Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of botulinum toxin A in 12 patients with spasticity and in eight patients with rigidity. The study design was a double-blind, placebo-controlled crossover trial with botulinum toxin A versus saline. Using the Ashworth Scale for spasticity and the Unified Parkinson's Disease Rating Scale for rigidity, we gave the patients a tone grade before and 2 weeks after treatment. Improvement in tone by two grades or more was considered clinically significant. In the spasticity group, botulinum toxin A reduced the tone of all patients significantly, improved functionality and nursing care in eight of 12 patients, and alleviated painful spasms in five of five patients. In the rigidity group, muscle tone was decreased in seven of eight patients, functionality improved in four of seven, and joint and muscle pain decreased in four of five. We conclude that botulinum toxin A is effective against the disabling effects of spasticity and rigidity. The treatment was well tolerated.
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PMID:Botulinum toxin A for spasticity, muscle spasms, and rigidity. 772 60

We report a 47-year-old woman with SLE, who developed meningeal signs and consciousness disturbance. She noted an onset of fever, and swelling and pain in her face, hands and feet in 1990. She was seen in another hospital and the diagnosis of SLE was made. She was treated with prednisolone with marked improvement in her symptoms. She was well with 5 mg of oral prednisolone daily until January of 1991, when she developed fever, myalgia and weakness in her legs. She was admitted to the medical service of our hospital on August 5. She was receiving 15 mg of prednisolone daily. Gram positive rods were cultured from her blood on August 5. She became incoherent 2 days later, and had a convulsive episode on August 8. After the convulsion, she lost consciousness from which she did not recover. Her CSF contained 304/3 microliters cells, 29 of which were neutrophils, 6 lymphocytes, 90 others, and 179 destructed cells. The CSF protein content was 345 mg/dl, and glucose 23 mg/dl. A neurological consultation was asked on August 9. Physical examination at that time revealed a semicomatous woman. Respiration was 30/min and regular. BP 132/82 mmHg, heart rate 122/min and regular, and BT 39.6 degrees C. General physical examination was unremarkable. Pertinent neurologic findings were positive Kernig sign and spasticity in all four limbs. Brain stem reflexes were retained. Upon painful stimulation, withdrawal response was elicited both lower extremities. She was treated with pipiracillin, latamoxef and phenobarbital, however, she had frequent seizures. She was deeply comatose on December 10. She became flaccid and no more meningeal signs were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 47-year-old woman with meningeal signs and consciousness disturbance]. 821 15

Lower extremity symptoms are caused by lesions at any level of the neuraxis, from cortex to muscle. HIV affects virtually every level of the nervous system, either directly or indirectly. The presence of pathology at multiple levels and by multiple processes further complicates the bedside diagnosis of a patient with AIDS and neurologic symptoms. Many neuropathies and other conditions that affect the lower extremities can be identified with careful history and physical examination, confirmed with limited testing, and can be treated successfully. Distal symmetric polyneuropathy is the most common lower extremity disorder, but it must be distinguished from similar-appearing neuropathies caused by medications, B12 deficiency, or vasculitis. Diffuse infiltrative lymphocytosis syndrome also causes a painful peripheral neuropathy that must be distinguished from distal symmetric polyneuropathy. Inflammatory demyelinating polyneuropathies are characterized by muscle weakness. They occur in early, asymptomatic HIV infection and respond to plasmapheresis or steroids. Mononeuropathies in patients with CD4 counts more than 200 often resolve on their own. Multiple mononeuropathies, which occur in patients with CD4 counts less than 50, are often associated with cytomegalovirus infection and may follow a rapidly progressive course unless treated promptly and aggressively. Progressive polyradiculopathy occurs late in the course of AIDS, is often caused by cytomegalovirus, is rapidly progressive, and generally is fatal unless recognized and treated promptly. Muscle weakness, myalgia, and fatigue are common in HIV and have multiple causes. Lower extremity spasticity may be caused by treatable etiologies such as spinal cord abscess, tumor, disc compression, B12 deficiency, or ischemia. Gait disturbances are common but nonspecific and may be caused by treatable neurologic disorders at any level of the neuraxis.
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PMID:Neurologic problems of the lower extremity associated with HIV and AIDS. 957 54

Spasticity and other muscle symptoms in the palliative care patient can contribute to suffering, significantly detracting from overall quality of life. Current therapy primarily includes use of centrally acting muscle relaxants, which are beneficial in treating some symptoms, but frequently have extensive side effects, such as sedation and muscle weakness. Tizanidine, a central alpha 2 adrenergic agonist, has been shown in clinical studies to be as effective as other commonly used antispastic agents, but without debilitating muscle weakness. Tizanidine can cause sedation, which is minimized by dose titration. When taken at night, patients report improvement in getting to sleep and little drowsiness or "hangover sensation" upon waking. Tizanidine is potentially helpful to many palliative care patients with chronic muscle pain and sleep disturbances.
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PMID:Tizanidine in the management of spasticity and musculoskeletal complaints in the palliative care population. 1109 20

The EMG interference pattern, built up of single motor unit action potentials, may be analyzed subjectively, or objectively by computer aided, quantitative methods, like counting of zero-crossings, counting of spikes, amplitude measurements, integration of the area under the curve, decomposition techniques, power spectrum analysis and turn/amplitude analysis. Since the shape of the interference pattern of healthy muscles is dependent on age, sex, force, muscle, temperature, fatigue, fitness level, recording site and surrounding tissue, electrode type, sensitivity, filters, sampling frequency and threshold level, all methods of analyzing the IP have to be standardized. Quantitative methods of analyzing the EMG interference pattern may be used for monitoring botulinum toxin therapy of dystonia and spasticity, quantifying spontaneous activity, assessment of chronic muscle pain, neuro-urological and proctological function, and diagnosing neuromuscular disorders. For diagnostic purposes, the methods favored are those that use needle electrodes and do not require measurement or monitoring of muscle force. The most well-evaluated methods are those using turn/amplitude analysis, like the cloud methods and the peak-ratio analysis. Peak-ratio analysis has the advantage that reference limits are easy to obtain and that its utility is well established and confirmed by several investigations. Overall, automatic methods of EMG interference pattern analysis are powerful tools for diagnostic and non-diagnostic purposes.
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PMID:EMG-interference pattern analysis. 1153 94

Neurolytic blockade is one of the therapeutic possibilities to treat spasticity of various muscles. In patients with spasticity of the adductor thigh muscles, a percutaneous approach to the obturator nerve is often difficult. We describe a new approach to the obturator nerve and we examine its feasibility. The second objective was to assess the efficacy of obturator neurolysis for the management of adductor thigh muscle pain and spasticity associated with hemiplegia or paraplegia. Nerve blocks were performed via a combined approach using fluoroscopy and nerve stimulation to identify the obturator nerve. Neurolysis was performed by injection of 65% ethanol. We performed 27 blocks in 23 patients. Technical evaluation was achieved in terms of number of attempted needle insertions, time to accurate location of the nerve and success rate. The efficacy of the block was assessed using four scores: degree of alleviation of muscle spasm and triple flexion of the lower limb, improvement of gait and facilitation of hygienic care. Success rate of the technique was 100% with a time to accurate nerve location of 130+/-35 s. Compared with scores measured immediately before the block, all studied parameters were significantly improved. Efficiency was significant on adductor muscle spasticity (p<0.001 at 1 day and p<0.01 at 60 and 120 months). Triple flexion was also significantly improved (p<0.05 from 1 to 120 days), as well as gait (p<0.02) and hygiene (p<0.01) scores. No complications occurred. The combined approach of the obturator nerve represents a new technique which proved to be accurate, fast, simple, highly successful and reproducible. Obturator neurolysis was confirmed as an efficient and cost-effective technique to reduce adductor muscle spasm and related pain and to improve gait and hygienic care in patients with neurological sequelae of stroke, head trauma or any lesion of the motor neurone.
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PMID:Neurolytic blockade of the obturator nerve for intractable spasticity of adductor thigh muscles. 1190 Apr 70

Considerable progress has been made in understanding and treating pain associated with pediatric AIDS. The World Health Organization (WHO) estimates that 1000 new pediatric HIV infections occur daily, with 67% in Africa and 30% in South and Southeast Asia. Perinatally infected children show two types of progression, a precocious form that is usually fatal by the 4th year and a less rapidly progressing form in which survival exceeds 80% at age 7. Neurologic effects are frequently apparent by 3-6 months in the severe form. The pain may result specifically from the HIV infection and its complications, from intercurrent or opportunistic infections, or from examinations and treatment. The emotional pain suffered by pediatric HIV patients is often very great. Seropositive children are more subject to bacterial infections than seropositive adults, and their infections are more recurrent, prolonged, and painful than those in immunocompetent children. Infants with HIV encephalopathy may suffer painful sensations from mild stimuli and extreme irritability and spasticity. Abdominal HIV pain often results from multifactorial etiologies, and the usual therapies may be of little efficacy. Children with full-blown AIDS may complain of joint or muscle pain or headaches that are of unexplained etiology. Indications for painful diagnostic procedures should be carefully considered before the child is subjected to them, and protocols for analgesia should be developed. Pain medications may be selected according to the WHO classification, in accordance with the intensity of the pain. Antidepressants and anticonvulsants may be used for neuropathic pain, and painful spasticity may be reduced with myorelaxants. Children are often responsive to behavioral methods such as relaxation, hypnosis, or distraction.
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PMID:[Pain from AIDS (child)]. 1234 7

This review article summarizes recent studies on myofascial trigger point (MTrP) to further clarify the mechanism of MTrP. MTrP is the major cause of muscle pain (myofascial pain) in clinical practice. There are multiple MTrP loci in an MTrP region. An MTrP locus contains a sensory component (sensitive locus) and a motor component (active locus). A sensitive locus is the site from which pain, referred pain (ReP), and local twitch response (LTR) can be elicited by needle stimulation. Sensitive loci are probably sensitized nociceptors based on a histological study. They are widely distributed in the whole muscle, but are concentrated in the endplate zone. An active locus is the site from which spontaneous electrical activity (SEA) can be recorded. Active loci are dysfunctional endplates since SEA is essentially the same as endplate noise (EPN) recorded from an abnormal endplate as reported by neurophysiologists. Both ReP and LTRs are mediated through spinal cord mechanisms, demonstrated in both human and animal studies. The pathogenesis of MTrPs appears to be related to the integration in the spinal cord (formation of MTrP circuits) in response to the disturbance of the nerve endings and abnormal contractile mechanism at multiple dysfunctional endplates. Methods usually applied to treat MTrPs include stretch, massage, thermotherapy, electrotherapy, laser therapy, MTrP injection, dry needling, and acupuncture. The mechanism of acupuncture is similar to dry needling or MTrP injection. The new technique of MTrP injection can also be used to treat neurogenic spasticity.
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PMID:New trends in myofascial pain syndrome. 1258 12

While pain is a common problem in multiple sclerosis (MS) patients, it is frequently overlooked and has to be asked for actively. Pain can be classified into 4 diagnostically and therapeutically relevant categories. 1. PAIN DIRECTLY RELATED TO MS: Painful paroxysmal symptoms like trigeminal neuralgia or painful tonic spasms are treated with carbamazepine as first choice, or lamotrigine, gabapentin, oxcarbazepine and other anticonvulsants. Painful "burning" dysaesthesia, the most frequent chronic pain syndrome, are treated with tricyclic antidepressants or carbamazepine, further options include gabapentin or lamotrigine. While escalation therapy may require opioids, the role of cannabinoids in the treatment of pain still has to be determined. 2. PAIN INDIRECTLY RELATED TO MS: Pain related to spasticity often improves with adequate physiotherapy. Drug treatment includes antispastic agents like baclofen or tizanidine, alternatively gabapentin. In severe cases botulinum toxin injections or intrathecal baclofen merit consideration. Physiotherapy and physical therapy may ameliorate malposition-induced joint and muscle pain. Moreover, painful pressure lesions should be avoided using optimally adjusted aids. 3. Treatment-related pain can occur with subcutaneous injections of beta interferons or glatiramer acetate and may be reduced by optimizing the injection technique and by local cooling. Systemic side effects of interferons like myalgias can be reduced by paracetamol or ibuprofen. 4. Pain unrelated to MS such as back pain or headache are frequent in MS patients and may be worsened by the disease. Treatment should be follow established guidelines. In summary, a careful analysis of the pain syndrome will allow the design of the appropriate treatment plan using various medical and non-medical options and thus will help to ameliorate the patients' quality of life.
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PMID:[Therapy of pain syndromes in multiple sclerosis -- an overview with evidence-based recommendations]. 1588 Mar 5

Loss of function, muscle pain and secondary muscoloskeletal complaints are common symptoms of patients with neuromuscular disease. Many patients develop a progressive handicap. Physiotherapeutic treatment is often used in the management of neuromuscular diseases. Different therapeutic strategies are useful depending on the stage and pathophysiology of the disease and with regard to the extent of the patient's handicap. The aims of the physiotherapy and realistic targets should be discussed critically with the patient at the beginning of the treatment. We propose different physiotherapeutic strategies depending on the stage of the underlying disease: 1) Patient is able to walk--active phase: education in self-training with regard to the risks of exhaustion. Manual and physical treatment of mycofascial complaints. 2) Progressive functional loss--assistive phase: support of compensation and daily functioning. 3) Patient in wheelchair or bedbound, loss of most voluntary functions--passive phase. The knowledge of the pathopysiology of the underlying disease is essential for the development of therapeutic strategies. Loss of upper neurons leads to the development of spasticity and muscle hypertonia whereas muscular atrophy and weakness is a prominent feature of lower motor neuron loss. Overtreatment and exhaustive training may lead to secondary muscle damage in primary myopathies. Training in short sessions with intervals between may have protective effects.
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PMID:[Basic principles of non-respiratory physiotherapy for neuromuscular diseases]. 1831 80


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