity, including demyelination from multiple sclerosis, congenital damage from diseases such as cerebral palsy, trauma to the brain or spinal cord, hemorrhage or infarction, and other pathologic conditions that interrupt neural pathways. Effects of spasticity range from mild muscle stiffness to severe, painful muscle contractures and repetitive spasms that reduce mobility and substantially impede normal activities of daily living. Botulinum toxin therapy reduces spasticity and pain associated with several disorders. Local treatment with botulinum toxins can be used as adjunctive therapy, along with oral antispasticity medications, or alone to provide localized decrease in symptoms of spasticity and pain. Botulinum toxin therapy may be particularly useful for patients with spasticity due to stroke, whose treatment can be tailored based on recovery of function over time. In addition, botulinum toxin therapy is safe for pediatric patients, including children with cerebral palsy, who may not be able to tolerate the cognitive side effects of oral medications. Results of studies evaluating botulinum toxin for the treatment of spasticity due to various causes are presented here.

Botulinum Toxins↗
PubMed2001

Sensitivity of qualitative and quantitative spasticity measures to clinical treatment with cryotherapy.

This study examined the extent to which a battery of tests could detect a reduction of plantarflexor spasticity resulting from cryotherapy. The tests included a traditional qualitative spasticity scale, three potential quantitative spasticity measures and a measure of voluntary ankle muscle function. Twenty-six adult traumatic-brain-injured subjects were examined; these included 22 males and 4 females. The mean age was 28.15 years (range: 18-57, SD 10.78). The five tests were performed in random sequence on both ankles of each subject, before and after a 20 minute cold pack application to the calf. Tests were: modified Ashworth scale (MAS) scoring; H-reflex testing with and without dorsiflexor contraction (Hdf/Hctrl ratio); H-reflex testing with and without Achilles tendon vibration (Hvib/Hctrl ratio); reflex threshold angle (RTA) and timed toe tapping (TIT). Cryotherapy resulted in lowered MAS scores consistent with a reduction in spasticity. Doubly multivariate repeated measures ANOVA revealed a significant difference (F = 24.16, P < 0.001) in test scores between the pre- and post-cryotherapy test batteries. Significant pre- and post-cryotherapy differences (P < or = 0.03) for all dependent measures contributed to the main effect for cryotherapy. However, among the potential quantitative measures of spasticity only the RTA test demonstrated appropriate sensitivity to the reduction in spasticity. In spite of spasticity reduction, TIT performance was impaired following muscle cooling. Failure of the H-reflex ratios to show a reduction consistent with reduced spasticity was attributed to competing alpha and gamma motoneuron effects resulting from peripheral cooling.

Adolescent↗
PubMed1997

Advances in hereditary spastic paraplegia.

Hereditary spastic paraplegia refers to a group of clinically similar disorders whose primary feature is insidiously progressive lower extremity weakness and spasticity. Hereditary spastic paraplegia is genetically diverse: loci for autosomal recessive (chromosome 8p), autosomal dominant (chromosome 2p, 14q, and 15q), and x-linked hereditary spastic paraplegia have been identified. The existence of hereditary spastic paraplegia families for whom the disorder is unlinked to these loci indicates the existence of additional, as yet undiscovered, hereditary spastic paraplegia loci. Hereditary spastic paraplegia exhibits axonal degeneration that is maximal at the terminal portions of the longest central nervous system axons. Efforts to positionally clone the hereditary spastic paraplegia gene are in progress.

Humans↗
PubMed1988

Spasticity in head trauma and CVA patients: etiology and management.

Spasticity is a common problem in patients following head trauma and cerebral vascular accident (CVA). Spasticity interferes with mobility and self-care activities which are critical for successful rehabilitative outcomes. While a patient with a spastic muscle about a joint may be able to voluntarily contract the muscle, relaxation of the muscle may be impossible. Severe spasticity can result in joint contractures which further impair function. Shearing movements due to spastic responses precipitate skin breakdown and may disrupt pressure sore repair. In addition, the inability to perform functional activities produces frustration and anxiety for patients and their significant others. The purpose of this article is to review the pathophysiologic basis of spasticity, outline treatment methods used to decrease spasticity, and suggest clinical management strategies for the nurse working with head trauma and CVA patients who exhibit spasticity.

Brain Injuries↗
PubMed2004

Does reducing spasticity translate into functional benefit? An exploratory meta-analysis.

BACKGROUND: Spasticity and loss of function in an affected arm are common after stroke. Although botulinum toxin is used to reduce spasticity, its functional benefits are less easily demonstrated. This paper reports an exploratory meta-analysis to investigate the relationship between reduced arm spasticity and improved arm function. METHOD: Individual data from stroke patients in two randomised controlled trials of intra-muscular botulinum toxin were pooled. The Modified Ashworth Scale (elbow, wrist, fingers) was used to calculate a "Composite Spasticity Index". Data from the arm section of the Barthel Activities of Daily Living Index (dressing, grooming, and feeding) and three subjective measures (putting arm through sleeve, cleaning palm, cutting fingernails) were summed to give a "Composite Functional Index". Change scores and the time of maximum change were also calculated. RESULTS: Maximum changes in both composite measures occurred concurrently in 47 patients. In 26 patients the improvement in spasticity preceded the improvement in function with 18 showing the reverse. There was a definite relationship between the maximum change in spasticity and the maximum change in arm function, independent of treatment (rho = -0.2822, p = 0.0008, n = 137). There was a clear relationship between the changes in spasticity and in arm function in patients treated with botulinum toxin (Dysport) at 500 or 1000 units (rho = -0.5679, p = 0.0090, n = 22; rho = -0.4430, p = 0.0018, n = 47), but not in those treated with placebo or 1500 units. CONCLUSIONS: Using a targeted meta-analytic approach, it is possible to demonstrate that reducing spasticity in the arm is associated with a significant improvement in arm function.

Activities of Daily Living↗
PubMed1998

Does spasticity contribute to walking dysfunction after stroke?

OBJECTIVES: Clinically, it is assumed that spasticity of the calf muscles interferes with walking after stroke. The aim was to examine this assumption by evaluating the contribution of spasticity in the gastrocnemius muscle to walking dysfunction in an ambulant stroke population several months after stroke. METHODS: Fourteen stroke patients who were able to walk independently and 15 neurologically normal control subjects were recruited. Both resting and action stretch reflexes of the gastrocnemius muscle were investigated under conditions that simulated walking. Resting tonic stretch reflexes were measured to assess spasticity whereas action tonic stretch reflexes were measured to assess the possible contribution of spasticity to gait dysfunction. RESULTS: Two thirds of the stroke patients exhibited resting tonic stretch reflexes which indicate spasticity, whereas none of the control subjects did. However, the stroke patients exhibited action tonic stretch reflexes that were of similar magnitude to the control subjects, suggesting that their reflex activity during walking was not different from that of control subjects. Furthermore, there was no evidence that the action stretch reflex in the stroke patients contributed a higher resistance to stretch than the control subjects. CONCLUSIONS: Whereas most of the stroke patients exhibited spasticity when measured both clinically and physiologically, they did not exhibit an increase in resistance to dorsiflexion due to exaggerated action tonic stretch reflexes. It is concluded that it is unlikely that spasticity causes problems in walking after stroke in ambulant patients. Therefore, it seems inappropriate to routinely reduce or inhibit the reflex response to improve functional movement in stroke rehabilitation. Factors other than spasticity should be considered when analysing walking after stroke, so that appropriate treatment is provided to patients.

Aged↗
PubMedDate not supplied

Central and peripheral motor conduction time in chronic alcoholics with polyneuropathy and/or spasticity.

We measured central and peripheral motor conduction time to demonstrate lesions in the upper and lower motor neurons of 11 chronic alcoholics with polyneuropathy without spasticity, 7 chronic alcoholics with spasticity with and without alcoholic polyneuropathy, and 16 healthy volunteers as controls. Peripheral motor conduction time was significantly prolonged in all extremities in all of the chronic alcoholics, and was accompanied by a considerable reduction in motor conduction velocity. Central motor conduction time was considerably prolonged in the lower extremities of the alcoholics with spasticity compared with both the controls and the alcoholics without spasticity. Central motor conduction time in the patients with alcoholic polyneuropathy without spasticity was slightly prolonged in comparison with the controls, but not significantly. Based on the electrophysiological findings, we conclude that peripheral neuropathy is a lesion common to chronic alcoholics whether or not they have clinically evident polyneuropathy. Chronic alcoholics with spasticity have significantly longer central motor conduction time in the lower extremities. Spasticity in chronic alcoholics develops not independently but concomitantly with peripheral neuropathy, suggesting that peripheral neuropathy develops earlier than spasticity.

Action Potentials↗
PubMed1999

Correlation of spasticity with hyperactive stretch reflexes and motor dysfunction in hemiplegia.

OBJECTIVES: To study the correlation between spasticity and motor dysfunction in the wrist-hand unit of adult hemiplegic patients, and to investigate the correlation between clinical spasticity and hyperactive stretch reflexes. STUDY DESIGN: A survey study with a sequential case series of subjects. SETTING: Neuromuscular Research Laboratory, School of Physical Therapy, Texas Woman's University, Houston, TX. SUBJECTS: Sequential sample recruited from local stroke support groups: 10 patients with chronic hemiplegia caused by cerebral vascular accident who had various degrees of spasticity in the wrist joint. OUTCOME MEASURES: Modified Ashworth Scale, amplitudes of stretch reflexes for wrist flexors, grip strength, active range of motion of the wrist joint, and Fugl-Meyer test. RESULTS: Strong reverse correlation was found between spasticity and grip strength, the Fugl-Meyer test scores, and the Box and Blocks test scores (p = .001 to .005). Results also indicated a strong and consistent correlation between spasticity and reflexive electromyographic activities of the stretch reflex recorded from active muscles (p = .005 and .007), but not between spasticity and torque response of the stretch reflex. CONCLUSIONS: The degree of wrist spasticity is associated with impaired hand function in hemiplegic patients, and hyperactive electromyographic response of the stretch reflex, recorded from active muscles, is a valid indicator of spasticity.

Aged↗
PubMedDate not supplied

Effects of thoraco-lumbar electric sensory stimulation on knee extensor spasticity of persons who survived cerebrovascular accident (CVA).

Spasticity is mostly due to an excess of impulses to alpha motor neurons partly resulting from a change of interneuron activity. Low threshold afferent has been reported to change the activity in interneuron. The purpose of this study is to investigate the effects of surface spinal paravertebral stimulation on knee extensor spasticity. Ten survivors of stroke, with knee extensor spasticity, received electric stimulation for five 45-minute periods through surface electrodes applied to the skin in the twelfth thoracic and first lumbar areas. The electric stimulations had an amplitude modulated alternating current (AC), with a carrier frequency of 2500 Hz, modulated to "beats" frequency of 20 Hz. Stimulation amplitude was raised to elicit sensory stimulation. The pre- and post-treatment evaluation included the modified Ashworth scale, active torque during controlled knee movements at various velocities, and electromyographic (EMG) activity during the torque measurements. Our results indicate that nine of ten subjects demonstrated a decrease in the modified Ashworth scale post-treatment. The EMG activity of the spastic quadriceps during active knee flexion was decreased post-treatment as compared with the value before treatment. The active torque value of knee flexion or extension at 30 degrees, 60 degrees, or 90 degrees/sec of angular velocity did not change significantly post-treatment. A trend of increasing spastic quadriceps EMG activity with respect to the angular velocity during an active knee flexion was established, with Ashworth scale considered. The level of EMG activity is higher when the Ashworth scale is higher. According to our results, the surface paravertebral sensory stimulation was effective in reducing quadriceps muscle spasticity of the subjects. Both the modified Ashworth scale and the EMG activity of spastic quadriceps during eccentric contraction are suggested as sensitive tools for measuring spasticity of persons who survived cerebrovascular accident (CVA).

Adult↗
PubMed2003

[Medical treatment of spasticity].

Spasticity is one of the clinical signs observed after a lesion of the pyramidal tract. Clinical manifestations are polymorphous and depend on the location of the lesion on the pre-motoneuron. Functional consequences are also variable. Only negative effects such as painful spasms, stiffness, distortions, are to be treated. Three different categories of drugs are available: GABA-like (baclofen, benzodiazepine), central alpha 2 agonists (tizanidine, clonidine) and peripheral anti-spastics (dantrolene). Baclofen remains the most commonly used anti-spastic. The preferential indication is spasticity from spinal cord disease, especially when the aetiology is multiple sclerosis. Efficacy of benzodiazepines (diazepam, tetrazepam, clonazepam) is comparable with baclofen; however, side effects (drowsiness) are more frequent. Benzodiazepines are indicated when spasticity is associated with anxiety. Tizanidine is an efficient and well tolerated antispastic. In France, prescription requires a temporary authorization of use. Dantrolen has a peripheral mechanism of action and can be prescribed in the different forms of spasticity. There are other compounds with anti-spastic properties (gabapentine, cyproheptadine, piracetam). Their advantage is rather limited when used alone. Generally, they are administrated in combinaison with usual anti-spastic drugs.

Adrenergic alpha-Agonists↗
PubMed2003

Surgical treatment of spasticity by selective posterior rhizotomy: 30 years experience.

BACKGROUND: Spasticity is a common neurologic disorder with adverse effects on the patient's function. Conservative management is unsuccessful in a significant proportion of patients and neurosurgical intervention should be considered. The mainstay of surgical treatment of spasticity is selective posterior rhizotomy, i.e., section of sensory nerve roots of the cauda equina. OBJECTIVE: To report our experience with selective posterior rhizotomy in the treatment of spasticity. METHODS: We retrospectively reviewed our experience in 154 patients who underwent SPR during 30 years. The indication for surgery was spasticity that significantly hindered the patient's function or care and was resistant to conservative treatment. All patients were evaluated for spasticity in the lower and upper limbs, the presence or absence of painful spasms, and sphincter disturbances. The decision as to which roots to be sectioned, and to what extent, was based mainly on clinical muscle testing. RESULTS: Reduction of spasticity in the lower limbs was obtained in every case, with improvement in movements in 86% of cases. Painful spasms were alleviated in 80% of cases. Amelioration of neurogenic bladder was observed in 42%. A minority of the patients also showed improvement in speech and cognitive performance. There was no perioperative mortality or major complications. CONCLUSION: SPR is a safe and effective method for the treatment of spasticity with long-lasting beneficial effects. We suggest that this method be considered more frequently for patients with spasticity that interferes with their quality of life.

Adolescent↗
PubMed2005

Starting position and stretching velocity effects on the reflex threshold angle of stretch reflex in the soleus muscle of normal and spastic subjects.

BACKGROUND AND PURPOSE: Although both starting position and stretching velocity play an important role in reflex response, their interaction with stretch reflexes has not been thoroughly investigated. This study examined the interaction effect of starting position and stretching velocity on the reflex threshold angle (RTA) of the stretch reflex in the soleus muscle of normal and spastic subjects. METHODS: The spastic group included 11 ankles from 7 subjects with a history of upper motor neuron lesions. Their ages ranged from 22 to 40 years. Another 10 healthy subjects served as the control group. RTAs of the stretch reflex in the soleus muscle were measured for a matrix of starting positions and stretching velocities. The matrix design enabled the use of a 2-way analysis model to investigate the effect of starting position and stretching velocity on the RTA. RESULTS: No interaction effect was found in either the phasic stretch reflex (PSR) or the tonic stretch reflex (TSR) in the spastic group, or in the PSR in the normal group. The RTA of the PSR in both spastic and normal groups was significantly affected by starting position but not by stretching velocity. In contrast, the RTA of the TSR in the spastic group was affected by both starting position and stretching velocity. Stretching velocity and starting position played independent roles in determining the RTA of both the PSR and the TSR of the spastic group and in the PSR of the normal group. CONCLUSIONS: The lack of interaction between length-sensitive and velocity-sensitive muscle spindles in both normal and spastic subjects supports the hypothesis that they independently modulate the stretch reflex. Results for the RTA of the TSR demonstrated that spasticity results in disinhibition of motoneuron excitability with different thresholds.

Adult↗