Botulinum toxin for spasticity in children with cerebral palsy: a comprehensive evaluation.
Pediatrics. 2007 Jul;120(1):49-58
Authors: (articles re: how to treat spasticity) Bjornson K, Hays R, Graubert C, Price R, Won F, McLaughlin JF, Cohen M
BACKGROUND: Spasticity is a prevalent disabling clinical symptom for children with cerebral palsy. Treatment of spasticity with botulinum toxin in children with cerebral palsy was first reported in 1993. Botulinum toxin provides a focal, controlled muscle weakness with reduction in spasticity. Interpretation of the literature is difficult because of the paucity of reliable measures of spasticity and challenges with measuring meaningful functional changes in children with disabilities. OBJECTIVE: This study documents the effects of botulinum toxin A injections into the gastrocnemius muscles in children with spastic diplegia. Outcomes are evaluated across all 5 domains of the National Centers for Medical and Rehabilitation Research domains of medical rehabilitation. METHODS: A randomized, double-masked, placebo-controlled design was applied to 33 children with spastic diplegia with a mean age of 5.5 and Gross Motor Function Classification System Levels of I through III. Participants received either 12 U/kg botulinum toxin A or placebo saline injections to bilateral gastrocnemius muscles. Outcomes were measured at baseline and 3, 8, 12, and 24 weeks after injection. RESULTS: Significant decreases in the electromyographic representation of spasticity were documented 3 weeks after botulinum toxin A treatment. A significant decrease in viscoelastic aspects of spasticity was present at 8 weeks, and subsequent increases in dorsiflexion range were documented at 12 weeks for the botulinum toxin A group. Improvement was found in performance goals at 12 weeks and in maximum voluntary torque and gross motor function at 24 weeks for the botulinum toxin A. There were no significant differences between groups in satisfaction with performance goals, energy expenditure, Ashworth scores, or frequency of adverse effects. CONCLUSIONS: The safety profile of 12 U/kg of botulinum toxin A is excellent. Although physiologic and mechanical effects of treatment with botulinum toxin A were documented with functional improvement at 6 months, family satisfaction with outcomes were no different. Communication is needed to ensure realistic expectations of treatment.
PMID: (Treat spasticity) 17606561 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Intrathecal catheter granuloma associated with isolated baclofen infusion.
Anesth Analg. 2006 Mar;102(3):848-52
Authors: (articles re: how to treat spasticity) Murphy PM, Skouvaklis DE, Amadeo RJ, Haberman C, Brazier DH, Cousins MJ
Intrathecal (IT) baclofen is an effective management strategy for controlling spasticity in patients unresponsive to maximal oral therapy. We present the case of a 57-yr-old woman who was rendered quadriplegic after a complete spinal cord transection at the C6 level. Her course was complicated by severe spasms, which were uncontrolled despite titrating orally administered baclofen to 80 mg/d. IT baclofen testing was performed with good response, and administration was commenced via an implanted intrathecal pump 6 mo after the injury at an initial dose of 200 microg/d. Catheter revision was required 2 wk later as a result of catheter displacement. The initial IT baclofen dose was gradually increased to achieve good control at a level of 400 microg/d. After a period of stability lasting 38 mo, her lower limb spasms dramatically increased in severity and remained poorly controlled despite repeated dose increases. Contrast pumpogram and computed tomography myelogram were performed to exclude a mechanical cause for this apparent increase in baclofen requirement. These investigations revealed neither catheter displacement nor fracture as suspected but, rather, displayed the presence of a catheter tip-associated mass. Catheter tip granuloma has not previously been described in a patient receiving IT baclofen alone. This suggests that although uncommon, the possibility of catheter-associated granuloma must be considered in all patients receiving IT baclofen presenting with altered neurological function or significant increase in drug requirement.
PMID: (Treat spasticity) 16492839 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Authors: (articles re: how to treat spasticity) Krigger KW
The presentation of cerebral palsy can be global mental and physical dysfunction or isolated disturbances in gait, cognition, growth, or sensation. It is the most common childhood physical disability and affects 2 to 2.5 children per 1,000 born in the United States. The differential diagnosis of cerebral palsy includes metabolic and genetic disorders. The goals of treatment are to improve functionality and capabilities toward independence. Multispecialty treatment teams should be developed around the needs of each patient to provide continuously updated global treatment care plans. Complications of cerebral palsy include spasticity and contractures; feeding difficulties; drooling; communication difficulties; osteopenia; osteoporosis; fractures; pain; and functional gastrointestinal abnormalities contributing to bowel obstruction, vomiting, and constipation. Valid and reliable assessment tools to establish baseline functions and monitor developmental gains have contributed to an increasing body of evidenced-based recommendations for cerebral palsy. Many of the historical treatments for this ailment are being challenged, and several new treatment modalities are available. Adult morbidity and mortality from ischemic heart disease, cerebrovascular disease, cancer, and trauma are higher in patients with cerebral palsy than in the general population.
PMID: (Treat spasticity) 16417071 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Sensorimotor function and axonal integrity in adrenomyeloneuropathy.
Arch Neurol. 2006 Jan;63(1):74-80
Authors: (articles re: how to treat spasticity) Zackowski KM, Dubey P, Raymond GV, Mori S, Bastian AJ, Moser HW
BACKGROUND: Gait abnormalities and sensorimotor disturbances are principal defects in adrenomyeloneuropathy (AMN). However, to our knowledge, their association with overall impairment and neuroanatomical changes has not been defined. OBJECTIVES: To understand how sensorimotor impairments create mobility deficits and to analyze how these impairments are related to specific metrics of axonal integrity. DESIGN: Cross-sectional study assessing impairments, including vibration sensation, strength, spasticity, and global measures of walking and balance. Fractional anisotropy was measured to evaluate the integrity of the corresponding brainstem tracts. PARTICIPANTS: Men with AMN and healthy control subjects. RESULTS: Individuals with sensory loss only showed minimal walking deficits. Concomitant strength and sensory loss resulted in slower walking, with abnormal knee control; increased spasticity led to an exaggerated trunk motion and a knee-flexed (crouched) posture. Hip strength was an independent predictor of walking velocity in subjects with AMN. Subjects with sensory loss only had greater sway amplitudes during standing balance testing, which did not worsen with additional impairments. There were significant associations among sway amplitude, great toe vibration sense, and dorsal column fractional anisotropy. Brainstem fractional anisotropy in AMN was significantly negatively correlated with impairment, indicating that overall tract integrity is associated with sensorimotor abnormalities in AMN. CONCLUSIONS: Impairment measures capture specific abnormalities in walking and balance that can be used to direct rehabilitation therapy in AMN. Tract-specific magnetic resonance imaging metrics, such as fractional anisotropy (used herein to evaluate structure-function relationships), significantly reflect disease severity in AMN.
PMID: (Treat spasticity) 16401738 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Disease-related phenotypes in a Drosophila model of hereditary spastic paraplegia are ameliorated by treatment with vinblastine.
J Clin Invest. 2005 Nov;115(11):3026-34
Authors: (articles re: how to treat spasticity) Orso G, Martinuzzi A, Rossetto MG, Sartori E, Feany M, Daga A
hereditary spastic paraplegias (HSPs) are a group of neurodegenerative diseases characterized by progressive weakness and spasticity of the lower limbs. Dominant mutations in the human SPG4 gene, encoding spastin, are responsible for the most frequent form of HSP. Spastin is an ATPase that binds microtubules and localizes to the spindle pole and distal axon in mammalian cell lines. Furthermore, its Drosophila homolog, Drosophila spastin (Dspastin), has been recently shown to regulate microtubule stability and synaptic function at the Drosophila larval neuromuscular junction. Here we report the generation of a spastin-linked HSP animal model and show that in Drosophila, neural knockdown of Dspastin and, conversely, neural overexpression of Dspastin containing a conserved pathogenic mutation both recapitulate some phenotypic aspects of the human disease, including adult onset, locomotor impairment, and neurodegeneration. At the subcellular level, neuronal expression of both Dspastin RNA interference and mutant Dspastin cause an excessive stabilization of microtubules in the neuromuscular junction synapse. In addition, we provide evidence that administration of the microtubule targeting drug vinblastine significantly attenuates these phenotypes in vivo. Our findings demonstrate that loss of spastin function elicits HSP-like phenotypes in Drosophila, provide novel insights into the molecular mechanism of spastin mutations, and raise the possibility that therapy with Vinca alkaloids may be efficacious in spastin-associated HSP and other disorders related to microtubule dysfunction.
PMID: (Treat spasticity) 16276413 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Authors: (articles re: how to treat spasticity) Penny EB, McCabe BD
Autosomal-dominant pure hereditary spastic paraplegia (AD-HSP) is characterized by the degeneration of long axons in corticospinal tracts and dorsal columns, resulting in spasticity and difficulty walking. Mutations in the SPG4 gene product spastin are the predominant genetic lesions associated with this inherited disease. In this issue, Orso et al. examine and reconcile existing Drosophila mutants of spastin and generate a new model for HSP by overexpression of a fly spastin transgene that carries a mutation prevalent in human AD-HSP (see the related article beginning on page 3026). Expression of this mutant spastin protein produces pathology in flies reminiscent of the human disease, including adult locomotion defects, in addition to causing aberrant synaptic morphology and altered microtubule stability. Both movement and synaptic defects in fly mutants were ameliorated by treatment with the microtubule-modifying agent vinblastine. The results are consistent with disease-causing mutations in human spastin producing dominant-negative proteins and confirm the usefulness of Drosophila genetic techniques to understand HSP and other neurodegenerative diseases.
PMID: (Treat spasticity) 16276409 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Authors: (articles re: how to treat spasticity) Calabresi PA
Multiple Sclerosis, an idiopathic inflammatory disease of the central nervous system, is characterized pathologically by demyelination and subsequent axonal degeneration. The disease commonly presents in young adults and affects twice as many women as men. Common presenting symptoms include numbness, weakness, visual impairment, loss of balance, dizziness, urinary bladder urgency, fatigue, and depression. The diagnosis of Multiple Sclerosis should be made by a physician with experience in identifying the disease. Diagnosis should be based on objective evidence of two or more neurologic signs that are localized to the brain or spinal cord and are disseminated in time and space (i.e., occur in different parts of the central nervous system at least three months apart). Magnetic resonance imaging with gadolinium contrast, especially during or following a first attack, can be helpful in providing evidence of lesions in other parts of the brain and spinal cord. A second magnetic resonance scan may be useful at least three months after the initial attack to identify new lesions and provide evidence of dissemination over time. It is critical to exclude other diseases that can mimic Multiple Sclerosis, including vascular disease, spinal cord compression, vitamin B12 deficiency, central nervous system infection (e.g., Lyme disease, syphilis), and other inflammatory conditions (e.g., sarcoidosis, systemic lupus erythematosus, Sj?gren's syndrome). Symptom-specific drugs can relieve spasticity, bladder dysfunction, depression, and fatigue. Five disease-modifying treatments for Multiple Sclerosis have been approved by the U.S. Food and Drug Administration. These treatments are partially effective in reducing exacerbations and may slow progression of disability.
PMID: (Treat spasticity) 15571060 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Authors: (articles re: how to treat spasticity) Hawker K, Frohman E, Racke M
BACKGROUND: Spasticity is a common and debilitating symptom of Multiple Sclerosis (MS). Current treatments are effective, but may be difficult to tolerate for many patients. OBJECTIVE: To determine if levetiracetam, a second-generation antiepileptic drug, may be useful for the treatment of spasticity in MS. METHODS: A retrospective medical record review of patients attending the Multiple Sclerosis Program at the University of Texas, Southwestern Medical Center at Dallas was performed. A series of 12 patients who had been treated with levetiracetam for spasticity was identified. Most of the patients were female (10/11), and the mean age was 41.0 years. The main outcome measure was a change in Penn spasm score or modified Ashworth score. Both scores are measured on a scale of 0 to 4. RESULTS: The Penn Spasm score (a measure of phasic spasticity) was decreased for all patients following treatment with levetiracetam. The mean +/- SD Penn Spasm score was 2.7 +/- 0.65 at baseline and decreased to 0.9 +/- 0.29 at follow-up. There was no change in modified Ashworth scores (a measure of tonic spasticity). Five patients reported adverse events; 1 patient discontinued treatment owing to an adverse event (edema). Three patients incidentally reported improvements in neuropathic pain. CONCLUSIONS: Levetiracetam was effective for reducing phasic spasticity but not tonic spasticity in this 12-patient case series. The drug was well tolerated and therefore shows promise as a treatment for phasic spasticity. Large, well-controlled trials are needed to confirm these findings.
PMID: (Treat spasticity) 14676055 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Rehabilitation medicine: 3. Management of adult spasticity.
CMAJ. 2003 Nov 25;169(11):1173-9
Authors: (articles re: how to treat spasticity) Satkunam LE
Spasticity refers to an abnormal, velocity-dependent (i.e., how fast the joint is moved through its range) increase in muscle tone resulting from interruption of the neural circuitry regulating the muscles and is a common complication of cerebral palsy, brain injuries, spinal cord injuries, Multiple Sclerosis and stroke. The muscle stretch reflex is thought to play an important role in spasticity generation. Spasticity can have a significant detrimental effect on daily functions, such as feeding, dressing, hygiene, bladder and bowel control, and mobility; patients' need for support can also influence the cost of care. Thus, managing these patients appropriately or referring them to those with expertise in this area is important. In this article, I review the pathophysiology of spasticity and the evaluation and management of adult patients with the condition. Two hypothetical cases are presented to illustrate the management of spasticity.
PMID: (Treat spasticity) 14638654 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Intramuscular injection of botulinum toxin for the treatment of wrist and finger spasticity after a stroke.
N Engl J Med. 2002 Aug 8;347(6):395-400
Authors: (articles re: how to treat spasticity) Brashear A, Gordon MF, Elovic E, Kassicieh VD, Marciniak C, Do M, Lee CH, Jenkins S, Turkel C,
BACKGROUND: Spasticity is a disabling complication of stroke, and it is uncertain whether intramuscular injections of botulinum toxin type A reduce disability in persons with spasticity of the wrist and fingers after a stroke. METHODS: We performed a randomized, double-blind, placebo-controlled, multicenter trial to assess the efficacy and safety of one-time injections of botulinum toxin A (200 to 240 units) in 126 subjects with increased flexor tone in the wrist and fingers after a stroke. The primary outcome measure was self-reported disability in four areas: personal hygiene, dressing, pain, and limb position (on a four-point scale ranging from no disability to severe disability) at six weeks; at base line, each subject selected one of these areas in which there was moderate-to-severe disability as the principal target of treatment. RESULTS: Subjects who received botulinum toxin A had greater improvement in flexor tone in the wrist and fingers at all follow-up visits through 12 weeks than did subjects who received placebo (P<0.001 for all comparisons). Subjects treated with botulinum toxin A had greater improvement in the principal target of treatment at weeks 4, 6, 8, and 12 (P<0.001, P<0.001, P=0.03, and P=0.02, respectively); at week 6, 40 of the 64 subjects in the botulinum-toxin group (62 percent), as compared with 17 of the 62 in the placebo group (27 percent), reported improvement of at least one point on the Disability Assessment Scale in the principal target of treatment (P<0.001). There were no major adverse events associated with injection of botulinum toxin A. CONCLUSIONS: Intramuscular injections of botulinum toxin A reduce spasticity of the wrist and finger muscles and associated disability in patients who have had a stroke.
PMID: (Treat spasticity) 12167681 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Friedreich ataxia: effects of genetic understanding on clinical evaluation and therapy.
Arch Neurol. 2002 May;59(5):743-7
Authors: (articles re: how to treat spasticity) Lynch DR, Farmer JM, Balcer LJ, Wilson RB
The discovery of the genetic cause of Friedreich ataxia has significantly affected our understanding of the disorder at both the clinical and basic science levels. Friedreich ataxia results from a deficiency of functional frataxin, a protein that appears to be involved in mitochondrial iron homeostasis. This leads to iron accumulation and mitochondrial abnormalities with consequent oxidant damage. The clinical spectrum of Friedreich ataxia has also expanded with the recognition of broader phenotypic features, including the absence of classical Friedreich ataxia features, later age at onset, and spasticity instead of ataxia. Although no proven therapy is yet available, antioxidants are a potential method for therapeutic intervention.
PMID: (Treat spasticity) 12020255 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Botulinum toxin type a neuromuscular blockade in the treatment of equinus foot deformity in cerebral palsy: a multicenter, open-label clinical trial.
Pediatrics. 2001 Nov;108(5):1062-71
Authors: (articles re: how to treat spasticity) Koman LA, Brashear A, Rosenfeld S, Chambers H, Russman B, Rang M, Root L, Ferrari E, Garcia de Yebenes Prous J, Smith BP, Turkel C, Walcott JM, Molloy PT
BACKGROUND: Focal spasticity of the gastrocnemius-soleus muscles causes equinus gait in children with cerebral palsy (CP). Botulinum toxin type A (BTX-A), a neuromuscular blocking agent, reduces muscle tone/overactivity in dystonia, stroke, and CP. OBJECTIVE: A prospective, open-label, multicenter clinical trial evaluated the long-term safety and efficacy of repeated intramuscular injections of BTX-A on equinus gait in CP children. METHODS: Nine centers enrolled 207 children. BTX-A injections (4 U/Kg) were given approximately every 3 months (maximum dose 200 U per treatment). Outcome measures included a Physician Rating Scale of gait, ankle range of motion measurements, and the incidence and profile of adverse events. RESULTS: One hundred fifty-five (75%) of 207 children completed at least 1 year with a total of 302 patient years of BTX-A treatment. The mean duration of BTX-A exposure was 1.46 years per patient. Dynamic gait pattern on the Physician Rating Scale improved in 46% of patients (86/185) at first follow-up. The response was maintained in 41% to 58% of patients for 2 years. Both gait pattern and ankle position improved at every visit. The most common treatment-related adverse events included increased stumbling, leg cramps, leg weakness, and calf atrophy in 1% to 11% of patients. No treatment-related serious adverse events were reported. Only 6% (7/117) of patients with pre- and postantibody samples had both detectable antibodies and a subsequent treatment failure. CONCLUSION: BTX-A proved both safe and effective in the chronic management of focal muscle spasticity in children with equinus gait.
PMID: (Treat spasticity) 11694682 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Rehabilitation of persons with central nervous system tumors.
Cancer. 2001 Aug 15;92(4 Suppl):1029-38
Authors: (articles re: how to treat spasticity) Kirshblum S, O'Dell MW, Ho C, Barr K
A tumor that affects the central nervous system can have a dramatic impact on the individual affected, as well as his or her family and friends. The tumor, regardless of extent or location, may affect the physical, social, vocational, and emotional capabilities of the individual. Basic aspects of rehabilitation for patients with tumors affecting the brain and spinal cord are reviewed in this article. The authors have found that the same principles of neurorehabilitation applied to persons with traumatic brain injury, stroke, and traumatic spinal cord injury are equally appropriate for persons with brain and spinal cord tumors. These principles include the prevention of medical complications; the treatment of medical problems such as pain, spasticity, and neuropathic bowel and bladder; and the improvement of patients' mobility and activities of daily living. Rehabilitation specialists can help prevent complications, maximize function, and improve the quality of life for patients with central nervous system tumors.
PMID: (Treat spasticity) 11519030 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Are cannabinoids an effective and safe treatment option in the management of pain? A qualitative systematic review.
BMJ. 2001 Jul 7;323(7303):13-6
Authors: (articles re: how to treat spasticity) Campbell FA, Tram?r MR, Carroll D, Reynolds DJ, Moore RA, McQuay HJ
OBJECTIVE: To establish whether cannabis is an effective and safe treatment option in the management of pain. DESIGN: Systematic review of randomised controlled trials. DATA SOURCES: Electronic databases Medline, Embase, Oxford Pain Database, and Cochrane Library; references from identified papers; hand searches. STUDY SELECTION: Trials of cannabis given by any route of administration (experimental intervention) with any analgesic or placebo (control intervention) in patients with acute, chronic non-malignant, or cancer pain. Outcomes examined were pain intensity scores, pain relief scores, and adverse effects. Validity of trials was assessed independently with the Oxford score. DATA EXTRACTION: Independent data extraction; discrepancies resolved by consensus. DATA SYNTHESIS: 20 randomised controlled trials were identified, 11 of which were excluded. Of the 9 included trials (222 patients), 5 trials related to cancer pain, 2 to chronic non-malignant pain, and 2 to acute postoperative pain. No randomised controlled trials evaluated cannabis; all tested active substances were cannabinoids. Oral delta-9-tetrahydrocannabinol (THC) 5-20 mg, an oral synthetic nitrogen analogue of THC 1 mg, and intramuscular levonantradol 1.5-3 mg were about as effective as codeine 50-120 mg, and oral benzopyranoperidine 2-4 mg was less effective than codeine 60-120 mg and no better than placebo. Adverse effects, most often psychotropic, were common. CONCLUSION: Cannabinoids are no more effective than codeine in controlling pain and have depressant effects on the central nervous system that limit their use. Their widespread introduction into clinical practice for pain management is therefore undesirable. In acute postoperative pain they should not be used. Before cannabinoids can be considered for treating spasticity and neuropathic pain, further valid randomised controlled studies are needed.
PMID: (Treat spasticity) 11440935 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Randomised double blind placebo controlled trial of the effect of botulinum toxin on walking in cerebral palsy.
Arch Dis Child. 2000 Dec;83(6):481-7
Authors: (articles re: how to treat spasticity) Ubhi T, Bhakta BB, Ives HL, Allgar V, Roussounis SH
BACKGROUND: cerebral palsy is the commonest cause of severe physical disability in childhood. For many years treatment has centred on the use of physiotherapy and orthotics to overcome the problems of leg spasticity, which interferes with walking and can lead to limb deformity. Intramuscular botulinum toxin (BT-A) offers a targeted form of therapy to reduce spasticity in specific muscle groups. AIMS: To determine whether intramuscular BT-A can improve walking in children with cerebral palsy. DESIGN: Randomised, double blind, placebo controlled trial. METHODS: Forty patients with spastic diplegia or hemiplegia were enrolled. Twenty two received botulinum toxin and 18 received placebo. The primary outcome measure was video gait analysis and secondary outcome measures were gross motor function measure (GMFM), physiological cost index (PCI), and passive ankle dorsiflexion. RESULTS: Video gait analysis showed clinically and statistically significant improvement in initial foot contact following BT-A at six weeks and 12 weeks compared to placebo. Forty eight per cent of BT-A treated children showed clinical improvement in VGA compared to 17% of placebo treated children. The GMFM (walking dimension) showed a statistically significant improvement in favour of the botulinum toxin treated group. Changes in PCI and passive ankle dorsiflexion were not statistically significant. CONCLUSION: The study gives further support to the use of intramuscular botulinum toxin type A as an adjunct to conventional physiotherapy and orthoses to reduce spasticity and improve functional mobility in children with spastic diplegic or hemiplegic cerebral palsy.
PMID: (Treat spasticity) 11087280 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Intrathecal baclofen pump implantation complicated by epidural lipomatosis.
Anesth Analg. 2000 Aug;91(2):429-31
Authors: (articles re: how to treat spasticity) Huraibi HA, Phillips J, Rose RJ, Pallatroni H, Westbrook H, Fanciullo GJ
Intrathecal baclofen is a useful therapy in patients with spasticity. We describe a patient who underwent an intrathecal pump implant, complicated by epidural lipomatosis that ultimately required a single level laminectomy and fat debulking before successful implantation.
PMID: (Treat spasticity) 10910862 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Long lasting spasticity in controlled vasospastic angina.
Heart. 1999 May;81(5):528-32
Authors: (articles re: how to treat spasticity) Ueda O, Kohchi K, Kishi Y, Numano F
OBJECTIVE: To evaluate changes in coronary artery spasticity in patients with vasospastic angina who had been stable for years under continuous drug treatment. METHODS: Follow up coronary angiography was performed under intracoronary ergonovine provocation in 27 well controlled patients with vasospastic angina and no organic stenosis; the tests were done > 24 months after the initial coronary angiography, in which occlusive spasm had been induced by the same regimen of ergonovine provocation. RESULTS: The mean (SD) follow up period was 47.2 (21.6) months. All patients had been free from angina attack for more than 24 months under treatment with antianginal drugs. During this follow up period, organic stenosis developed in only one case. Occlusive spasm was observed during follow up coronary angiography in 23 patients. Spasm with 90% narrowing was observed in three other patients, and diffuse significant narrowing was seen in the final patient. No significant difference was found in spasticity (p = 0.75) between the initial and the follow up tests. CONCLUSIONS: Repeated ergonovine provocation during coronary angiography after a controlled period of several years showed that coronary spasm remains inducible in most patients. Discontinuance of drug treatment during the remission from anginal attacks achieved by medication may put the patient at high risk.
PMID: (Treat spasticity) 10212173 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Authors: (articles re: how to treat spasticity) Andersson PB, Goodkin DE
About 350,000 persons in the United States have Multiple Sclerosis, and primary care physicians are often called on to provide symptomatic therapy for these patients. We review our current pharmacologic approach to the management of Multiple Sclerosis exacerbations and the symptoms of spasticity, fatigue, bladder and bowel involvement, neurobehavioral complaints, pain syndromes, dystonic spasms, and tremor and ataxia.
PMID: (Treat spasticity) 8993211 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Arm span as measurement of response to growth hormone (GH) treatment in a group of children with meningomyelocele and GH deficiency.
J Clin Endocrinol Metab. 1996 Apr;81(4):1654-6
Authors: (articles re: how to treat spasticity) Satin-Smith MS, Katz LL, Thornton P, Gruccio D, Moshang T
Children with meningomyelocele (MMC) frequently have impaired linear growth. A number have associated structural brain defects with resultant GH deficiency (GHD). Reproducible measurements of height or length in MMC patients are often hampered by lower limb contractures, spasticity, and scoliosis. Arm span has been proposed as a more reproducible measure of linear growth. Five MMC children documented to have GHD were treated with recombinant human GH (hGH) for 1-3 yr. Their height, arm span, and growth velocity were compared with 32 children with idiopathic GHD treated similarly with hGH. These measures are compared with normal children by being expressed as standard deviation scores. The results of this study indicate that arm span measurements in GHD MMC patients are almost identical to height measurements in idiopathic GHD patients both before and during hGH therapy. The physical condition of children with MMC makes reproducible longitudinal height measurements difficult. Routine determinations of arm span measurements for children with MMC will assist in recognizing growth failure as well as monitoring treatment results.
PMID: (Treat spasticity) 8636383 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
The sedative and sympatholytic effects of oral tizanidine in healthy volunteers.
Anesth Analg. 1996 Apr;82(4):817-20
Authors: (articles re: how to treat spasticity) Miettinen TJ, Kanto JH, Salonen MA, Scheinin M
Tizanidine, an imidazoline derivative with alpha 2-receptor-mediated central muscle relaxant activity, is in widespread clinical use for the treatment of spasticity. To evaluate its possible role in anesthesia we assessed the sedative and sympatholytic effects of orally administered tizanidine in a double-blind, placebo-controlled, randomized, cross-over study in six healthy male volunteers. Three different doses of tizanidine (4, 8, and 12 mg) were tested and compared to clonidine 150 micrograms. The sedative and sympatholytic effects of tizanidine 12 mg were comparable in magnitude to those of clonidine 150 micrograms, but the effects of clonidine were longer lasting. Similarly, the observed decreases in arterial blood pressure (diastolic, 13% and 19%; systolic, 10% and 8% for tizanidine and clonidine, respectively) and salivation were comparable in magnitude but of shorter duration after tizanidine 12 mg than after clonidine. Clonidine and tizanidine 12 mg had also similar effects on the secretion of growth hormone. Our results indicate that the effects of a single 12-mg oral dose of tizanidine resemble those of 150 micrograms oral clonidine, but are of shorter duration. Tizanidine may thus be a useful alternative to clonidine as an orally active, short-acting alpha 2-adrenoceptor agonist in the perioperative period.
PMID: (Treat spasticity) 8615503 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Interjoint coordination during pointing movements is disrupted in spastic hemiparesis.
Brain. 1996 Feb;119 ( Pt 1):281-93
Authors: (articles re: how to treat spasticity) Levin MF
Approaches to the rehabilitation of movement in spastic hemiparetic patients depend on knowledge of the underlying mechanisms of movement deficits. The goals of this study were to characterize end-point trajectories and interjoint coordination of arm pointing movements to different targets on a horizontal planar surface and to correlate disruptions in motor control in the affected arm of hemiparetic subjects with the level of spasticity and the degree of functional impairment measured clinically. Arm movements were studied in six normal and 10 hemiparetic subjects. Data from the affected arms of hemiparetic subjects were compared with those from their non-affected arms and to data from the arms of normal subjects. Subjects were seated in front of a horizontal surface adjusted to the height of the sternal notch with the trunk stabilized. They made planar arm reaching movements (20 and 40 cm) to four different targets located directly in front of them and in the ipsilateral and contralateral workspace. Kinematic data from the finger, wrist, elbow and shoulder were recorded with a three-dimensional optical tracking system. Results showed that movement amplitudes were lower and movement times were significantly prolonged in the affected arms. Although trajectories were marked by deviations from smooth straight lines and characterized by increased dispersion and segmentation, even those subjects with the most severe spasticity could reach into all parts of the workspace with both their affected and non-affected arms. This indicated that movement planning in terms of extrapersonal space was unaffected in these subjects. On the other hand, the interjoint coordination of movements made into or out of the typical extensor or flexor synergies was equally disrupted. These findings suggest a bi-level control organization of pointing movements in both normal and hemiparetic subjects: the level of trajectory planning in extrapersonal space and the level specifying interjoint coordination according to the trajectory plan. Deficits in motor performance in stroke patients may be associated with problems at the second control level. This implies some strategies for the rehabilitation of stroke patients with motor disorders. Treatment aimed at improving arm function should be oriented toward restoring the normal sensorimotor relationships between the joints. We also found that while clinical spasticity scores were correlated with some aspects of motor performance, they provided little information about the movement deficit itself.
PMID: (Treat spasticity) 8624689 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
A controlled trial of riluzole in amyotrophic lateral sclerosis. ALS/Riluzole Study Group.
N Engl J Med. 1994 Mar 3;330(9):585-91
Authors: (articles re: how to treat spasticity) Bensimon G, Lacomblez L, Meininger V
BACKGROUND. Amyotrophic lateral sclerosis is a progressive motor neuron disease for which there is no adequate treatment. Some research suggests that the excitatory amino acid neurotransmitter glutamate may be involved in the pathogenesis. METHODS. To evaluate the efficacy and safety of the antiglutamate agent riluzole, we conducted a prospective, double-blind, placebo-controlled trial in 155 outpatients with amyotrophic lateral sclerosis. The dose of riluzole was 100 mg per day. Randomization was stratified according to the site of disease onset (the bulbar region or the limbs). The primary end points were survival and rates of change in functional status. The main secondary end point was change in muscle strength. Analyses were undertaken after 12 months of treatment and at the end of the placebo-controlled period (median follow-up, 573 days). RESULTS. After 12 months, 45 of 78 patients (58 percent) in the placebo group were still alive, as compared with 57 of 77 patients (74 percent) in the riluzole group (P = 0.014). For patients with bulbar-onset disease, one-year survival rates were 35 percent (6 of 17) with placebo and 73 percent (11 of 15) with riluzole (P = 0.014), whereas for those with limb-onset disease one-year survival was 64 percent and 74 percent, respectively (P = 0.17). The survival advantage with riluzole was smaller (37 percent [29 of 78] with placebo vs. 49 percent [38 of 77] with riluzole) at the end of the placebo-controlled period, but it remained significant in the overall population (P = 0.046) as well as in the patients with bulbar-onset disease (18 percent [3 of 17] vs. 53 percent [8 of 15], P = 0.013). The deterioration of muscle strength was significantly slower in the riluzole group than in the placebo group (P = 0.028). Adverse reactions to riluzole included asthenia, spasticity, and mild elevations in aminotransferase levels. Twenty-seven patients in the riluzole group withdrew from the study, as compared with 17 in the placebo group. CONCLUSIONS. The antiglutamate agent riluzole appears to slow the progression of amyotrophic lateral sclerosis, and it may improve survival in patients with disease of bulbar onset.
PMID: (Treat spasticity) 8302340 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Determinants of outcome in lesions of the thoracic aorta in patients with multiorgan system trauma.
Chest. 1992 Feb;101(2):331-5
Authors: (articles re: how to treat spasticity) Cernaianu AC, Cilley JH, Baldino WA, Spence RK, DelRossi AJ
Of all patients presenting at our level 1 trauma center with multiorgan system injuries, 33 have been identified with acute lesions of the thoracic aorta. Mean severity injury score was 24 +/- 3. Four patients underwent resuscitative thoracotomy upon arrival in the emergency department. One survived and fully recovered. The rest underwent diagnostic procedures and repair of aortic lesions in conjunction with surgical treatment of other injured organ systems. The overall survival rate was 82 percent. Survivors arrived significantly faster to the ED and had lesser degree of multiorgan system injuries. There was no difference in the time spent to make the diagnosis of acute aortic disruption for survivors and nonsurvivors, nor was a difference in time to arrive in the operating room once the diagnosis of aortic injury has been established. Morbidity was related to ischemia to distal organs in four patients of whom two presented with multiple lesions of the thoracic aorta; two remained paralyzed and two had only lower limb spasticity. All discharged survivors were alive at 12 months' follow-up. The type of surgical repair did not influence the outcome of patients with single, typical aortic lesions; however, "clamp/sew" technique was not adequate when multiple aortic tears were found intraoperatively. The outcome of surgical treatment of the traumatic aortic lesions of patients with polytrauma may be influenced by the speed of arrival to the ED, the magnitude of multiorgan system involvement, and the application of appropriate surgical technique for repair according to the intrathoracic findings and the timing of aortic repair vis-a-vis other surgical treatment.
PMID: (Treat spasticity) 1735250 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
The significance of spasticity in the upper and lower limbs in myelomeningocele.
J Bone Joint Surg Br. 1986 Mar;68(2):213-7
Authors: (articles re: how to treat spasticity) Mazur JM, Stillwell A, Menelaus M
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.
PMID: (Treat spasticity) 3958005 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
The surgical treatment of equinovarus deformity in adults with spasticity.
J Bone Joint Surg Br. 1978 Nov;60-B(4):533-5
Authors: (articles re: how to treat spasticity) Roper BA, Williams A, King JB
Adults with deformities of the lower limb due to spasticity may be considerably improved by operation, but thorough pre-operative assessment as an inpatient is essential in order to pinpoint the disability. The commonest deformity is equinovarus which often responds to simple operative procedures. The results of seventy-seven operative procedures in fifty patients are recorded. Correction once achieved is stable and the deformity does not recur.
PMID: (Treat spasticity) 711804 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]
Hypoxanthine-guanine phosphoribosyltransferase: characteristics of the mutant enzyme in erythrocytes from patients with the Lesch-Nyhan syndrome.
J Clin Invest. 1972 Jul;51(7):1805-12
Authors: (articles re: how to treat spasticity) Arnold WJ, Meade JC, Kelley WN
The Lesch-Nyhan syndrome is characterized clinically by choreoathetosis, spasticity, selfmutilation, and mental and growth retardation. Biochemically, there is a striking reduction of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) activity in affected individuals. We have examined erythrocytes from 14 patients with the Lesch-Nyhan syndrome for the presence of hypoxanthine-guanine phosphoribosyltransferase activity and enzyme protein. In contrast to the usual finding of no detectable hypoxanthine-guanine phosphoribosyltransferase activity, we have found low levels (0.002-0.79 nmoles/mg protein per hr) of hypoxanthine-guanine phosphoribosyltransferase activity in erythrocyte lysates from five of these patients. In three of the five patients, hypoxanthine-guanine phosphoribosyltransferase activity appeared to be substantially more labile in vivo than normal using erythrocytes which had been separated according to their density (age).Immunochemical studies using a monospecific antiserum prepared from a homogeneous preparation of normal human erythrocyte hypoxanthine-guanine phosphoribosyltransferase revealed immunoreactive protein (CRM) in hemolysate from all 14 patients with the Lesch-Nyhan syndrome. The immunoreactive protein from each patient gave a reaction of complete identity with normal erythrocyte hypoxanthine-guanine phosphoribosyltransferase and was present in quantities equal to those observed in normal erythrocytes. In addition, a constant amount of CRM was found in erythrocytes of increasing density (age) from patients with the Lesch-Nyhan syndrome despite the decreasing hypoxanthine-guanine phosphoribosyltransferase activity.These studies confirm previous data which indicate that the mutations leading to the Lesch-Nyhan syndrome are usually, if not always on the structural gene coding for hypoxanthine-guanine phosphoribosyltransferase. In addition, although the mutant proteins appear to be present in normal amounts, they are often very labile in vivo with respect to enzymatic activity. These observations suggest that therapy directed at stabilization or activation of enzyme activity in vivo may be of potential benefit.
PMID: (Treat spasticity) 4624352 [PubMed (articles re: how to treat spasticity) - indexed for MEDLINE (Treat spasticity) ]