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PubMed2004

Image-guided HIFU neurolysis of peripheral nerves to treat spasticity and pain.

Spasticity, a major complication of central nervous system disorders, signified by uncontrollable muscle contractions, is very difficult to treat effectively. We report on the use of ultrasound (US) image-guided high-intensity focused US (HIFU) to target and suppress the function of the sciatic nerve complex of rabbits in vivo, as a possible treatment of spasticity. The image-guided HIFU device included a 3.2-MHz spherically curved transducer and an intraoperative imaging probe. A focal acoustic intensity of 1480 to 1850 W/cm(2), applied using a scanning method, was effective in achieving complete conduction block in 100% of 22 nerve complexes with HIFU treatment times of 36 +/- 14 s (mean +/- SD). Gross examination showed blanching of the nerve at the HIFU treatment site and lesion volumes of 2.8 +/- 1.4 cm(3) encompassing the nerve complex. Histologic examination indicated axonal demyelination and necrosis of Schwann cells as probable mechanisms of nerve block. With accurate localization and targeting of peripheral nerves using US imaging, HIFU could become a promising tool for the suppression of spasticity.

Animals↗
PubMed1995

Selective dorsal rhizotomy to decrease spasticity in cerebral palsy.

Until recently, treatment of muscle spasticity in children with cerebral palsy has consisted of physical therapy, bracing, and surgery to release and lengthen tight tendons of contracted muscles and correct muscle contractures. Selective dorsal rhizotomy is a surgical intervention that selectively cuts the spinal sensory nerve rootlets carrying the most abnormal signals, thereby reducing spasticity in all muscle groups of the affected extremities. It is not a cure for spastic cerebral palsy. Children who have this procedure can gain significant increases in knee and thigh ranges of motion and increased strength and muscle control if they have good family support and follow through with intensive postoperative physical therapy.

Cerebral Palsy↗
PubMed2000

Gabapentin effect on spasticity in multiple sclerosis: a placebo-controlled, randomized trial.

OBJECTIVE: To investigate the effect of gabapentin on subject self-report and physician-administered spasticity scales in individuals with multiple sclerosis. DESIGN: Prospective, double-masked, placebo-controlled, crossover design. SETTING: The Multiple Sclerosis Center at the Denver Veterans Affairs Medical Center. INTERVENTION: Subjects were titrated to either 900 mg gabapentin orally three times a day or placebo over a 6-day period. Subjects underwent a 14-day washout and then were crossed over. No other changes were made to their medication regimen. MAIN OUTCOME MEASURES: The outcome measures were divided into two categories: subject self-report scales physician-administered scales. Subject self-report scales included the spasm frequency scale, spasm severity scale, interference with function scale, painful spasm scale, and global assessment scale. Physician-administered scales included the Modified Ashworth Scale, clonus scale, deep tendon reflexes, plantar stimulation response, and the Kurtzke Expanded Disability Status (EDSS) Scale. Digit Span and Digit Symbol subtests of the WAIS-R Intelligence Scale were administered to assess for possible impaired concentration. The Fatigue Impact Scale was administered to assess for changes in fatigue. The adjective generation technique was administered to assess for alterations in mood. RESULTS: A statistically significant reduction in the impairment of spasticity was found in the gabapentin-treated subjects compared with placebo as measured by the self-report scales of the spasm severity scale, interference with function scale, painful spasm scale, and global assessment scale and by the physician-administered scales of the Modified Ashworth and plantar stimulation response. No significant difference was noted in the Digit Span, Digit Symbol, adjective generation technique, and EDSS. CONCLUSION: Gabapentin reduces the impairment of spasticity, compared with placebo, without the side effects of worsening concentration and fatigue.

Acetates↗
PubMed2003

Quantitative evaluation of reflex and voluntary activity in children with spasticity.

OBJECTIVE: To determine whether increased reflexes are related to functional impairment in children with spasticity. DESIGN: Descriptive measurement study. SETTING: Rehabilitation department in Poland. PARTICIPANTS: Sixteen able-bodied children and 29 children with spasticity. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Measurement of modulation function of knee tendon reflexes by isometric knee extension, maximum isometric knee flexion, and extension torques, and scoring of ambulation in patients. RESULTS: In able-bodied children, the reflex modulation function increased with voluntary knee extension, reached maximum at 5% to 20% of voluntary extension, and then decreased. The reflex modulation function in patients fell into 2 major categories. In the majority of affected limbs, the modulation function was inverse, with maximum reflex response at relaxation, and decreased with an increase of voluntary extension. In the remaining limbs, the shape of the reflex modulation function was normal, although other parameters changed. Isometric torques decreased more in flexion (65%) than in extension (39%). A torque decrease was a result of cocontraction more often during knee flexion (65%) than in knee extension (24%). The larger the reflexes, the more flexion torque decreased and ambulation deteriorated. This pattern occurred in patients with inverse modulation function but not in those with normal modulation function. The reciprocal inhibition from knee flexors to extensors could be affected in patients with inverse modulation function and cocontraction during flexion, whereas other mechanisms occurred in other patients. CONCLUSIONS: The experimental design has potential as a quantitative measure of abnormal control in children with spasticity and can lead to more precise treatment selection criteria.

Adolescent↗
PubMed1996

Gait analysis of spinal cord injured subjects: effects of injury level and spasticity.

OBJECTIVE: To identify abnormalities in the gait of spinal cord injured (SCI) subjects, particularly in relation to injury level and spasticity. DESIGN: Case-control study comparing the gait of SCI individuals with matched controls. Video-motion analysis was used to collect data on temporal and kinematic variables. Spasticity was assessed using the Ashworth score and pendulum test. Data regarding age, height, weight, mechanism, and level of injury were also collected. SETTING: Spinal cord injury clinic of a tertiary care hospital. PARTICIPANTS: Twenty-seven SCI individuals volunteered to participate in the study. All had retained walking ability (Frankel D) and could ambulate independently for a minimum of 10m with or without walking aids. Individuals with cauda equina injuries were excluded from the study. Age, gender, etiology of injury, and interval since injury were not used as exclusion criteria. Ten age-, sex-, and anthropomorphically matched controls were also recruited. RESULTS: Subjects with thoracic injures demonstrated reduced cadence, forward velocity, and knee angular velocity, whereas lumbar injuries resulted in reduced stride length and ankle velocities. These differences were statistically significant (p < .05). Gait in individuals with cervical injuries was not significantly different. CONCLUSIONS: Kinematic gait analysis is a sensitive means of quantifying gait abnormalities. Spasticity and injury level determine the pattern of abnormality in gait after spinal cord injury.

Adult↗
PubMed1996

Botulinum toxin A in the treatment of spasticity: functional implications and patient selection.

OBJECTIVE: To explore the range of functional indications and benefit of botulinum toxin A (BTA) in spastic patients. DESIGN: Case report of a series of patients selected for BTA treatment. Clinical information was collected in a prospective fashion on each patient. SETTING: Freestanding acute rehabilitation hospital. PATIENTS: 39 consecutive patients with 40 limbs with acquired spasticity. INTERVENTION: All 39 patients received BTA injections into muscles targeted for treatment based on functional indications. MAIN OUTCOME MEASURES: Objective evaluation of outcome was measured by Ashworth Scale, goniometry, ambulation score, and brace wear scale. Subjective measures included patient self report of improvement and pain relief. RESULTS: Mean BTA dose per limb was 180 units, mean number of muscles injected per limb was 2. Twenty-nine patients had subjective and/or objective improvement with treatment. Mean Ashworth Scale improvement was one point. Mean gain in active range of motion (AROM) was 17.0 degrees, and in passive range of motion (PROM) 18.4 degrees. Brace tolerance improved in 14 of 22 patients and pain relief occurred in 10 of 13 patients. There were no adverse effects, and there was no difference in duration of effect compared to dystonia patients. CONCLUSION: BTA is a useful intervention in the treatment of spasticity, with the majority of patients demonstrating improvement on objective measures of tone and function, and reporting improvement on subjective measures. Careful patient selection will maximize functional benefit.

Activities of Daily Living↗
PubMed1996

Clinical measurement of spasticity using the pendulum test: comparison of electrogoniometric and videotape analyses.

OBJECTIVE: To compare pendulum test data obtained using an electrogoniometer with data obtained by videotape. The issue of video digitization error was also addressed. DESIGN: The study compared pendulum test relaxation indices determined from data simultaneously collected using (1) a video (VID) camera and (2) an electrogonimeter (EG). SETTING: A spinal cord injury rehabilitation center. SUBJECTS: Three persons with a spinal cord injury (SCI) exhibiting mild, moderate, and severe spasticity, respectively, and a fourth, non-SCI subject. MAIN OUTCOME MEASURE: Relaxation index as a descriptor of lower limb muscle spasticity measured using the pendulum test. RESULTS: Multiple-digitization of VID data did not affect the reliability of this technique. It was noted that reflective markers located on body landmarks resulted in more reliable data as opposed to markers placed on the EG. Both EG and VID data were accurate and reliable. CONCLUSIONS: In the VID method, using one digitization by a single operator is sufficient. The appropriate placement of light reflector markers are on body points. EG and VID are both reliable, highly correlated, and interchangeable in measuring spasticity using the pendulum test.

Adult↗
PubMed1996

Intrathecal baclofen administration for control of severe spinal spasticity: functional improvement and long-term follow-up.

OBJECTIVES: To assess long-term efficacy and functional benefits of intrathecal baclofen for severe spinal spasticity. DESIGN: A prospective before-after trial. SETTING: A neurological rehabilitation department of a university hospital. Pump implantation was realized in neurosurgery; follow-up was carried out mostly on an outpatient basis. PATIENTS: Eighteen patients with severe and disabling spinal spasticity received intrathecal baclofen by an implantable pump; average follow-up was 37.4 months (range, 9 to 72). MAIN OUTCOME MEASURES: Spasticity (Ashworth and spasms frequency scores); disability (Functional Independence Measure [FIM]). RESULTS: A significant decrease in tone and spasms was observed in all patients. Tolerance appeared during the first 6 to 9 months. Later on, efficacy remained stable, except in cases of mechanical problems of the pump or catheter. Functional assessment found a highly significant (p < .001) increase of FIM score (particularly for bathing, dressing lower body, transfers, and in some cases, locomotion). This was particularly marked in patients with thoracic spinal cord lesion. In cases of severe upper limb dysfunction, FIM was only improved for wheelchair displacements, due to a better sitting position, but nursing became easier and life comfort was enhanced. Severe side effects (overdose) were observed in two cases. CONCLUSION: Efficacy remained stable after 6 to 9 months. Marked improvement of functional independence was observed in paraplegic patients. Improvement was less spectacular in patients with severe upper limb dysfunction, but nevertheless appreciable in terms of life comfort and use of attendants.

Activities of Daily Living↗
PubMed2000

Botulinum toxin type-A treatment in spastic paraparesis: a neurophysiological study.

OBJECTIVE: The aim of this study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. SUBJECTS AND METHOD: Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. RESULTS: In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. CONCLUSIONS: Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

Adult↗
PubMed2002

Friedreich ataxia with minimal GAA expansion presenting as adult-onset spastic ataxia.

Around a quarter of Friedreich ataxia (FA) patients, despite being homozygous for GAA expansion within the FRDA gene, show atypical presentations. Our aim is to describe the case of three brothers with long-term follow-up suffering from late onset FA manifested with spastic ataxia. The three patients belong to a family with occipital dysplasia (OD) and Chiari I malformation previously reported by us. We have carried out serial examinations since 1977. Electrophysiological and neuroimaging studies, and molecular genetic analyses of hereditary ataxias are available in all three patients. Onset of symptoms occurred between 25 and 35 years. The clinical picture consisted of progressive spastic gait, truncal and limb ataxia, dysarthria, nystagmus, hyperreflexia with knee and ankle clonus and extensor plantar response, and mild hypopallesthesia. Ages at present vary between 50 and 59. One patient is wheelchair-bound but the other two are able to walk with support. Leaving OD aside, skeletal anomalies are not prominent. All three patients showed cardiomyopathy. MR imaging revealed atrophy of the cerebellum and spinal cord. Motor and sensory nerve conduction velocities were normal. Central conduction time of both motor and sensory pathways was delayed or unobtainable. All three patients were homozygous for the GAA expansion, the smaller expanded allele ranging between 131 and 156 repeats. Four heterozygotic carriers were detected among non-ataxic relatives including one with OD; furthermore, an asymptomatic OD patient showed normal genotype. We conclude that adult onset spastic ataxia is a distinctive FA phenotype associated with minimal GAA expansion. This phenotype represents a new cause of selective distal degeneration of central sensory axons. The present concurrence of OD and FA reflects coincidental cosegregation of two different inherited disorders.

Adult↗
PubMed1993

Urinary dysfunction in tropical spastic paraparesis: preliminary urodynamic survey.

Tropical spastic paraparesis is an infection caused by human T lymphotropic virus type 1 (HTLV-1). We present the urodynamic findings in 4 female and 1 male patient with tropical spastic paraparesis. All patients underwent synchronous video-pressure-flow urodynamics, while 3 also underwent electromyographic examination. Of the 5 patients 4 presented with detrusor external sphincter dyssynergia and 1 had detrusor hyperreflexia with a coordinated sphincter contraction. The preliminary results of this series suggest that patients with tropical spastic paraparesis and voiding symptoms should undergo urodynamic examination so that diagnosis and appropriate therapy may be instituted.

Adult↗
PubMed2003

Defective human T-cell lymphotropic virus type I (HTLV-I) provirus in seronegative tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM) patients.

Infection with human T-cell lymphotropic virus type I (HTLV-I) have been associated with the development of the tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM). We studied the presence of HTLV-I provirus in peripheral blood mononuclear cells (PBMC) from 72 Chilean patients with progressive spastic paraparesis by polymerase chain reaction: 32 seropositive and 40 seronegative cases. We amplified different genomic regions of HTLV-I using primers of 5' ltr, tax, env/tax, pX, pol and env genes. These genes were detected from all seropositive patients. The seronegative patients were negative with 5' ltr, pol, env, and pX primers. However, amplified product of tax and env/tax genes was detected from 16 and four seronegative patients, respectively. Three of them were positive with both genetic regions. The results of this study show that the complete HTLV-I provirus is found in 100% of seropositive cases. In seronegative cases, clinically very similar of seropositive cases, was found only tax gene in 42.5% (17/40) of patients. These results suggest the presence of a defective HTLV-I provirus in some seronegative patients with progressive spastic paraparesis, and suggest a pathogenic role of this truncate provirus for a group of TSP/HAM.

Adult↗
PubMedDate not supplied

Spastic dysphonia: a patient profile of 200 cases.

A comprehensive case history profile of spastic dysphonia patients was established, using 200 patients matched to 200 controls. The case histories and epidemiologic profiles for male and female patients revealed few dissimilarities. Likewise, intergroup (patients-controls) health history profiles differed in only a few specific instances. The data suggest non-psychogenic, non-behavioral causation of spastic dysphonia; however, neither a definitive cluster or clusters of events at onset nor any unequivocal epidemiologic factor was accountable for spastic dysphonia. Short of qualified improvement with voice therapy in some patients, no form of treatment other than recurrent laryngeal nerve section was shown to be of any significant help for the patient population sampled.

Adult↗
PubMed1998

A new form of complicated hereditary spastic paraplegia with cataracts, atretic ear canals and hypopigmentation.

A 16-year-old Hispanic boy born of consanguineous parents is described as having a history of cataracts, progressive lower-extremity spasticity and atrophy starting at 4 years of age, atretic ear canals with hearing dysfunction and diffuse patchy cutaneous hypopigmented areas. Clinical examination showed the typical signs of spastic paraplegia with increased tone, hyperreflexia, muscle atrophy and contractures. Sensation, autonomic and cerebellar functions were not disturbed. Neuroimaging studies were normal. Laboratory findings did not support a diagnosis of metabolic disturbance or infectious disease. This is considered a new form of complicated hereditary spastic paraplegia (HSP), transmitted presumably in an autosomal recessive pattern.

Adolescent↗
PubMed1999

A clinical study of a large inbred kindred with pure familial spastic paraplegia.

BACKGROUND AND OBJECTIVES: Spastic paraplegia, an uncommon neurodegenerative disorder with phenotypic and genotypic heterogeneity, is mainly characterized by progressive weakness and spasticity of the lower limbs. We here present a large inbred family with pure familial spastic paraplegia outlining the clinical picture, the age at onset and the possible mode of inheritance. METHODS: This family was ascertained through two probands after which we structured an extended 10 generation pedigree. We examined 43 available family members to identify affected individuals based on fixed criteria. The clinical presentation and phenotypic specifics of this disease were studied in the affected members. We analyzed the possible mode of inheritance and the age at onset in this family. RESULTS: This 10 generation family reported about 50 affected individuals distributed over 5 consecutive generations. We identified 13 affected individuals out of the examined 43 and five individuals were classified as probably affected. We noticed the clinical specifics of this disorder in this family and identified some unique features not described in previous reports. DISCUSSION AND CONCLUSION: The mode of inheritance is either autosomal recessive or autosomal dominant with incomplete penetrance or variable expression of the age at onset. The age at onset seems to decrease with successive generations, either due to a true anticipatory phenomenon or to increased awareness. The unique features of this disorder in this family are discussed.

Adolescent↗
PubMed2003

The use of botulinum toxin type A treatment in children with spasticity.

The current modalities in managing spastic children have some limitations; thus, alternative therapeutic agents are in need. The purpose of this study is to investigate whether intramuscular botulinum toxin type A administration may be an alternative agent in the treatment of children with cerebral palsy. Eighteen children who were aged between 3 and 17 years and manifested cerebral palsy were administered intramuscular botulinum toxin type A with a total dose of 6 U/kg body weight. Outcome measurements were determined with four methods, including Ashworth Spasticity Scale, standardized videotape assessments, observational gait analysis, and walking velocity. Ashworth Spasticity Scale and videotape assessments were statistically significant before and after treatment in all muscles (P < 0.001). The best improvement in video gait analysis was evident at week 8. The botulinum toxin type A injections yielded an improved walking velocity at all visits. The observational gait analysis and walking velocity demonstrated an improvement after treatment in the gastrocnemius-injected group (P < 0.001). In conclusion, intramuscular botulinum toxin type A administration may be effective in children with cerebral palsy, especially at week 4 and when injected in gastrocnemius.

Adolescent↗
PubMed1999

The effect of tiagabine on spasticity in children with intractable epilepsy: a pilot study.

Preliminary pharmacologic evidence suggests that tiagabine, a new presynaptic gamma-aminobutyric acid-uptake inhibitor developed as an antiepileptic drug, may also relieve spasticity. This pilot study assessed the drug's efficacy in 14 children with congenital or acquired spastic quadriplegia and concomitant intractable epilepsy refractory to treatment with multiple antiepileptic drugs. The primary outcome variable was change in motor function; the secondary outcome was change in seizure frequency. Tiagabine was initiated at 0.1-0.2 mg/kg/day and then gradually titrated upward until seizures ceased, adverse effects supervened, or the maximum dose of 1.1 mg/kg/day was reached. When a modified Ashworth scale was used to assess motor function, a mean improvement of approximately 50% was observed. Common findings included improved tone, strength, coordination, range of motion, and relaxation of extremities, with less ataxia and wobbling. Mean reduction in seizure frequency was 50-74%. Randomized, double-blind controlled studies are needed to confirm the suggested efficacy of tiagabine in relieving chronic spasticity in children with neurodevelopmental disorders.

Anticonvulsants↗
PubMed2004

Autosomal recessive hereditary spastic paraparesis with thin corpus callosum; report of two sisters.

OBJECTIVES: To describe the clinical, cognitive, neurophysiological and radiological features of autosomal recessive hereditary spastic paraparesis (ARHSP) with thin corpus callosum. PATIENTS AND METHODS: Two sisters with spastic paraparesis. RESULTS: MRI brain scans demonstrated thinning of the corpus callosum. The clinical features were progressive spastic paraparesis beginning in the second decade, dysarthria, minor dystonia and chorea, distal weakness and cognitive impairment with frontal dysfunction. Motor compound action potentials are reduced and EMG demonstrated minor chronic denervation. Magnetic stimulation studies demonstrated increased threshold consistent with pyramidal system axonal loss. CONCLUSIONS: AHRSP with thinned corpus callosum is a distinct clinical and genetic entity that may occur in non-Japanese individuals.

Adult↗