Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spasticity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMedDate not supplied

[Clinical treatment (non surgical) of spasticity in cerebral palsy].

OBJECTIVE: A review about the procedures used in the non surgical management of spasticity in children with cerebral palsy. DEVELOPMENT: Therapeutic modalities for the management of spasticity in cerebral palsy include: (1) elimination of factors aggravating spasticity: pain, fatigue, stress, excitement, cold, illness, sleep disturbance, immobility, and hormonal changes; (2) rehabilitative therapies, there are four major groups: (a) biomechanical approach, (b) neurophysiologic approach, (c) developmental approach and (d) sensory approach; (3) orthosis; (4) oral pharmacotherapy: baclofen, tizanidine, diacepam and dantroleno; (5) chemical denervation: phenol injections and botulinum toxin injections. The medical management of spasticity in cerebral palsy is based on: 1. Oral pharmacotherapy: (a) baclofen, binds GABAB receptors of spinal interneurons presynaptically, inhibits release of excitatory neurotransmitters in the spinal cord; (b) tizanidine, binds alfa 2 adrenergic receptors presinaptically, inhibits release of excitatory neurotransmitters in the spinal cord; (c) diacepam, augments GABA mediated inhibition in the spinal cord and supraspinally;(d) dantrolene, inhibits release of calcium from sarcoplasmic reticulum in muscle, weakens muscle contraction in response to myofiber excitation. 2. Chemical denervation: (a) phenol injection perineurally or into the motor point disrupts efferent signals from hyperexcitable anterior horn cells causing necrosis of axons or muscle; (b) botulinum toxin injection in selected muscles blocks the release of acetylcholine presynaptically and weakens the force of muscle contraction produced by hyperexcitable motoneurons. CONCLUSIONS: At the present time, there is not irrefutable evidence of a sustain benefit of physical rehabilitation in the management of spasticity. There are few studies with oral pharmacological agents involving children with cerebral palsy to define its role. On the other hand, botulinum toxin A is effective, well tolerated, and safe in the treatment of spasticity in children with cerebral palsy.

Botulinum Toxins, Type A↗
PubMed2003

[Spasticity and botulinum toxin in 2003. An update].

After the spastic foot in cerebral palsy, there are now wider indications for botulinum toxin injections in spasticity. Post stroke upper limb spasticity has been usefully treated by botulinum toxin in several studies, including double blind placebo-controlled studies. Two serotypes and one serotype B are marketed, with various properties. Botulinum toxin has been studied in multiple etiologies of spasticity. In multiple sclerosis, few studies revealed an efficacy in angulations and comfort. In spinal cord injuries, gait and sphincter disorders can be improved. In post stroke spasticity, lower limb angulations are improved, but gait remained difficult to evaluate. In upper limb spasticity, angulation, function and quality of life were improved in double blind, placebo controlled studies. Comparisons of costs and efficacy are made between botulinum toxin and the other antispastic methods.

Anti-Dyskinesia Agents↗
PubMed2003

[Neurosurgical treatment of spasticity: indications in children].

Today, we have several efficient neurosurgical treatments of spasticity in children with cerebral palsy. A good indication is possible only if a consensus about the goal of the surgery is found between the surgeon, the child and his/her family, and the reeducation team. This goal is not always functional. Clinical examination is not limited to the analytical assessment of spasticity, but must take into account the general and orthopedic state of the child, and his/her functional evolution, cognitive abilities, habits and general environment. The struggle against spasticity is part of a therapeutical programme which extends over several years. It must be considered before muscular contractures. On lower limbs, in the cases of general spasticity, we propose posterior rhizotomy or intrathecal baclofen administration. Posterior rhizotomy is proposed when a more aggressive intervention is preferred for some muscular groups or when the child's general environment does not allow for the medical care imposed by intrathecal administration. In the case of localized spasticity, botulinum toxin injection permits delaying until the child reaches the age for selective neurotomy. On upper limbs, in children with quadriplegia the indication is essentially physical and occupational therapy. We cannot count on the positive side effects of rhizotomy or intrathecal administration of baclofen on the upper limbs. In children with hemiplegia, with localized or global spasticity of the upper limb, botulinum toxin is proposed as the first form of treatment. Neurotomy or rhizotomy can follow toxin, according to the efficacy of the toxin.

Child↗
PubMed2003

[Intrathecal baclofen in the treatment of severe spastic tetraplegia and dystonia in children and adolescents].

INTRODUCTION: Continuous intrathecal baclofen has been used over the past years especially in adult patients with spasticity of spinal origin. Children and young adults with severe spasticity and dystonia of cerebral origin are difficult to treat in spite of optimal systemic antispasmotic therapy with baclofen, tizanidine, dantrolene and/or diazepam. Intrathecal baclofen has therefore been applied in a group of young patients. MATERIAL AND METHODS: Eight children and young adults from East Denmark with spasticity and 12 with dystonia aged 3-18 years (median 10.9 years) were tested, operated and treated with continuous intrathecal baclofen for a period of 2-64 months (median 22.2 months). Registration of efficacy, fillings, adjustments of baclofen and other therapies were performed in an out patient setting since 1995. RESULTS: Spasticity in lower extremities was reduced from Ashworth score 3.5-4.5 (median 4.2) to Ashworth score 2.5-4.0 (median 2.9; p < 0.001) during infusion with baclofen 5-33 micrograms/kg/24 hours (median 19 micrograms/kg/24 hours). The infusion catheter tip was placed at levels Th1-Th12 (median Th7.5). Peroral baclofen was reduced from an average of 5.0 to 0.44 mg/kg/24 hours, tizanidine from 0.4 to 0.1 mg/kg/24 hours, and dantrolene from 4.0 to 0.4 mg/kg/24 hours. After initial adjustments successively increased dosages of average 0.46 microgram/kg/month were needed to maintain the same level of efficacy. In questionnaires parents or guardians rated less spasticity in lower extremities in 15 out of 19 patients, and less pain in 13 out of 19 patients. CONCLUSION: Continuous intrathecal baclofen was effective in treating severe spasticity and dystonia of cerebral origin with major effect on muscles of the lower extremities, pelvis, and back and in particular opisthotonus was relieved. Efficacy on upper extremities was far less pronounced.

Adolescent↗
PubMed2004

Clinical features of hereditary spastic paraplegia with thin corpus callosum: report of 5 Chinese cases.

BACKGROUND: Hereditary spastic paraplegia is a clinically and genetically heterogeneous group of neurodegenerative disorders of the motor system, characterized by slowly progressive spasticity and weakness of the lower extremities. This study was conducted to investigate the clinical features of hereditary spastic paraplegia with thin corpus callosum (HSP-TCC). METHODS: Clinical data from five patients and thirty-five previously published case reports of HSP-TCC were analyzed retrospectively. RESULTS: Most patients were adolescents at the onset of the disease, presenting with spastic paraparesis of the lower limbs and mental impairment. Some patients also had other clinical features, including spasticity of the upper limbs, cerebellar ataxia, and sensory disturbances. Cranial MRIs of the five patients revealed an extremely thin corpus callosum, sometimes with widened cerebral sulci and ventricles, as well as with cerebellar and cerebral atrophy. CONCLUSION: The main clinical features of HSP-TCC include slowly progressive spastic paraplegia, mental impairment during the second decade of life, and an extremely thin corpus callosum as shown on cranial MRIs.

Adolescent↗
PubMed1992

[Treatment of spasticity with botulinum toxin].

Spasticity following upper motor neuron lesion can be alleviated by few treatments such as physiotherapy, drugs and neurosurgery. However, they all have side effects, limitations or lack of selectivity. We tentatively used the paralyzing effects of botulinum toxin. Since the late 1970's the use of this toxin has increased and it has been extended to numerous muscles and diseases of various causes. In this pilot and open study we use botulinum toxin in spasticity. Eight patients (7 stroke, 1 head injury) with longstanding severe spasticity (minimum: 12 months, maximum: 15 years) were included. Spasticity greatly interfered with their activity in daily life and was resistant to oral antispastic medications. Six patients suffered from pain and 4 had cutaneous lesions especially maceration of the palm of the hand. A-botulinum toxin was injected with a 30-gauged needle. The sites chosen for injection were the following muscles: biceps brachii, brachioradialis, flexor digitorum, flexor carpi, tibialis anterior, flexor digitorum longus. Altogether 41 injections were performed. There were no side effects. Spasticity was improved in all patients. Five patients reported significant pain relief on a visual analogical scale. Most of them reported a benefit in their limb tone and referred to subjective improvement in the activity of daily life and nursing. The beneficial effects of one injection lasted more than 5 months. Seven patients received a second course of treatment. A double-blind study of botulinum toxin in spasticity is to be undertaken to assess its effectiveness and safety when prescribed in the required dose to treat this condition.

Adult↗
PubMed1988

Microsurgical procedures in the peripheral nerves and the dorsal root entry zone for the treatment of spasticity.

When spasticity becomes severe and harmful, in spite of physical and medical therapy, neurosurgery can give functional improvement. This paper deals with the long term results of Selective Peripheral Neurotomies of the Tibial Nerve and Selective Posterior Rhizotomies in the Dorsal Root Entry Zone, in 123 patients with spastic disorders localized to the limbs. The micro-techniques and intra-operative electro-stimulation for identification of the nervous structures responsible for the spastic components, can give a substantial reduction of the harmful spasticity, without suppressing the useful muscle tone and impairing the residual motor and sensory functions. The results were effective, with a 1 to 13 year follow-up (5 on average), in 89% of 47 Selective Peripheral Neurotomies of the tibial nerve for spastic foot, in 92% of 53 Selective Posterior Rhizotomies for paraplegia and in 87% of 23 Selective Posterior Rhizotomies for hemiplegia. In the most severe situations ("comfort" indications), correction of the abnormal postures and relief of pain facilitated nursing and physiotherapy. Sometimes there was reappearance of some useful voluntary movements. In the less affected patients ("functional" indications), the suppression of the harmful spastic components made the persistant capacities more effective.

Adolescent↗
PubMed1995

[Treatment of spastic paraparesis with botulinum toxin with reference to beneficial effects, disease severity and long-term treatment].

We administered local botulinum toxin injections on the leg adductors of 12 patients with spastic paraparesis (9 patients with HAM, 2 patients with spinal spastic paraparesis, 1 patient with an identified degenerative disease). Two of them were wheelchair-bound and the other patients could walk with or without help. The patients were assessed by the time to walk 10 m and the spasticity score which was derived from the degree of muscle tone and spasm frequency of leg adductors. After the initial injection, 7 of the 12 patients improved spasticity scores and 8 of the 10 patients could walk 10 m within a shorter time. The time to walk 10 m was markedly shortened in moderate cases. However, one patient complained of leg weakness and the time to walk 10 m was prolonged. Five of the 12 patients received injections 3 to 7 times, and were followed up for a mean of 16.2 months. In 4 of the 5 patients, repeated injections could maintain the improvement of spasticity score and time to walk 10 m. However, injection was discontinued in one patient because of leg weakness. The other side effects were pain and swelling at the injected site and dysarthria. However, these side effects were slight and transient and did not require treatment. No other systemic side effects were observed. In conclusion, the beneficial effects of botulinum injections to spastic paraparesis were (1) improvement of objective symptoms in mild cases, (2) improvement of ADL in moderate cases, and (3) improvement of objective symptoms and ease of nursing care in severe cases. Furthermore, we confirmed the long-term efficacy and safety of botulinum toxin.

Adult↗
PubMedDate not supplied

Intrathecal baclofen application in patients with supraspinal spasticity secondary to severe traumatic brain injury.

Intrathecal application of baclofen is considered the treatment of choice in patients suffering from spinal spasticity insufficiently responding to conventional oral antispastic medication. This approach has also been used successfully in cases with spasticity of supraspinal origin. To achieve a good therapeutic response in the latter condition the amount of intrathecal baclofen has to be approximately twice the dosage required in spinal spasticity. We report on 8 patients suffering from supraspinal spasticity due to severe traumatic brain injury. Intrathecal baclofen reduced spasticity in all patients (mean Ashworth Score from 3.9 to 1.6; mean Reflex Score from 4.0 to 1.4). In some cases improvement of motor performance and in one case recovery of bladder function were noted. In two patients focal epileptic seizures with secondary generalization seemed to be associated with the application of baclofen. The local intrathecal application of baclofen has proven to be an effective therapy in otherwise intractable cases of severe supraspinal spasticity.

Acute Disease↗
PubMed1994

Examination of the segmental pathophysiological mechanisms of spasticity.

The purpose of this investigation was to ascertain a complex of electromyographic methods suitable for evaluation of the basic segmental pathophysiological mechanisms of spasticity. Clinical and electromyographic examinations were performed on 120 patients with spastic hemiparesis after stroke. Patients muscle tone, muscle force and tendon reflexes were assessed by the well known clinical five point scales. A battery of electromyographic methods was used to analyze different segmental mechanisms of spasticity: for alpha motoneurone activity--the F-wave parameters; for gamma motoneurone activity--the TA/H amplitude ratio; for common interneurone activity--the flexor reflex parameters; for presynaptic inhibition--the Hvibrated/Hmaximal amplitude ratio. Our results revealed that nearly all of the patients have increased alpha motoneurone activity on the spastic side. In most of the patients at least two of the segmental mechanisms are altered. Different mechanisms participate with different frequency in development of spasticity. We suppose that alpha-motoneurone hyperactivity usually develops secondary after alteration of some other segmental mechanism. In conclusion the applied complex of electromyographic methods gives the possibility for evaluation of the individual pathophysiological profile of patients with spasticity. This is a background for appropriate treatment.

Aged↗
PubMed1993

Impaired activation pattern in antagonistic elbow muscles of patients with spastic hemiparesis: contribution to movement disorder.

Surface electromyographic "EMG" activity in biceps brachii (agonist muscle) and triceps brachii (antagonist muscle) as well as the discharge behaviour of motor units "MUs" (needle recording) in biceps brachii muscle were recorded during slow (0.33 Hz) and fast (0.66 Hz) voluntary elbow flexion movements (auditory matching task) in fifty patients with spastic hemiplegia. In the spastic limbs, a long lasting, small amplitude tonic co-contraction of antagonist muscles was seen during slow flexions (SF) in 29 cases. This effect was strongest during the fast elbow flexion movements (FF). In 33 patients a triphasic pattern of muscle activation was observed on the unaffected side but not on the spastic side. The amplitude of the agonist surface EMG was significantly reduced and the amplitudes of the MU potentials recruited during maximal effort were generally smaller on the spastic side compared to the unaffected side. The agonist-antagonist activation pattern was analysed with respect to three clinically identifiable functional recovery stages of voluntary movements in the spastic limbs, namely synergistic, isolated and useful movements. The MU amplitudes and the amplitude of the surface EMG activity in the agonist muscle recorded during FF movements became significantly larger whereas the amplitude of the antagonist tonic activity became smaller with increasing functional recovery of the limb. It is concluded that impaired recruitment of type II motor units in the agonist muscles and the inability to selectively activate the agonist muscle contribute to the deficit in motor performance in spastic paresis.

Adult↗
PubMed1993

[Local injection treatment with botulinum toxin A in severe arm and leg spasticity].

In patients with predominantly focal spasticity, oral antispastic drugs are relatively ineffective or cause unwanted side effects of central origin. Therefore we treated patients disabled by focal spasticity with local injections of Botulinum-Toxin A (Porton Products BOTOX). Efficacy, dosage, side-effects and injection technique were examined. 11 patients (mean age 48 years) with severe focal spasticity of the flexor muscles of the hand and arm (5 patients), the adductor muscles of the legs (5) or the plantar flexors of the foot (1) due to multiple sclerosis, cervical myelopathy or stroke-related hemi-paresis were treated with BOTOX. Rating scales, including Ashford spasticity scale, pain scale and a hygienic rating scale, were used to evaluate the efficacy. 25 to 30 ng (1000-1200 MU Porton) were injected in the flexor group of the hand or arm and 42 to 50 ng (1680-2000 MU Porton) BOTOX in the adductor group of one leg. 10 of the patients showed an improvement of at least one point on the scales for spasticity, pain and hygiene. Effects could be observed after 4-7 days and lasted for 6-13 weeks. There were no unwanted side-effects. We conclude that BOTOX is an alternative to the systemic application of antispastic drugs. Focal spasticity and pain can be successfully reduced and hygienic care is facilitated.

Adult↗
PubMed1993

[Chemical neurolysis using alcohol (alcoholization) in the treatment of spasticity in the hemiplegic].

Spasticity is a source of disability for the hemiplegic patient. It leads to various disorders influencing the quality of gait: at the lower limb varus equinus foot deformity, toe-claw and/or hip adduction with adductors spasticity. At the upper limb, flexion deformity of the wrist and the hand makes grasp and grip ineffective and spasticity of the Pectoralis Major muscle is considered as a main cause of sympathetic dystrophy. Neurolysis with alcohol injection in the nerve trunk or at the motor point destroys the gamma fibers and reduces spasticity, without impairing motor command. The effects on spasticity, motricity, and deformity of 33 chemical neurolysis with alcohol are analysed with a six months follow-up (27 hemiplegic patients, 28 to 62 years old, mean = 54.5). The authors have used 60% alcohol concentration. Sciatic nerve injection significantly reduces triceps spasticity (7/11), improves the range motion of the ankle, and allows the patient to take off the ankle device. Those fair results are still present at the fourth month after injection. Similar results are reported after injection of the obturator nerve for hip adduction deformity (2/3), median nerve injection for wrist and hand deformity (6/6). Pectoralis Major injection in the motor point is effective for 10 of the 13 cases, preventing sympathetic reflex dystrophy or contributing to its dramatic improvement.

Adult↗
PubMed1997

Clinicophysiologic concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion.

Spasticity is a disorder of the sensorimotor system characterized by a velocity-dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. It is one component of the upper motoneuron syndrome, along with released flexor reflexes, weakness, and loss of dexterity. Spasticity is an important "positive" diagnostic sign of the upper motoneuron syndrome, and when it restricts motion, disability may result. The "negative" signs--weakness and loss of dexterity--invariably alter patient function when they occur. In an upper motoneuron syndrome, the alpha motoneuron pool becomes hyperexcitable at the segmental level. This hyperexcitability is hypothesized to occur through a variety of mechanisms, not all of which have yet been demonstrated in humans. Spasticity caused by spinal cord lesions is often marked by a slow increase in excitation and over-activity of both flexors and extensors with reactions possibly occurring many segments away from the stimulus. Cerebral lesions often cause rapid build-up of excitation with a bias toward involvement of antigravity muscles. Chronic spasticity can lead to changes in the rheologic properties of the involved and neighboring muscles. Stiffness, contracture, atrophy, and fibrosis may interact with pathologic regulatory mechanisms to prevent normal control of limb position and movement. In the clinical exam, it is important to distinguish between the resistance due to spasticity and that due to rheologic changes, because the distinction has therapeutic implications. Diagnostic nerve or motor point blocks and dynamic or multichannel EMG are useful to distinguish the contributions of spasticity and stiffness to the clinical problem.

Adult↗
PubMed1997

A clinical overview of treatment decisions in the management of spasticity.

Spasticity from an upper motor neuron syndrome may cause a variety of symptoms that interfere with function. Decisions regarding spasticity treatment are influenced by the chronicity, severity, and distribution of the spasticity; the locus of injury; the presence and severity of co-morbidities; the availability of support; and the goals of treatment. Not all spasticity can or even should be treated; tone reduction is indicated only if spasticity interferes with some level of function, positioning, care, or comfort. Treatment goals should be well outlined before treatment begins. Botulinum toxin may be used to treat focal spasticity as part of an overall treatment plan.

Adult↗
PubMed1998

[Treatment of spasticity with injections of botulinum toxin. Review of the literature].

Botulinum toxin injections are a new treatment for limb spasticity. Intramuscular injections can be performed in spastic muscles; efficacy occurs one or two weeks later, with a mean duration of three months. Clinical action is related to chemical denervation of presynaptic motor end nerves by the botulinum toxin. Double blind studies versus placebo have demonstrated the improvement of limb spasticity after injections of botulinum toxin. Ashworth scales, articular angulations, pain and spasms improve both in upper and lower limb spasticity. Functional scores are not changed in the upper limb, but quality of life improves. Kinematic parameters of gait are improved in lower limb spasticity, especially in children with cerebral palsy disorders. There were no reports of serious side effects. Botulinum toxin is a safe and effective treatment of localized spasticity in adults and children.

Animals↗
PubMed1998

[Treatment of spasticity with the intrathecal administration of baclofen].

Direct intrathecal administration of baclofen in the treatment of severe spasticity was proposed in 1984 by Richard Penn with the objective to carry out a selective spinal distribution of the active principle thus avoiding supraspinal side effects. We presented our first results at the French Language Association of Neurosurgery in 1985 within the framework of a report on "Functional neurosurgery of cerebral palsy" (Neurochirurgie, 1985, 31 (suppl 1): 1-118). This study aims to specify the selection criteria and current indications of this method for the treatment of severe chronic diffused spasticity of spinal and cerebral origin in adults and in children. This report relates to our experience concerning 60 patients (10 children) that benefit from the use of a totally implantable system for chronic administration. The total follow-up of all patients was 48 months (from 3 to 140 months). The initial effective daily amount of baclofen was 156 micrograms/24 hours and progressed in time to reach in the long run 280 micrograms/24 hours, with a very broad interindividual variability from 36 to 1050 micrograms/24 hours. All the patients benefited from a reduction in muscular hypertonicity as well as painful muscular spasms. On the other hand, the functional improvement was very variable from one patient to another and depended primarily on the initial clinical state and the etiology of the spasticity. The results observed were more significant in post-traumatic paraplegia than those secondary to demyelination disease even if they were stabilized with regard to spasticity of spinal origin. This mode of administration currently plays a significant role in the treatment of spasticity of cerebral origin, in particular in children presenting a motor disorder of cerebral origin with spastic prevalence. The current limitations of this type of treatment are technical because of the frequent catheter malfunctions, but are due essentially to the importance and constraint of the multi-disciplinary organization needed for the out-patient follow-up.

Baclofen↗
PubMed2003

Genetic heterogeneity in inherited spastic paraplegia associated with epilepsy.

We have recently mapped a new rare form of spastic paraplegia complicated by bilateral cataracts, gastroesophageal reflux with persistent vomiting, and amyotrophy to chromosome 10q23.3-q24.2. This locus, named SPG9, is located in an interval spanning about 12 cM of genomic DNA, between markers D10S536 and D10S603, where different neurological disorders have been mapped. In particular, a gene for partial epilepsy has been assigned to a 3 cM interval between markers D10S185 and D10S577, which is completely included in the SPG9 critical region. A few families affected with spastic paraplegia and epilepsy have been reported; in the present study, we tested a pedigree with concurrence of spastic paraplegia, epilepsy, and mental retardation inherited as an autosomal dominant trait, using markers located in the SPG9 interval. Haplotype reconstruction excluded the linkage to 10q23.3-q24.2. In addition, the seven different loci so far reported to be associated with autosomal dominant pure forms of spastic paraplegia have been tested and excluded by linkage analysis and haplotype reconstruction, including SPG4 on chromosome 2p22-p21, where a familial form of spastic paraplegia associated with dementia and epilepsy has been mapped. These data confirm genetic heterogeneity in familial spastic paraplegia with epilepsy and suggest a specific locus for the family here analyzed.

DNA↗