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PubMed2001

Open-label dose-titration safety and efficacy study of tizanidine hydrochloride in the treatment of spasticity associated with chronic stroke.

BACKGROUND AND PURPOSE: Spasticity is a frequently observed motor impairment that develops after stroke; it can cause pain and disability in those affected. The objective of the present study was to evaluate the safety and efficacy of tizanidine, a centrally acting alpha(2)-adrenergic agonist, in the treatment of stroke-related spasticity. METHODS: Forty-seven patients, who were a minimum of 6 months poststroke and had significant spasticity, were studied at 4 centers. Tizanidine was administered in an open-label manner for 16 weeks, beginning at 2 mg/d and slowly titrated to a maximum of 36 mg/d. The Modified Ashworth Scale, muscle strength testing, functional assessments, and Pain and Functional Spasticity Questionnaires were administered at baseline and at 4, 8, 16, and 18 weeks (after 1 week off tizanidine). RESULTS: Spasticity was significantly improved between baseline and week 16, with a decrease in total upper extremity Modified Ashworth Scale score of 2.80+/-0.47 (P<0.0001). No decline in strength was noted. Treatment with tizanidine resulted in a significant improvement in pain intensity (P=0.0375), quality of life (P=0.0001), and physician assessment of disability (P=0.0001). The most frequent side effects were somnolence (62%) and dizziness (32%). No serious adverse events were considered to be drug related. Ten of 47 patients (21%) were able to reach the maximum daily dosage of 36 mg. CONCLUSIONS: Overall, the data suggest that tizanidine is safe and efficacious in the treatment of stroke-related spasticity, preserving muscle strength while reducing muscle tone and painful spasms in affected patients.

Clonidine↗
PubMed2003

Neurosurgical treatment of spasticity and other pediatric movement disorders.

For children whose spasticity and movement disorders are inadequately treated by oral medications and botulinum toxins, neurosurgical procedures are now available to effectively treat spasticity, tremor, and many cases of dystonia. Spastic diplegia can be treated with selective lumbar rhizotomies, which significantly decrease spasticity, increase range of motion, and improve Gross Motor Function Measure scores. Children with spastic quadriparesis and those with secondary dystonia can be treated with intrathecal baclofen, which diminishes both spasticity and dystonia and is associated with improved function and quality of life. Children with primary dystonia and those with tremor can be treated with deep brain stimulation of the internal globus pallidus and thalamus, respectively. Some children with chorea respond to deep brain stimulation. There are no effective neurosurgical treatments for athetosis or ataxia. The effectiveness of neurosurgical treatments of pediatric movement disorders has increased significantly in the past 15 years.

Athetosis↗
PubMed2006

Childhood-onset spastic paraplegia with NIPAL gene mutation.

Hereditary spastic paraplegia is a heterogeneous group of inherited neurodegenerative disorders in which the predominant clinical feature is gait disturbance owing to spasticity and weakness of the lower limbs. Autosomal dominant hereditary spastic paraplegia is the predominant form of the disorder. To date, 10 autosomal dominant hereditary spastic paraplegia gene loci and genes for 6 of them have been identified. Spastic paraplegia 6, with a typical teenage onset and considered to be one of the more severe forms of the disease, is due to mutations in the gene NIPA1. We report a childhood-onset, aggressive, spastic paraparesis in a North American family with a c.316G>A mutation of the NIPA1 gene, confirming c.316 as a mutational hot spot.

Adult↗
PubMed2003

Bladder stones - red herring for resurgence of spasticity in a spinal cord injury patient with implantation of Medtronic Synchromed pump for intrathecal delivery of baclofen - a case report.

BACKGROUND: Increased spasms in spinal cord injury (SCI) patients, whose spasticity was previously well controlled with intrathecal baclofen therapy, are due to (in order of frequency) drug tolerance, increased stimulus, low reservoir volume, catheter malfunction, disease progression, human error, and pump mechanical failure. We present a SCI patient, in whom bladder calculi acted as red herring for increased spasticity whereas the real cause was spontaneous extrusion of catheter from intrathecal space. CASE PRESENTATION: A 44-year-old male sustained a fracture of C5/6 and incomplete tetraplegia at C-8 level. Medtronic Synchromed pump for intrathecal baclofen therapy was implanted 13 months later to control severe spasticity. The tip of catheter was placed at T-10 level. The initial dose of baclofen was 300 micrograms/day of baclofen, administered by a simple continuous infusion. During a nine-month period, he required increasing doses of baclofen (875 micrograms/day) to control spasticity. X-ray of abdomen showed multiple radio opaque shadows in the region of urinary bladder. No malfunction of the pump was detected. Therefore, increased spasticity was attributed to bladder stones. Electrohydraulic lithotripsy of bladder stones was carried out successfully. Even after removal of bladder stones, this patient required further increases in the dose of intrathecal baclofen (950, 1050, 1200 and then 1300 micrograms/day). Careful evaluation of pump-catheter system revealed that the catheter had extruded spontaneously and was lying in the paraspinal space at L-4, where the catheter had been anchored before it entered the subarachnoid space. A new catheter was passed into the subarachnoid space and the tip of catheter was located at T-8 level. The dose of intrathecal baclofen was decreased to 300 micrograms/day. CONCLUSION: Vesical calculi acted as red herring for resurgence of spasticity. The real cause for increased spasms was spontaneous extrusion of whole length of catheter from subarachnoid space. Repeated bending forwards and straightening of torso for pressure relief and during transfers from wheel chair probably contributed to spontaneous extrusion of catheter from spinal canal in this patient.

Adult↗
PubMed2002

Prevalence of spasticity post stroke.

OBJECTIVES: To establish the prevalence of spasticity 12 months after stroke and examine its relationship with functional ability. DESIGN: A cohort study of prevalence of spasticity at 12 months post stroke. SETTING: Initially hospitalized but subsequently community-dwelling stroke survivors in Liverpool, UK. SUBJECTS: One hundred and six consecutively presenting stroke patients surviving to 12 months. MAIN OUTCOME MEASURES: Muscle tone measured at the elbow using the Modified Ashworth Scale and at several joints, in the arms and legs, using the Tone Assessment Scale; functional ability using the modified Barthel Index. RESULTS: Increased muscle tone (spasticity) was present in 29 (27%) and 38 (36%) of the 106 patients when measured using the Modified Ashworth Scale and Tone Assessment Scale respectively. Combining the results from both scales produced a prevalence of 40 (38%). Those with spasticity had significantly lower Barthel scores at 12 months (p < 0.0001). CONCLUSION: When estimating the prevalence of spasticity it is essential to assess both arms and legs, using both scales. Despite measuring tone at several joints, spasticity was demonstrated in only 40 (38%) patients, lower than previous estimates.

Aged↗
PubMed2002

Spastic paraplegia, ataxia, mental retardation (SPAR): a novel genetic disorder.

OBJECTIVE: To describe a kindred with a dominantly inherited neurologic disorder manifested either as uncomplicated spastic paraplegia or ataxia, spastic paraplegia, and mental retardation. METHODS: Neurologic examinations and molecular genetic analysis (exclusion of known SCA and HSP genes and loci; and trinucleotide repeat expansion detection [RED]) were performed in six affected and four unaffected subjects in this family. MRI, electromyography (EMG), and nerve conduction studies were performed in three affected subjects. RESULTS: The phenotype of this dominantly inherited syndrome varied in succeeding generations. Pure spastic paraplegia was present in the earliest generation; subsequent generations had ataxia and mental retardation. MRI showed marked atrophy of the spinal cord in all patients and cerebellar atrophy in those with ataxia. Laboratory analysis showed that the disorder was not caused by mutations in genes that cause SCA-1, SCA-2, SCA-3, SCA-6, SCA-7, SCA-8, and SCA-12; not linked to other known loci for autosomal dominant ataxia (SCA-4, SCA-5, SCA-10, SCA-11, SCA-13, SCA-14, and SCA-16); and not linked to known loci for autosomal dominant hereditary spastic paraplegia (HSP) (SPG-3, SPG-4, SPG-6, SPG-8, SPG-9, SPG-10, SPG-12, and SPG-13) or autosomal recessive HSP SPG-7. Analysis of intergenerational differences in age at onset of symptoms suggests genetic anticipation. Using RED, the authors did not detect expanded CAG, CCT, TGG, or CGT repeats that segregate with the disease. CONCLUSIONS: The authors describe an unusual, dominantly inherited neurologic disorder in which the phenotype (pure spastic paraplegia or spastic ataxia with variable mental retardation) differed in subsequent generations. The molecular explanation for apparent genetic anticipation does not appear to involve trinucleotide repeat expansion.

Adolescent↗
PubMed1985

Evaluation of spinal cord stimulation for postapoplectic spastic hemiplegia.

We used spinal cord stimulation (SCS) in patients with postapoplectic spastic hemiplegia in an attempt to reduce the spasticity. Three patients with spastic hemiplegia due to apoplexia were selected for the treatment. Reduction of spasticity was observed 3 to 9 days after the stimulation. Electrophysiological evaluation of the spasticity from the H reflex revealed a remarkable improvement in all three patients. The mechanism of reduction of spasticity has not yet been clarified, although a direct or indirect effect on the reticulospinal tract is thought to play a role.

Aged↗
PubMed1986

The significance of spasticity in the upper and lower limbs in myelomeningocele.

One hundred and nine children with myelodysplasia were evaluated and classified according to the level and type of paralysis and its effect on functional ability. Thirty-one per cent of the patients were paralysed at the thoracic level, 26% at the upper lumbar level, 30% at the lower lumbar level and 13% at the sacral level. Fifty-four per cent of these patients demonstrated the classic flaccid paralysis in the lower limbs with normal upper limbs; 9% were flaccid in the lower limbs, but were spastic in the upper; 24% were spastic in the lower limbs; 13% were spastic in the upper and lower limbs. Patients with spastic lower limbs required more orthopaedic procedures, more days in hospital and in casts, and were less likely to walk than those with flaccid paralysis. Patients with spastic upper limbs were less likely to be independent in activities of daily living and were more likely to require special schools than patients with normal upper limbs. In addition to the spinal cord level of the lesion, the degree of spasticity is important in the evaluation, treatment and prognosis of myelodysplastic patients.

Activities of Daily Living↗
PubMed1988

Oxcarbazepine and spasticity: further observations.

The previously described anti-spastic effect of oxcarbazepine and 10,11-dihydro-10-hydroxycarbamazepine was found accidentally in 2 patients undergoing a double-blind comparative study for evaluation of antiepileptic effect. In this study oxcarbazepine was given orally in doses of 300-2700 mg daily to one patient with transverse myelitis and to two patients with multiple sclerosis, all of whom had clinically disabling spasticity in the form of difficulty in walking, lower limb rigidity, spastic contractions of the lower limbs and ankle clonus. Anti-spastic effect was observed at doses between 600-1200 mg daily and consisted in a substantial decrease in the above symptoms of spasticity. The anti-spastic effect appears at a dose immediately below that which produces nausea, dizziness and somnolence.

Adult↗
PubMed2005

Botulinum toxin type A for the treatment of the upper limb spasticity after stroke: a meta-analysis.

Muscle over-activity is one of the cardinal features of spasticity and it is a common disability of stroke patients. In this group, spasticity is responsible for several limitations that interfere in their daily activities and quality of life. To treat spasticity, neurologists usually prescribe drugs as baclofen, tizanidine or benzodiazepines or even use definitive treatment as phenol or surgery. Authors suggest the use of botulinum toxin type A (BTX-A) for spasticity in the upper limbs after stroke, but there are few papers with adequate methodology supporting this idea. In this article we summarize the data of previous double-blind, randomised clinical trials to asses, with a meta-analysis, if BTX-A is an adequate treatment for spasticity due to stroke. The results show a statistical superiority of BTX-A ov%r placebo on reducing muscle tone by the Modified Ashworth Scale (WMD= 0.95 [0.74 to 1.17]) in patients with post-stroke upper limb spasticity.

Botulinum Toxins, Type A↗
PubMed2005

Soft-tissue releases to treat spastic hip subluxation in children with cerebral palsy.

BACKGROUND: Spastic hip subluxation and dislocation are common problems in children with cerebral palsy. Soft-tissue releases have proved to be beneficial in the prevention of spastic hip dislocation. A protocol for treatment based on patient age, hip abduction, and hip migration percentage was established in 1988. The purpose of this study was to assess the outcome in sixty-five children treated according to this protocol and followed for a minimum of eight years. METHODS: The medical records and radiographs of sixty-five children, from an original series of seventy-four patients, who met the inclusion criteria were available for review. Forty-seven children had spastic quadriplegia and were unable to walk; eighteen children had spastic diplegia and were able to walk independently or with assistive devices. The mean age at the time of the surgery was 4.4 years. Open adductor tenotomy and psoas muscle recession or iliopsoas tenotomy were performed on 129 hips, which were followed for a mean of 10.8 years. The mean age at the time of follow-up was fifteen years. Hips were grouped according to the hip migration percentage preoperatively, at one year postoperatively, and at the time of final follow-up. The final outcome for the patient was defined according to the worse hip. An analysis was performed to identify potential factors influencing outcome. RESULTS: Thirty-two patients (49%) had a good result, eleven (17%) had a fair result, three (4%) had a poor result, and nineteen (30%) had a failure. The mean hip migration percentage was 34% preoperatively and 18% at the time of final follow-up. Nineteen patients required subsequent osseous reconstructive procedures, and eleven required repeat soft-tissue releases. The migration percentage at one year postoperatively was the most predictive of the final outcome (p = 0.001). Patients who had been able to walk preoperatively had a better long-term outcome (p = 0.01). Neither the preoperative hip migration percentage nor the age at surgery significantly affected the outcome. CONCLUSIONS: Soft-tissue release was effective for long-term prevention of hip dislocation in 67% (forty-three) of sixty-five children with spastic hip subluxation. Two preoperative factors that were related to a favorable outcome were a spastic diplegic pattern of involvement and the ability to walk. The hip migration percentage at one year postoperatively was a good predictor of final outcome.

Cerebral Palsy↗
PubMed2004

A benefit-risk assessment of baclofen in severe spinal spasticity.

Baclofen is used for treatment of the spasticity of spinal origin that is a common sequela of spinal cord injury and multiple sclerosis; spasticity occurs in about 50% of patients affected by these disorders. In open-label studies of oral baclofen, the drug improved spasticity in 70-87% of patients; additionally, improvement in spasms was reported in 75-96% of patients. In double-blind, crossover, placebo-controlled trials, baclofen was reported to be effective, producing statistically significant improvements in spasticity. Tizanidine is the antispasticity drug that has been most widely compared with oral baclofen; studies have generally found the two drugs to have equivalent efficacy. However, tizanidine has better tolerability, in particular weakness was reported to be occur less frequently with tizanidine than with baclofen. The main adverse effects of oral baclofen include: sedation or somnolence, excessive weakness, vertigo and psychological disturbances. The incidence of adverse effects is reported to range from 10% to 75%. The majority of adverse effects are not severe; most are dose related, transient and/or reversible. The main risks of oral baclofen administration are related to withdrawal: seizures, psychic symptoms and hyperthermia can occur. These symptoms improve after the reintroduction of baclofen, usually without sequelae. When not related to withdrawal; these symptoms mainly present in patients with brain damage and in the elderly. The limited data on baclofen toxicity in patients with renal disease suggest that administration of the drug in these persons may carry an unnecessarily high risk. Intrathecal baclofen is indicated for use in patients with spasticity of spinal origin unresponsive to treatment with maximum doses of oral baclofen, tizanidine and/or dantrolene. The benefits of continuous intrathecal baclofen infusion have been demonstrated: >80% and >65% of patients have improvement in tone and spasms, respectively. The main risks of intrathecal baclofen infusion are symptoms related to overdose or withdrawal; the latter is more important because of the associated severe effects on clinical status and the possibility of death, but it is responsive to rapid treatment. Overdose primarily arises from drug test doses or human error during refill and programming of the pump, and withdrawal most commonly occurs as a result of a problem with the delivery system. Since the adverse consequences do not exceed the benefits of oral and intrathecal baclofen for patients with spinal spasticity, the benefit/risk assessment is favourable.

Administration, Oral↗
PubMed2006

Botulinum toxin treatment of adult spasticity : a benefit-risk assessment.

Injections of botulinum toxin have revolutionised the treatment of focal spasticity. Before their advent, the medical treatment for focal spasticity involved oral anti-spasticity drugs, which had decidedly non-focal adverse effects, and phenol injections. Phenol injections could be difficult to perform, could cause sensory complications and had effects that were of uncertain duration and magnitude. Furthermore, few neurologists knew how to perform them as they were mostly the province of rehabilitation specialists. Botulinum toxin can produce focal, controllable muscle weakness of predictable duration, without sensory adverse effects. Randomised clinical trials (RCTs) involving patients with spasticity resulting from a variety of diseases (mainly stroke and multiple sclerosis) have clearly shown that botulinum toxin type A (Dysport and Botox) can temporarily (for approximately 3 months) reduce spastic hypertonia in the elbow, wrist and finger flexors of the upper limbs, and the hip adductors and ankle plantar flexors in the lower limbs. The clinical benefits from this reduction of neurological impairment are best shown in the upper limb, with less disability of passive function and reduced caregiver burden. In the lower limbs, there is improved perineal hygiene from hip adductor injections. The benefits of reducing ankle plantar flexor tone are less well established. Pain is also reduced, possibly by mechanisms other than muscle weakness. Improved active function has not yet been clearly demonstrated in RCTs, only in open-label trials. The safety of botulinum toxin-A is impressive, with minimal (mainly local) adverse effects. There are little data on the use of botulinum toxin type B (Myobloc or Neurobloc) in spasticity and the only RCT that has examined this did not show tone reduction; dry mouth appeared to be a very common adverse effect. There are also very little data to allow a benefit-risk comparison of phenol and botulinum toxin injections; each have their clinical and technical advantages and disadvantages, and phenol is much less costly than botulinum toxin.

Adult↗
PubMed2003

Spasticity associated with cerebral palsy in children: guidelines for the use of botulinum A toxin.

Botulinum A toxin produces selective and reversible chemodenervation that can be employed to balance muscle forces across joints in children with cerebral palsy (CP). Currently, there are two commercially available botulinum A toxin formulations (BOTOX) and Dysport). The amount of botulinum A toxin required depends upon the number of muscles that are targeted, and the size of the patient. In order to achieve adequate chemodenervation with botulinum A toxin, the following conditions must be met: (i) a sufficient number of units of toxin must be injected in order to neutralize neuromuscular junction (NMJ) activity; (ii) an appropriate drug volume is required in order to optimize the delivery of the toxin to the NMJs; and (iii) localization of the injecting needle through the fascia of the target muscle is necessary. Localization of the injection may be facilitated by active electromyography, ultrasonography, palpation of the muscle belly, and/or use of anatomic landmarks. Botulinum A toxin injections are indicated for use in pediatric patients with CP to: (i) improve motor function by balancing muscle forces across joints; (ii) improve health-related quality of life by decreasing spasticity and/or decreasing caregiver burden; (iii) decrease pain from spasticity; (iv) enhance self-esteem by diminishing inappropriate motor responses; and (v) provide a presurgical diagnostic tool. Following intramuscular injections of botulinum A toxin, short-term benefits of reduced spasticity are observed in approximately 70-82% of children. The intermediate term (1-2 years) efficacy rate is approximately 50%. The most common deformity treated with toxin injections in pediatric patients with CP is equinus foot deformity. However, efficacy of toxin injections for the management of crouched gait, pelvic flexion contracture, cervical spasticity, seating difficulties, and upper extremity deformity also has been documented. In addition, toxin injections have been shown to manage painful muscle spasticity associated with surgery or application of casts and painful cervical spasticity with or without dystonia. Toxin injections can also be used as a diagnostic tool to determine the appropriateness of other interventions by observing the muscle response to the injection in order to gain additional information for the development of a treatment plan. Botulinum A toxin, when used in appropriate doses, is well tolerated.

Botulinum Toxins↗
PubMed1977

Posterior partial rootlet section in the treatment of spasticity.

Twenty-six patients were operated on using a techinal modification of Förster's method of treating spasticity, which consists of a partial section of the roolets constituting the posterior roots. Many patients had mild cerebral spastic quadriplegia or spastic diplegia: several of them were nearly independent when standing or walking, and two of them completely independent. The spastic disorders that were not made worse by voluntary movements were reduced or abolished in all but one patient, in whom rootlet section was insufficient. The spastic disorders that were made worse by voluntary movements were only partially reduced; after operation they were scarcely evident or absent in a static position, but evident during voluntary movements. No improvement was observed in one patient who suffered from spastic disorders that were evident only during voluntary movements, or in one patient suffering from dystonia. The procedure caused no sensory disorders. The operation was especially useful in patients who were acquiring or had already acquired independence when standing or walking.

Adolescent↗
PubMed2004

The effect of selective tibial neurotomy and rehabilitation in a quadriplegic patient with ankle spasticity following traumatic brain injury.

Ankle spasticity following brain injury leads to abnormal posture and joint contracture; making standing or walking impossible. This study investigates the efficacy of selective tibial neurotomy (STN) and intensive rehabilitation in a patient who suffered ankle spasticity after brain injury. This case describes a 37-year-old man whose traumatic brain injury (TBI) resulted in severe right ankle spasticity and contracture. He was unable to stand due to severe right ankle spasticity and contracture. Intensive rehabilitation and STN allowed him to walk without brace at 6 months and run at 12 months after STN. STN is an effective procedure to resolve localized spasticity of the ankle and it may be considered as a management strategy after local injection to alleviate ankle spasticity and/or contracture prior to orthopaedic surgery.

Adult↗
PubMed2005

Biomechanical assessment with electromyography of post-stroke ankle plantar flexor spasticity.

Spasticity has been defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflex (muscle tone). Muscle tone consists of mechanical-elastic characteristics, reflex muscle contraction and other elements. The aims of this study were to determine whether to assess spasticity quantitatively, and to characterize biomechanical and electromyographic spasticity assessment parameters. These assessment parameters were described by investigating the correlation between clinical measures and the response to passive sinusoidal movement with consecutive velocity increments. Twenty post-stroke hemiplegic patients and twenty normal healthy volunteers were included in the study. Five consecutive sinusoidal passive movements of the ankle were performed at specific velocities (60, 120, 180, and 240 degrees/ sec). We recorded the peak torque, work, and threshold angle using a computerized isokinetic dynamometer, and simultaneously measured the rectified integrated electromyographic activity. We compared these parameters both between groups and between different velocities. The peak torque, threshold angle, work, and rectified integrated electromyographic activity were significantly higher in the post-stroke spastic group at all angular velocities than in the normal control group. The threshold angle and integrated electromyographic activity increased significantly and linearly as angular velocity increased, but the peak torque and work were not increased in the post-stroke spastic group. Peak torque, work, and threshold angle were significantly correlated to the Modified Ashworth scale, but the integrated electromyographic activity was not. The biomechanical and electromyographic approach may be useful to quantitatively assess spasticity. However, it may also be very important to consider the different characteristics of each biomechanical parameter.

Adult↗
PubMedDate not supplied

[Botulin toxin as treatment for spasticity and dystonia in infantile cerebral paralysis].

UNLABELLED: Treatment of spasticity and dystonía in PCI with Botulinum toxin A. BACKGROUND: Botulinum-A (NxTxBoA) toxin produce neuromuscular blockade, it has been effective with therapeutic purposes in strabismus, focal dystonias and spasticity. OBJECTIVE: Evaluate the therapeutically effects off NxTxBoA in cerebral palsy (CP) spastic and/or dystonic in children. Prospective study. MATERIAL AND METHODS: 12 CP patients (8 spastic and 4 spastic/dystonic) were treated with NxTxBoA in affected muscles at least for 2 doses by up 12 months. The indication was: improve limb function, to avoid surgical correction or improve hygienic or dressing. Ashworth Spasticity Scale (ASS), functional scale for Dystonic Sindou-Millet (SMS) and O'Brien Global Assessment Scale (OGAS) were used to evaluate improvement. STATISTICAL METHODS: No parametric tests, Wilcoxon's rang's test and sign test were used with p < 0.05. RESULTS: Total doses session was 3-10 U/kg. AAS showed muscle spasticity improvement in two grades in 8 patients, and one grade in the rest (p = 0.004). SMS showed the muscle dystonic improve up 60% in two patients improve 50% in others (p = 0.006). OGAS demonstrated a good correlation. Mean treatment effect during 4.8 months (rank 4 to 10 m). Two patients had side effects, general weakness, instability, and focal haematoma. CONCLUSIONS: Botulinum toxin type A proved a highly useful adjuvant therapy and conservative management in CP.

Adolescent↗