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)

Spasticity is a velocity-dependent pathologic increase in muscle resistance to stretch, and occurs in a variety of neurologic disorders. We report our controlled open study using botulinum toxin A for treatment of adductor spasticity in five patients with advanced multiple sclerosis. Clinical evaluation of spasticity and stiffness of joints is based on the Ashworth Scale and grade of passive abduction. Three patients showed no response; the two others experienced an excellent and longlasting effect. We also describe briefly the different spastic conditions where this treatment has been used successfully.
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PMID:[Treatment of spasticity with botulinum toxin]. 923 78

Severe muscle spasticity is common in patients with neurological disease. It is often associated with pain and distressing spasms, and frequently leads to functional motor disability. Antispasticity drugs usually result in systemic adverse effects, and peripheral nerve blocks have some disadvantages such as sensory loss and painful dysaesthesiae. In recent years botulinum toxin type A (BT/A) has been advocated for the treatment of muscle spasticity. We studied, using a functional assessment scale, the effects of BT/A on the patients' symptoms and the functional disability due to spasticity in five children and eight adults who were referred for treatment. In 10 patients the treatment goals were achieved, and children generally had a better and more sustained response than adults. There were no adverse effects reported. The present study suggests that BT/A is safe and effective in improving the motor functional disability which is often associated with severe localized muscle spasticity.
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PMID:A study of the effectiveness of botulinum toxin type A (Dysport) in the management of muscle spasticity. 949 39

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

We describe a patient presenting with progressive bulbar dysfunction and spasticity that clinically mimicked amyotrophic lateral sclerosis (ALS). Electromyography, however, showed no evidence of denervation and revealed a rare combination of peripheral and central myokymia. We feel that this pattern of myokymia represented a marker of neural injury from remote radiation therapy. Nervous system disorders resulting from therapeutic radiation are described, and potential pathophysiologic mechanisms underlying myokymia are discussed.
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PMID:Delayed radiation-induced bulbar palsy mimicking ALS. 1079 8

Spasticity is a frequent feature of neurological disease in adults and children. Commonly associated symptoms include impaired movement, painful muscle spasms, stiffness and disturbed sleep. Severe or long-standing spasticity may lead to contractures and joint ankylosis, which can severely restrict the patient's care and rehabilitation. Here, we review the management of patients with spasticity, concentrating on the role of drug treatment.
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PMID:The management of spasticity. 1091 99

Botulinum toxin (BTX), a potent biologic neurotoxin, commonly is associated with lethal outbreaks of food poisoning; however, it also plays a role as a therapeutic agent. Since the 1970s physicians have investigated BTX therapy in patients with neurologic disorders. The number of applications greatly expanded over the years to include certain focal dystonias (blepharospasm, torticollis, laryngeal dystonias, writer's cramp), strabismus, and a wide variety of other indications (gastrointestinal disorders, cosmetic wrinkle correction, spasticity, hyperhidrosis). BTX's safety and efficacy are reviewed.
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PMID:Pharmacotherapy with botulinum toxin: harnessing nature's most potent neurotoxin. 1099 1

The main purpose of this study was to investigate the effects of electrical nerve stimulation on alpha motoneurons excitability. The electrophysiological parameters of H-reflex and F-wave were assessed for this object. These experiments was performed on ten non-athletic healthy men without neurologic disorders with mean age 25.6 years (SD 4.4) and three spastic hemiplegic patients with mean age 65.33 years (SD 6.32). In the experimental protocol, electrical stimulation (TENS) applied on common peroneal nerve with frequency 99 Hz and duration 0.25 ms for 30 minutes. H-reflex and F-wave of the soleus muscle were recorded in three stages sequenced immediately, 5 minutes and 10 minutes later on. The parameters such as amplitudes and latencies of H-reflex and F-wave were compared with the data of first record before stimulation. Finally, after 30 minutes application of TENS the following results were obtained: 1. The mean peak to peak amplitude of H-reflexes and F-waves were significantly decreased after application of TENS in normal subjects. (P < 0.05) 2. H/M ratios and F/M ratios were significantly decreased after application of TENS in normal subjects. (P < 0.05) 3. The mean latency of H-reflexes and F-waves were significantly increased after application of TENS in normal subjects. (P < 0.05) 4. In spastic patients, the mean peak to peak amplitude of H-reflexes and F-waves, H/M and F/M ratios were significantly decreased and the mean latencies of H-reflexes and F-waves were significantly increased after application of TENS. The reduction of amplitude of H-reflexes and F-waves, H/M and F/M ratios demonstrated reduction of spasticity in patients group. The above-mentioned parameters are parts of electrophysiological indicators about assessment of spasticity.
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PMID:The effects of electrical nerve stimulation of the lower extremity on H-reflex and F-wave parameters. 1123 62

The prevalence of bowel dysfunction in multiple sclerosis (MS) patients is higher than in the general population. Up to 70% of patients complain of constipation or faecal incontinence, which may also coexist. This overlap can relate to neurological disease affecting both the bowel and the pelvic floor muscles, or to treatments given. Bowel dysfunction is a source of considerable ongoing psychosocial disability in many patients with MS. Symptoms related to the bladder and the bowel are rated by patients as the third most important, limiting their ability to work, after spasticity and incoordination. Bowel management in patients with MS is currently empirical. Although general recommendations include maintaining a high fibre diet, high fluid intake, regular bowel routine, and the use of enemas or laxatives, the evidence to support the efficacy of these recommendations is scant. This review will examine the current state of knowledge regarding the pathophysiological mechanisms underlying bowel dysfunction in MS, outline the importance of proper clinical assessment of constipation and faecal incontinence during the diagnostic work-up, and propose various management possibilities. In the absence of clinical trial data on bowel management in MS, these should be considered as a consensus on clinical practice from a team specialized in bowel dysfunction.
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PMID:Pathophysiology and management of bowel dysfunction in multiple sclerosis. 1133 78

A comparative study of pharmacodynamics and clinical efficacy of nimodipine, nifedipine and foridon in ischemic stroke (late recovery and residual period) was performed in 97 patients with ischemic stroke. It was found that nimodipine, nifedipine and foridon at late recovery or residual stages significantly improved higher psychic functions, promoted regression of neurologic disorders and optimized social rehabilitation. Nimodipine, primarily, decreased the intensity of neurological disorders, improved higher psychic functions and had a positive impact on cerebral hemodynamics. Nifedipine primarily improved central hemodynamics (increased stroke output and ejection fraction). Foridon is most effective selective pharmacodynamic impact on peripheral hemodynamics (stimulated arteriolar blood flow, diminished venous capacity and spasticity), i.e. normalized peripheral blood flow.
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PMID:[Comparative clinico-pharmacological characteristics of nimodipine, nifedipine and foridon in the treatment of patients with ischemic stroke in late rehabilitative and residual periods]. 1241 26

The hereditary spastic paraplegias (HSPs) are inherited neurologic disorders in which the primary symptom is insidiously progressive difficulty walking due to lower extremity weakness and spasticity. There have been great strides in our knowledge of this group of disabling disorders; 20 HSP loci and 9 HSP genes have been discovered. Insights into the molecular causes of HSPs are beginning to emerge. This review summarizes these advances in HSPs' genetics.
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PMID:The hereditary spastic paraplegias: nine genes and counting. 1536


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