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Query: UMLS:C0026838 (spasticity)
6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spasticity has been described as "a motor disorder, characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex as one component of the upper motor neuron syndrome". In patients with complete spinal cord lesions, severe untreatable spasticity can make movement, sitting and hygiene difficult or impossible while it may alter gait and personal care in patients with partial lesions. From a clinical point of view, it is useful to distinguish spinal cord spasticity from supraspinal spasticity. Traditionally, the Ashworth scale is the most widely used to quantify the tone of single muscles. In order to quantify hypereflexia, the Reflex Scale is also used. In the spinal spasticity which is characterized by spasms, the Spasm Frequency Scale is useful in order to monitor their frequency. Initially, management of spasticity is based on non-invasive treatments that later become more invasive. The first approach. the conservative treatment, usually includes elimination of the nociceptive stimuli, rehabilitative therapy (physical and occupational), orthopaedic prostheses and plaster corsets. These treatments, do not resolve spasticity in about 33% of cases. In these severe cases, more invasive procedures such as muscle infiltrations with botulin toxin and intrathecal baclofen infusion can be used.
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PMID:Intrathecal baclofen therapy in patients with severe spasticity. 1769 73

Post-stroke spasticity is an important cause of disability in adults, due to muscle hyperactivity, which results in limb stiffness and muscle spasm. The prognosis for these patients depends on several features such as early management and adequate physical therapy to avoid muscle shortening, pain, and their consequences. Although several papers have shown that intramuscular injections of botulinum toxin type A (BT-A) decreases spasticity in post-stroke patients, few authors have demonstrated functional improvement after this therapy. In order to assess if individualized BT-A injections improves upper limb function in post-stroke spastic patients, we prospectively followed 20 consecutive patients of 18 years of age or more with spastic hemiparesis secondary to stroke. Fulg-Meyer scale modified for upper limbs, measure of functional independence (MFI), Ashworth modified scale, and goniometry were applied in the beginning of the investigation and in the 16th and 32nd weeks. BT-A was applied at baseline and in the 16th week. All subjects were submitted to rehabilitation therapy. All patients showed improvement according to Ashworth modified scale and increase in the range of motion, which were sustained until the 32nd week (p<0.05). The assessment of the first three parameters of the Fulg-Meyer scale and the evaluations of the motor part of the Functional Independence Measure showed statistically improvement until the end of the study. We conclude that proper choice of muscles and individualized doses of BT-A can improve function in selected post-stroke patients.
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PMID:Does botulinum toxin improve the function of the patient with spasticity after stroke? 1787 96

Dantrolene sodium was effective in controlling spasticity and improving function in 11 of 13 patients taking part in a 14-week double-blind crossover study. Clonus and lower-extremity tendon jerks were reduced in almost all patients (10 and 11 respectively) during dantrolene sodium therapy at 200 to 400 mg/day. Activities of daily living showed marked improvement in 3 cases and moderate improvement in 8. All 13 patients reported decreases in the frequency of intermittent painful spasm. Side effects were minimal and consisted mainly of an initial 3- to 4-day period of weakness and lightheadedness.
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PMID:Efficacy of dantrolene sodium in the treatment of spasticity. 1789 68

Clinical signs and symptoms of spasticity include hypertonia, involuntary movements (spasms, clonus), decreased range of motion, contractures, and often spasm-related pain. When spasticity is refractory to medical management, patients may be referred for intrathecal baclofen (ITB) pump placement. We reviewed a cohort of amyotrophic lateral sclerosis (ALS) patients with intractable spasticity requiring ITB to further define the impact of ITB on pain relief in this patient population. From 2003 to 2005, eight patients (mean age 43.8 years; 5 men, 3 women) with ALS received ITB for pain associated with intractable spasticity at our institution. Mean disease duration preoperatively was 47.4 months, mean follow-up was 9.8 months, and pain was evaluated using a 0-10 scoring system. All patients experienced spasticity relief in response to a preoperative bolus test injection of ITB (25-50 microg) via lumbar puncture. Following ITB pump placement, the average reduction of pain was 54% (P = 0.0082). Six patients (75%) experienced pain score reduction, three of whom had complete pain relief. Postoperative pain reduction was predicted by the degree of pain reduction following preoperative ITB test injection. These results support ITB as a treatment modality for pain associated with spasticity in ALS.
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PMID:Intrathecal baclofen for spasticity-related pain in amyotrophic lateral sclerosis: efficacy and factors associated with pain relief. 1789 58

Botulinum toxin is a natural purified protein and one of the strongest biological poisons--neurotoxin. It is produced by the bacterium Clostridium botulinum. Its medical usage started in USA in 1981 and in Europe in 1992. There are seven different immune types of the toxin: A, B, C1, D, E, F and G. Toxin types A and B are used to decrease muscular spasticity. Botulinum toxin prevents the formation of acetylcholine from cholinergic nerve tissues in muscles, which in the end irreversibly destroys neuromuscular synapses. It is called temporary local chemodenervation. It does not affect the synthesis of acetylcholine. As it affects neuromuscular bond it also affects one of the symptoms of cerebral palsy--spasticity. Decreasing the spasticity of children with cerebral palsy leads to the improvement of conscious movements, muscles are less toned, passive mobility is improved, orthosis tolerance is also improved, and the child is enabled to perform easier and better motor functions such as crawling, standing and walking. Since the action of Botulinum toxin is limited to 2-6 months, new neural collaterals are formed and neuromuscular conductivity is reestablished which in the end once again develops a muscular spasm. This leads to a conclusion that botulinum toxin should again be applied into spastic muscles. It is very important for good effect of Botulinum toxin to set the goals of the therapy in advance. The goals include improvement of a function, prevention of contractions and deformities, ease of care and decrease of pain for children with cerebral palsy. After application of botulinum toxin, it is necessary to perform adequate and intensive physical treatment with regular monitoring of effects. This work shows a case of a boy with spastic form of cerebral palsy. After being rehabilitated using Vojta therapy and Bobath concept and the conduct of certain physical procedures, botulinum toxin is administered into his lower limbs' muscles and kinesiotherapy is intensified. After the administration of botulinum toxin significant functional improvement is noted.
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PMID:Treatment of the spasticity in children with cerebral palsy. 1803 97

Intrathecal baclofen injection (ITB) has been available since April, 2006 in Japan. According to the clinical trial data, ITB reduced continuously the average Ashworth spasticity score (1 no spasticity-5 completely contracted) from 3.85 to 1.84 or below as well as the average spasm score (0 no spasm-4 more than 10 spasms hour) from 2.56 to 0.75. It also reduced the number of patients with severe pain from 45% to 17% as well as the number of patients with severe compressive sensation from 65% to 11%. The effect was very dramatic and there have been no severe side effect. ITB seems effective and useful to patients suffered from marked spasticity. It appears also safe when appropriate patients are selected and careful procedures are taken. Because ITB needs surgical procedures, neurosurgeon or orthopedic surgeons have been involved so far. We neurologist, however, should at least know about ITB and its powerful effect against severe spasticity while we must be aware of dangerous situation due to overdose and secession of the baclofen.
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PMID:[Intrathecal baclofen therapy to spasticity]. 1821 Aug 45

Elevated muscular tone associated with spastic syndromes can cause excessive contractility at the upper esophageal sphincter and impede swallowing. A 47-year-old male patient with spasticity predominantly of the lower extremities after a subarachnoid hemorrhage suffered from severe dysphagia and chronic salivary aspiration. He was dependent on a cuffed tracheostomy tube and a percutaneous enterogastric feeding tube. Barium swallow and esophageal manometry revealed cricopharyngeal spasm, while laryngeal elevation and pharyngeal contractility were well preserved. We endoscopically injected 180 MU botulinum toxin A into the cricopharyngeus muscle. Two days post injection, swallowing function had improved and oral nutrition was possible. This improvement lasted for six weeks. After another injection 8 weeks later, an undesired diffusion into the hypopharynx occurred and manometry showed diminished contractility without amelioration of dysphagia. Botulinum toxin therapy of cricopharyngeal spasm improves swallowing function in a subgroup of patients with spastic syndromes. The therapeutic effect is of limited duration. Toxin diffusion into the pharynx should be avoided. Manometry is useful in planning and monitoring the therapy.
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PMID:Botulinum toxin a treatment of cricopharyngeal dysphagia after subarachnoid hemorrhage. 1843 65

Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum as a complex of proteins containing the neurotoxin itself and other nontoxic proteins. Activation of the neurotoxin occurs upon proteolytic cleavage into the heavy and light chains. This di-chain moiety is essential for neurotoxin and each chain is playing a unique role; the heavy chain mediates neurospecifics cell binding and entry, whereas the light chain, a protease, catalyzes the cleavage and inactivation of neuronal proteins that mediate neurotransmitter release. There are seven BoNT serotypes (A,B,CI,D,E,F, and G), all of which inhibit acetylcholine release, though their intracellular target proteins, the characteristics of their actions, and their potencies vary substantially. BoNT type A has been the most widely studied and applied serotype for therapeutic purposes. It has been a mainstay in the treatment of cervical dystonia, blepharospasm, and hemifacial spasm for years. BoNT has more recently emerged as an increasingly important therapeutic option in the clinical management of a broad array of conditions, including other focal dystonias, spasticity, cerebral palsy, equinovarus, gastrointestinal (GI) and urogenital disorders, hypersecretory disorders, facial lines due to hyperfunctional facial muscles and recently, musculoskeletal pain disorders and headache.
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PMID:[Mechanism of therapy effects by botulinum neurotoxin]. 1854 57

Botulinum toxin type A (BTX-A) has been used to treat several neurological conditions such as sialorrhea, hyperhydrosis, dystonia, hemifacial spasm, spasticity and pain. Although spasticity has been successfully treated with BTX-A, few are the authors studying the use of BTX-A to treat shoulder pain secondary to stroke. In order to study if BTX-A is effective to treat post-stroke shoulder pain, we followed up during 4 months 16 patients with sustained shoulder pain. Patients received BTX-A according to previous discussion with the rehabilitation group to determine the muscles and dose to be injected and were evaluated by the join range of motion and analogic pain scale. There was decrease of pain during shoulder motion, mainly during the movements of extension and rotation. We conclude that BTX-A is a safe and efficacious therapy.
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PMID:Botulinum toxin type A for refractory post-stroke shoulder pain. 1854 85

Continuous infusion of intrathecal baclofen (ITB) via a subcutaneously implanted pump has developed over the last 20 years as a powerful tool in the management of spasticity in various adult and paediatric neurological conditions. Acting more focally on spinal GABA receptors, ITB causes fewer systemic side effects than orally administered baclofen. The result is facilitation of daily caring, and symptomatic relief from painful spasm. With increasing experience of ITB use, novel applications and indications are emerging. These include the management of dystonia and chronic neuropathic pain. However, despite some recent authoritative reviews, there is still uncertainty about optimal use and evaluation of this therapy. Many challenges remain. How can efficacy of therapy best be assessed both at primary testing and after pump implantation? What is the precise mechanism of baclofen action in different brain and spinal disorders associated with spasticity and dystonia? Does placement of the spinal catheter tip influence efficacy? What is the cranio-caudal gradient of CSF baclofen levels at given pump flow rates and does this matter? What CSF baclofen levels are efficacious in various conditions? Why do some patients with the same primary condition require large differences in ITB dose? What are the relative merits of programmable versus constant infusion rate pumps? What are the implications of setting up multidisciplinary teams for long term follow up? This review evaluates these questions and highlights other areas for further investigation.
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PMID:Intrathecal baclofen therapy for neurological disorders: a sound knowledge base but many challenges remain. 1864 60


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