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PubMed2001

Modulation of presynaptic inhibition and disynaptic reciprocal Ia inhibition during voluntary movement in spasticity.

The aim of the study was to investigate whether impaired control of transmission in spinal inhibitory pathways contributes to the functional disability of patients with spasticity. To this end, transmission in the pathways mediating disynaptic reciprocal Ia inhibition and presynaptic inhibition was investigated in 23 healthy subjects and 20 patients with spastic multiple sclerosis during ankle dorsiflexion and plantar flexion. In healthy subjects, but not in spastic patients, the soleus H reflex was depressed at the onset of dorsiflexion (300 ms rise time, 20% of maximal voluntary effort). At the onset of plantar flexion, the soleus H reflex was more facilitated in the healthy subjects than in the patients. The H reflex increased more with increasing level of tonic plantar flexion and decreased more with dorsiflexion in the healthy subjects than in the spastic patients. Transmission in the disynaptic Ia reciprocal inhibitory pathway from ankle dorsiflexors to plantar flexors was investigated by conditioning the soleus H reflex by previous stimulation of the common peroneal nerve (conditioning-test interval 2-3 ms; stimulation intensity 1.05 times the motor response threshold). At the onset of dorsiflexion, stimulation of the common peroneal nerve evoked a significantly larger inhibition than at rest in the healthy subjects but not in the spastic patients. At the onset of plantar flexion the inhibition decreased in the healthy subjects, but because only weak inhibition was observed at rest in the patients it was not possible to determine whether a similar decrease occurred in this group. There were no differences in the modulation of inhibition during tonic plantar flexion and dorsiflexion in the two populations. Presynaptic inhibition of Ia afferents terminating on soleus motor neurones was evaluated from the monosynaptic Ia facilitation of the soleus H reflex evoked by femoral nerve stimulation. Femoral nerve facilitation was decreased at the onset of dorsiflexion and increased at the onset of plantar flexion in the healthy subjects and patients, but the changes were significantly greater in the healthy subjects. There was no difference between the two populations in the modulation of presynaptic inhibition during tonic plantar flexion and dorsiflexion. It is suggested that the abnormal regulation of disynaptic reciprocal inhibition and presynaptic inhibition in patients with spasticity is responsible for the abnormal modulation of stretch reflexes in relation to voluntary movement in these patients. Lack of an increase in reciprocal inhibition and presynaptic inhibition at the onset of dorsiflexion may be responsible for the tendency to elicitation of unwanted stretch reflex activity and co-contraction of antagonistic muscles in patients with spasticity.

Adult↗
PubMed2000

Intrathecal baclofen for intractable cerebral spasticity: a prospective placebo-controlled, double-blind study.

OBJECTIVE: To conduct a placebo-controlled prospective study of the effectiveness of intrathecal bolus injections and continuous administration of baclofen on functional parameters in patients with severe spasticity of cerebral origin. To compare this functional evaluation with spasticity scores in different muscle groups. METHODS: In 11 patients with spasticity of cerebral origin (mainly cerebral palsy), double-blind scoring of spasticity (Ashworth scale score and visual analog score), spasms, pain, and functional abilities was performed during tests with bolus injections including a placebo control. Eight patients were considered good responders and received a subcutaneous device for intrathecal drug delivery. Six of these patients were followed up for 2 years, during which they underwent the same scoring procedures as after their bolus injections. These patients were subjected to a blinded dose reduction test. RESULTS: There was a noticeable placebo effect on spasticity scores during tests with bolus injections. Eight patients demonstrated a significant beneficial effect of intrathecal bolus injections compared with this placebo effect. Functional improvements were noted in most patients. During continuous infusion, Ashworth scale scores were less favorable but still significantly lower than at baseline. Subjective evaluation (visual analog scores) remained positive, functional improvements were maintained, and patient comfort was invariably and significantly improved. CONCLUSION: Intrathecal administration of baclofen is a safe and effective treatment for spasticity of cerebral origin. Functional improvement was demonstrated. The presence of a placebo effect on the spasticity scores suggests the need for double-blind screening in each patient.

Adolescent↗
PubMed2003

Intrathecal baclofen for spasticity management in Rett syndrome.

Intrathecal baclofen infusions have proven to be effective for management of spasticity during the last two decades. Efficacy of intrathecal baclofen for spasticity of spinal origin has been well established and has shown promise in treatment of spasticity that is not spinal in origin. Rett syndrome is a neurodevelopmental disorder primarily affecting girls and women. Manifested in the advanced stages of this syndrome is increased spasticity leading to functional decline. Presented is a case report of a 32-yr-old white woman with Rett syndrome, diagnosed before the age of 2 yr, and significant spasticity that was successfully managed with intrathecal baclofen. After placement of an intrathecal baclofen pump, the dose was increased slowly during 1 yr to 800 microg/day with good clinical response. There was observed a significant decrease in upper and lower limb Ashworth scores, from an average of 3-4 to 2-3, during this 1-yr period. The decrease in spasticity in this patient eventually led to improved range of motion, positioning, skin care, hygiene, and quality of life. Intrathecal baclofen is an effective option in managing severe spasticity from Rett syndrome.

Adult↗
PubMed1977

Recurrence risks in families of children with symmetrical spasticity.

This study was undertaken to evaluate the recurrence risks for sibs of patients with symmetrical spasticity (either quadriplegia or diplegia) in the absence of factors known to cause spastic cerebral palsy (e.g. pre-term birth, perinatal hypoxia). Among 669 children in the West Midlands with spastic cerebral palsy, 24 had symmetrical spasticity and normal birth histories. This group was clinically and genetically heterogenous. Among their 55 sibs, six had a spastic disorder similar to that in the index patient, and one further sib, who had died young, had been mentally retarded. Of particular interest were two families with an autosomal recessive condition of post-natal microcephaly, myoclonic epilepsy and spastic quadriplegia; and one family, and possibly a sporadic case of X-linked athetoid cerebral palsy. The recurrence risk in this series of approximately 1 in 9 suggests that about half the children with symmetrical spastic cerebral palsy and a normal birth history may have a recessive condition.

Adolescent↗
PubMed1979

Gait electromyography in normal and spastic children, with special reference to quadriceps femoris and hamstring muscles.

Telemetered gait electromyography was used to investigate gait patterns and the phasic behavior of the quadriceps femoris and medial hamstring muscles in 26 normal children and 32 children with spastic cerebral palsy. The average child with spastic cerebral palsy was found to have a shorter stance phase than the normal, but the cadence, while more variable, was nearly the same as normal. The spastic muscles typically exhibited prolonged phasic activity or a dysphasic pattern. Most of the patients with spastic hamstrings also had spastic quadriceps, suggesting that over-weakening the hamstrings may produce an unwanted genu recurvatum or hyperextended knee gait. Care must be taken to balance hamstring spasticity with quadriceps spasticity. A final result with slight knee flexion is preferable to hyperextension.

Adolescent↗
PubMed1988

Effects of dorsal bilateral rhizotomy treatment on transmitter systems in the spinal cord of normal and spastic dogs.

The high-affinity uptakes of [3H]serotonin, [3H]-glutamate, and gamma-[3H]aminobutyric acid were studied using a myelin-free crude synaptosomal fraction prepared from the spinal cords of normal dogs and spastic dogs following sham treatment or dorsal bilateral rhizotomy surgery. Compared to sham-operated controls, rhizotomy surgery of normal dogs produced, after 1 week, a 30% reduction in the Vmax value of [3H]glutamate, but did not alter the uptake of gamma-[3H]aminobutyric acid. This treatment also produced a 60% decrease in the Vmax value of [3H]serotonin. Comparison of the effect of rhizotomy surgery on normal and spastic dogs revealed that the spastic group had 60% higher Vmax values for uptakes of [3H]glutamate and gamma-[3H]aminobutyric acid. Comparison of sham-operated spastic dogs and rhizotomy-treated spastic animals showed that there was a 25% decrease in the uptake of both amino acids in the rhizotomy-treated spastic group. Overall, the data (a) support the hypothesis that glutamate is the neurotransmitter from some of the primary afferents, and (b) suggest that sprouting of interneuronal amino acid transmitter systems may occur in the spinal cords of spastic dogs.

Animals↗
PubMedDate not supplied

Frequency response characteristics of ankle plantar flexors in humans following spinal cord injury: relation to degree of spasticity.

Frequency response characteristics of the ankle plantar flexors were studied in adults both with and without spinal cord injury (SCI) to determine how the muscle contractile properties change after SCI. and to see if there is a relation between the severity of spasticity and how the properties change. Ten controls and ten complete, chronic spinal cord injured subjects were tested, where the tibial nerve was stimulated electrically in a stochastic manner with the ankle fixed isometrically at various joint angles. A nonparametric linear frequency response function was derived, from which a second-order transfer function was calculated. The contractile dynamics were then characterized by the three classic second-order parameters: gain, damping ratio, and natural frequency. We found that in subjects with low degrees of spasticity (as determined by clinical evaluation), the contractile dynamics presented the largest changes, in which the speed of contraction increased significantly while there were no statistical differences in the gains between the two groups. This similarity emerged even though there was noticeable atrophy in the SCI patient group. Differences between the controls and subjects with high levels of spasticity were markedly different, in that these SCI subjects had slower contractile speeds than the controls, but significantly lower gains. Moderately spastic subjects fell somewhere in between, where the speed of muscle contraction increased modestly yet the gain was significantly smaller than that of the control subjects. These findings indicate that in subjects with chronic spinal cord injury, the severity of spasticity can significantly influence the degree of change in muscle contractile properties. It appears that high degrees of spasticity tend to preserve contractile dynamics, while in less spastic subjects, muscle contractile properties may display faster response characteristics.

Achilles Tendon↗
PubMed2005

Spastin mutations are frequent in sporadic spastic paraparesis and their spectrum is different from that observed in familial cases.

BACKGROUND: SPG4 encodes spastin, a member of the AAA protein family, and is the major gene responsible for autosomal dominant spastic paraplegia. It accounts for 10-40% of families with pure (or eventually complicated) hereditary spastic paraparesis (HSP). OBJECTIVE: To assess the frequency of SPG4 mutation in patients with spastic paraplegia but without family histories. METHODS: 146 mostly European probands with progressive spastic paraplegia were studied (103 with pure spastic paraplegia and 43 with additional features). Major neurological causes of paraplegia were excluded. None had a family history of paraplegia. DNA was screened by DHPLC for mutations in the 17 coding exons of the SPG4 gene. Sequence variants were characterised by direct sequencing. A panel of 600 control chromosomes was used to rule out polymorphisms. RESULTS: The overall rate of mutations was 12%; 19 different mutations were identified in 18 patients, 13 of which were novel. In one family, where both parents were examined and found to be normal, the mutation was transmitted by the asymptomatic mother, indicating reduced penetrance. The parents of other patients were not available for analysis but were reported to be normal. There was no evidence for de novo mutations. The mutations found in these apparently isolated patients were mostly of the missense type and tended to be associated with a less severe phenotype than previously described in patients with inherited mutations. CONCLUSIONS: The unexpected presence of SPG4 gene mutations in patients with sporadic spastic paraplegia suggests that gene testing should be done in individuals with pure or complicated spastic paraplegia without family histories.

Adenosine Triphosphatases↗
PubMed1993

X linked spastic paraplegia (SPG2): clinical heterogeneity at a single gene locus.

X linked hereditary spastic paraplegia is a rare condition that has been divided into two forms (the pure spastic form and the complicated form) as a function of clinical course and severity. A gene for pure hereditary spastic paraplegia (SPG2) has been mapped to the proximal long arm of the X chromosome (Xq21) by linkage to the DXS17 locus, while a gene for a complicated form of the disease has been mapped to the distal long arm by linkage to the DXS52 locus (Xq28). Here we report on the mapping of a gene for complicated hereditary spastic paraplegia to the Xq21 region by linkage to the probe S9 at the DXS17 locus (Z = 5 at theta = 0.04) in a three generation pedigree. Multipoint linkage analysis supports the distal location of the disease gene with respect to the DXYS1-DXS17 block (cen-DXYS1-DXS3-DXS17-SPG2-tel). The observation of a complicated form of spastic paraplegia mapping to Xq21 raises the difficult issue of variable phenotypic expression, allelic heterogeneity, or even close proximity of two genes for hereditary spastic paraplegia in this region. However, since our study provides clinical evidence for intrafamilial heterogeneity in complicated X linked spastic paraplegia, the present data support the hypothesis of variable clinical expression of a single gene at the SPG2 locus, as previously suggested for SPG1. Finally, we report here what we believe to be the first evidence of clinical expression in heterozygous carriers, a feature that is relevant to genetic counselling in at risk females.

Adolescent↗
PubMed2000

Impact of botulinum toxin type A on disability and carer burden due to arm spasticity after stroke: a randomised double blind placebo controlled trial.

OBJECTIVES: After stroke, abnormal arm posture due to spasticity in a functionally useless arm may interfere with self care tasks. In these patients botulinum toxin treatment presents an opportunity to reduce disability. The purpose was to investigate whether reduction in spasticity after botulinum toxin treatment translates into reduction in disability and carer burden. METHODS: Forty patients with stroke with spasticity in a functionally useless arm (median duration 3.1 years) were randomised to receive intramuscular botulinum toxin type A (BT-A; Dysport) (n=20) or placebo (n=20) in a total dose of 1000 MU divided between elbow, wrist, and finger flexors. Spasticity (using the modified Ashworth scale), muscle power, joint movement, and pain were assessed. Disability and carer burden were measured using an eight item and a four item scale respectively. Two baseline and three post-treatment assessments (weeks 2, 6, and 12) were made. Concurrent treatments as far as possible remained unchanged and not optimised. RESULTS: Disability improved at week 6 with BT-A compared with placebo. This effect, present at week 2, wore off by week 12. Reduction in carer burden was seen at week 6 with BT-A and continued for at least 12 weeks. Forearm flexor spasticity was reduced with BT-A up to 12 weeks after treatment. Although significant improvement in elbow flexor spasticity was seen at week 2 with BT-A compared with placebo, this effect was not evident at weeks 6 and 12. Arm pain was not improved after BT-A. Grip strength was reduced with BT-A. No serious BT-A related adverse effects were reported. CONCLUSION: BT-A is useful for treating patients with stroke who have self care difficulties due to arm spasticity. The decision to treat should also include relief of carer burden. As muscle weakness may occur, its potential impact on functional activities must be assessed before intervention.

Adolescent↗
PubMed2006

Spastic tail muscles recover from myofiber atrophy and myosin heavy chain transformations in chronic spinal rats.

Without intervention after spinal cord injury (SCI), paralyzed skeletal muscles undergo myofiber atrophy and slow-to-fast myofiber type transformations. We hypothesized that chronic spasticity-associated neuromuscular activity after SCI would promote recovery from such deleterious changes. We examined segmental tail muscles of chronic spinal rats with long-standing tail spasticity (7 mo after sacral spinal cord transection; older chronic spinals), chronic spinal rats that experienced less spasticity early after injury (young chronic spinals), and rats without spasticity after transection and bilateral deafferentation (spinal isolated). These were compared with tail muscles of age-matched normal rats. Using immunohistochemistry, we observed myofiber distributions of 15.9 +/- 3.5% type I, 18.7 +/- 10.7% type IIA, 60.8 +/- 12.6% type IID(X), and 2.3 +/- 1.3% type IIB (means +/- SD) in young normals, which were not different in older normals. Young chronic spinals demonstrated transformations toward faster myofiber types with decreased type I and increased type IID(X) paralleled by atrophy of all myofiber types compared with young normals. Spinal isolated rats also demonstrated decreased type I myofiber proportions and increased type II myofiber proportions, and severe myofiber atrophy. After 4 mo of complete spasticity (older chronic spinals), myofiber type transformations were reversed, with no significant differences in type I, IIA, IID(X), or IIB proportions compared with age-matched normals. Moreover, after this prolonged spasticity, type I, IIA, and IIB myofibers recovered from atrophy, and type IID(X) myofibers partially recovered. Our results indicate that early after transection or after long-term spinal isolation, relatively inactive tail myofibers atrophy and transform toward faster myofiber types. However, long-term spasticity apparently produces neuromuscular activity that promotes recovery of myofiber types and myofiber sizes.

Aging↗
PubMed1990

Spasticity in cerebral palsy and the selective posterior rhizotomy procedure.

A review of the selective posterior rhizotomy procedure for reduction of spasticity in cerebral palsy is presented. The history of the procedure, selection of patients, operative technique, and results are described. The neurophysiologic basis for spasticity is considered, as well as the role of spasticity in the complex motor disorder of cerebral palsy. Cerebral palsy is a multifaceted disorder of which spasticity is only one aspect. Reduction of spasticity can be effectively achieved using the current technique of selective posterior rhizotomy, but careful patient selection and establishment of realistic goals are vital to successful outcome. Postoperative physical and occupational therapy are felt to be essential for regaining strength and improving motor function following the rhizotomy procedure. Further study in the areas of spasticity, cerebral palsy, and the effects of rhizotomy is expected to advance our treatment of spastic children.

Cerebral Palsy↗
PubMed1993

Intrathecal baclofen for severe spasticity secondary to spinal cord injury.

OBJECTIVE: To evaluate the use of intrathecal baclofen for the treatment of muscle spasticity in patients with spinal cord injury. DATA SOURCES: A MEDLINE search was used to identify relevant and pertinent literature. Information was obtained from open-label clinical trials, abstracts, conference proceedings, and review articles. Index terms in the search included baclofen, spasticity, intrathecal drug infusion, spinal cord disease, and neurosurgery. DATA EXTRACTION: Studies were selected for review if they evaluated intrathecal baclofen in patients with spinal cord injury. Emphasis was placed on human studies published in the English language. Trials were reviewed by dosage regimen, therapeutic response, adverse effects, and complications. DATA SYNTHESIS: Thus far, intrathecal baclofen administration shows promise in the treatment of spasticity resulting from spinal cord trauma. Few complications and adverse effects have been reported. CONCLUSIONS: Muscle spasms and spasticity constitute a significant problem in spinal cord injuries, interfering with rehabilitation and leading to inconveniences and complications in these patients. Oral baclofen is the drug of choice for spasticity due to spinal cord trauma. It often is ineffective, however, because of the large dosages required to cross the blood-brain barrier and the subsequent appearance of central nervous system adverse effects. These adverse effects are not tolerated by many patients. Intrathecally administered baclofen has been approved by the Food and Drug Administration (FDA) for the treatment of spasticity in patients with spinal cord injury who are refractory to or cannot tolerate oral baclofen. It is intended for use only in implantable pumps approved by the FDA for the administration of baclofen into the intrathecal space. Intrathecal administration achieves high concentrations in the spinal cord with small dosages, thus reducing the incidence of central nervous system adverse effects. To date, approximately 350 patients with spinal cord injury have been treated with intrathecal baclofen. Reductions in spasticity have been demonstrated in both open-label and placebo-controlled trials. Patients also often make substantial gains in activities of daily living. Few adverse effects and complications have been reported. However, tolerance to the clinical effects of intrathecal baclofen has been reported. Further studies are needed to determine specific patient populations that may benefit most from intrathecal baclofen administration. Individual dosage ranges and follow-up care also need to be defined more completely. In addition, the question of whether tolerance detracts from long-term clinical benefits with intrathecal baclofen needs to be addressed.

Baclofen↗
PubMed2000

A double-blind placebo-controlled study of botulinum toxin in upper limb spasticity after stroke or head injury.

OBJECTIVE: To assess dose-response relationships to a single dose of botulinum toxin 'A' in upper limb spasticity associated with stroke or head injury. DESIGN: A double-blind placebo-controlled randomized dose ranging study. SETTING: A regional centre for neuroscience and a neurorehabilitation outpatient clinic. SUBJECTS: Twenty-one hemiplegic patients with troublesome upper limb spasticity. Nineteen with stroke and two with head injury. MAIN OUTCOME MEASURES: Spasticity (modified Ashworth), range of movement, posture (postural alignment and finger curl), disability (upper body dressing time and Frenchay Arm Test), patient-reported global assessment scale. RESULTS: Combining data from all doses of botulinum toxin there was a significant reduction in spasticity at the wrist and fingers associated with a greater range of passive movement at the wrist and less finger curl at rest. There was a tendency for a further reduction in spasticity at elbow and wrist to occur with increasing dose but not for finger spasticity or curl. Effects present at six weeks were lost by 12 weeks except for a small improvement in elbow range of movement at the 1,500 Mu dose. There was no change in upper limb disability but a significant increase in patients' global assessment of benefit. CONCLUSION: Botulinum toxin produced beneficial effects in spasticity and passive range of movement in the hemiplegic upper limb. Increasing the dose increased the magnitude of response for impairments in some muscle groups but had little effect on duration of response.

Adult↗
PubMed2002

Are we underestimating the clinical efficacy of botulinum toxin (type A)? Quantifying changes in spasticity, strength and upper limb function after injections of Botox to the elbow flexors in a unilateral stroke population.

OBJECTIVE: To quantify the clinical efficacy of botulinum toxin type A in treating elbow flexor spasticity in a unilateral stroke population. LOCATION: A spasticity clinic at a regional neurological rehabilitation centre. STUDY DESIGN: A convenience sample longitudinal study. Fourteen subjects with elbow flexor spasticity secondary to a stroke were recruited. Two repeated measures, one before and another four weeks after treatment, were taken to quantify clinical efficacy. OUTCOME MEASURES: Elbow flexor spasticity was simultaneously rated with the modified Ashworth scale (MAS) and quantified by measuring the surface EMG from the flexors using a custom-built device. Strength at the elbow (isometric), grip strength and upper limb function (Action Research Arm test) were also assessed. TREATMENT: Injections of botulinum toxin type A (Botox) to the m.biceps brachii (mean dose 70 U), m.brachioradialis (mean dose 56.5 U) and m.flexor digitorum longus (mean dose 83.3 U). RESULTS: Following treatment, spasticity (as measured by flexor EMG activity) reduced but the MAS was unable to detect this improvement. In some subjects, isometric flexor strength at the elbow as well as grip strength increased. This was contrary to the expected weakening following treatment with botulinum toxin type A and suggests an optimization of motor control. CONCLUSION: Treatment with Botox reduces spasticity but does not necessarily cause a reduction in the force generating capabilities at the joint. The improvement in strength may have contributed to the improvements in upper limb function. The MAS is an inappropriate measure of spasticity.

Adult↗
PubMed2006

The Tardieu Scale differentiates contracture from spasticity whereas the Ashworth Scale is confounded by it.

OBJECTIVE: To compare the Tardieu Scale as a clinical measure of spasticity after stroke with the Ashworth Scale. DESIGN: Cross-sectional study. PARTICIPANTS: Sixteen people, living in the community three years after their stroke. MAIN MEASURES: The Ashworth Scale and Tardieu Scale as well as laboratory measures of spasticity (stretch-induced electromyographic (EMG) activity) and contracture (maximum passive joint excursion) were collected from the affected elbow flexors and extensors and ankle plantarflexors and dorsiflexors by three examiners who were blinded to the results of the other measures. RESULTS: The percentage exact agreement (PEA) between the Tardieu Scale and a laboratory measure of spasticity was 100% for both the elbow flexors and ankle plantarflexors. This was significantly (P= 0.02) greater than the PEA of 63% for both muscles between the Ashworth Scale and the same laboratory measure of spasticity. For contracture, the PEA between the Tardieu Scale and a laboratory measure was 94% for both the elbow flexors and the ankle plantarflexors. Pearson correlation coefficients between the Tardieu Scale and laboratory measures of spasticity were 0.86 for the elbow flexors and 0.62 for the ankle plantarflexors and between the Tardieu Scale and laboratory measures of contracture were 0.89 for the elbow flexors and 0.84 for the ankle plantarflexors. CONCLUSION: In all cases that spasticity was overestimated by the Ashworth Scale, participants had a contracture. These findings suggest that the Tardieu Scale differentiates spasticity from contracture whereas the Ashworth Scale is confounded by it.

Aged↗
PubMed2004

Selective posterior rhizotomy for painful spasticity in the lower limbs of hemiplegic patients after stroke: report of two cases.

OBJECTIVE AND IMPORTANCE: Selective posterior rhizotomy (SPR) has been performed mainly in children with cerebral palsy. Seldom has the use of SPR been reported for reduction of spasticity after stroke. We describe two elderly patients with hemiplegia who underwent unilateral SPR for pain caused by spasticity after stroke. CLINICAL PRESENTATION: The first patient was a 68-year-old woman who experienced spasticity and pain in her right leg during the chronic stage of a left cerebral infarction. The second patient was an 89-year-old man who had intolerable spastic pain in his left hemiplegic leg 3 months after a right cerebral infarction. INTERVENTION: Both patients underwent unilateral SPR on the spastic side to reduce the pain. After surgery, the patients' pain resolved. In the first patient, the ability to perform activities of daily living also improved. CONCLUSION: Antispastic medications are often sufficient for treatment of post-stroke spasticity. In selected cases, however, SPR can be beneficial for improving painful spasticity.

Aged↗
PubMed1998

Spasticity and strength changes as a function of selective dorsal rhizotomy.

OBJECT: The goal of this investigation was to quantify changes in hamstring muscle spasticity and strength in children with cerebral palsy (CP) as a function of their having undergone a selective dorsal rhizotomy. METHODS: Nineteen children with CP (CP group) and six children with able bodies (AB group) underwent testing with a dynamometer. For the spasticity measure, the dynamometer measured the resistive torque of the hamstring muscles during passive knee extension at four different speeds. Torque-angle data were processed to calculate the work done by the machine to extend the knee for each speed. Linear regression was used to calculate the slope of the line of best fit for the work-velocity data. The slope simultaneously encompassed three key elements associated with spasticity (velocity, resistance, and stretch) and was considered the measure of spasticity. For the strength test, the dynamometer moved the leg from full knee extension to flexion while a maximum concentric contraction of the hamstring muscles was performed. Torque-angle data were processed to calculate the work done on the machine by the child. Hamstring spasticity values for the CP group were significantly greater than similar values for the AB group prior to surgery; however, they were not significantly different after surgery. Hamstring strength values for the CP group remained significantly less than those for the AB group after surgery, but were significantly increased relative to their presurgery values. CONCLUSIONS: The results of spasticity testing in the present investigation agreed with those of previous studies, indicating a reduction in spasticity for the CP group. The results of strength testing did not agree with those in the previous literature; a significant increase in strength was observed for the CP group.

Adolescent↗