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)

Drug-induced diseases constitute up to 5% of hospital admissions,a figure which almost certainly understates the total morbidity due to drugs1. Sever drug-induced myopathies are uncommon, but milder forms may be more prevalent than is generally appreciated, since skeletal muscle constitutes some 45% of total body-weight and has a major metabolic role in addition to its mechanical function2. Knowledge of possible effects of drugs on the neuromuscular system is of increasing importance both because the range of therapeutic agents continues to expand and because the resulting syndromes, through usually reversible at the outset, may progress and lead to grave consequences if the drug responsible is not stopped. Drug-induced neuropathies3 will not be considered here, but it will be appreciated that muscle weakness may also be feature of such disorders and that some drugs may cause both a neuropathy and a myopathy. The features of the main drug-induced syndromes are summarised in the table. To these one could justifiably add the unwanted effects of srugs given for the treatment of central-nervous-system or neuromuscular disorders per se-e.g., the cholinergic block which may be produced by anticholinesterases alone or with corticosteroids in the myasthenic,4 and the profound weakness which may supervene after relief of spasticity with dantrolene sodium5.
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PMID:Drug-induced myopathies in man. 7 27

The effects of dantrolene sodium, an anti-spasticity drug with a site of action within the muscle fibres, were studied in 19 patients with spastic paresis. Oral doses were successively increased from 100 mg/day to a maximal tolerated level or up to 800 mg/day. Trial periods were 8-13 weeks. The responses of stretch reflexes to local cooling over the spastic muscles were used to differentiate alpha and gamma spasticity. In the knee extensor and flexor muscle groups, cryo-negative alpha-spasticity was seen in 25 and cryo-positive gamma-spasticity in 4 muscle groups. Ankle clonus was cryo-positive in 14 of 15 cases. Resistance to passive knee joint movements, ankle clonus and isometric or isokinetic muscle strength was determined quantitatively. The gait was recorded by intermittent-light photography and the muscle activation patterns in gait were studied in recordings of the average EMG from limb muscles. Functional disability and spasms were assessed from clinical examinations and interviews. Passive resistance at slow (6%/sec) and fast (30 degrees/sec) knee joint movements decreased by 32% in the extensor muscles (p = 0.005 resp. 0.001) and by 23-26% in the flexor muscles (not significant). Reduced passive resistance was observed in 16 of the muscles with alpha-spasticity and in all 4 of the muscle groups with gamma-spasticity. Clonus was diminished or abolished in 14 of 15 patients with this sign. Maximal isometric or isokinetic muscle strength was unaltered in the majority of the patients. In a few the strength was increased, in some it was decreased. The averaged EMG activity during walking as studied in 10 patients were increased in 35 of the 57 muscle groups examined. In some muscle groups, exaggerated activity attributable to spastic reflexes was reduced. Motor disability was decreased significantly in 10 patients. It was not significantly changed in 5 and deteriorated in 4 patients. Drowsiness and subjective muscle weakness were the most frequent side-effects. SGOT and SGPT were increased in 3 cases.
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PMID:Action of dantrolene sodium in spasticity with low dependence on fusimotor drive. 13 20

Reciprocal reflex connections were studied in capsular hemiplegia and spastic paresis with spinal cord lesions, using Lloyd's technique. Effects of conditioning stimulation of the tibial or peroneal nerve on the H reflex in the antagonists were examined. Stimulus intensity was controlled with reference to the threshold of the M wave. Weaker stimulation than this threshold was regarded as stimulation of group I afferents. It aroused no subjection sensation in intact subjects. Early and strong inhibition, comparable to Ia inhibition in the cat (Lloyd 1946), was observed from weak stimulation of the tibial nerve on the pre-tibial (flexor) H reflex, but not from the peroneal nerve on the triceps surae (extensor) H reflex in capsular hemiplegia. Alcohol block of extensor motor points resulted in reduction of spasticity without further paralysis in the blocked muscle and a remarkable increase in strength of the antagonist pre-tibial muscles. These results suggest that an extensor spasticity withe flexor weakness, which is common in capsular hemiplegia, may be due to an imbalance of reflex activities via Ia muscle afferents, and that a part of flexor weakness can be restored by "disinhibition' by reduction of Ia inflow from extensor muscles. Ia inhibition was also observed in one third of cases with spinal cord lesions at rest. It returned to normal after recovery from spastic paresis by radical therapy in some cases.
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PMID:Reciprocal Ia inhibition in spastic paralysis in man. 28 52

Dantrolene sodium or dantrolene1 is 1([5-(nitrophenyl)furfurylidend] amino) hydantoin sodium hydrate. It is indicated for use in chronic disorders characterised by skeletal muscle spasticity, such as spinal cord injury, stroke, cerebral palsy and multiple sclerosis. Dantrolene is believed to act directly on the contractile mechanism of skeletal muscle to decrease the force of contraction in the absence of any demonstrated effects on neural pathways, on the neuromuscular junction, or on the excitable properties of the muscle fibre membranes. Controlled trials have demonstrated that dantrolene is superior to placebo in adults or children with spasticity from various causes, as evidenced by clinical assessments of disability and daily activities, and by muscle and reflex responses to mechanical and electrical stimulation. It is somewhat less effective in patients with multiple sclerosis than in those with spasticity from other causes. There has been a general clinical impression in controlled trials that dantrolene caused less sedation than would have been expected from therapeutically comparable doses of diazepam. In 2 controlled trials, there was no significant difference between dantrolene and diazepam in terms of reductions in spasticity, clonus, and hyperreflexia, but side-effects such as drowsiness and inco-ordination occurred significantly more frequently on diazepam. Long-term studies have indicated continuing benefit for patients taking dantrolene, though the incidence of side-effects has often been high and there has been a suggestion of exacerbation of seizures in children with cerebral palsy. Dantrolene may be of value in the medical treatment of spasm of the external urethral sphincter due to neurological and non-neurological disease, and animal studies suggest a potential use in the management of malignant hyperpyrexia. Chemical evidence of liver dysfunction may occur in 0.7 to 1% of patients on long-term treatment with dantrolene, with symptomatic hepatitis in 0.35 to 0.5% and fatal hepatitis in 0.1 to 0.2%. The drug commonly causes transient drowsiness, dizziness, weakness, general malaise, fatigue and diarrhoea at the start of therapy. Muscle weakness may be the principal limiting side-effect in ambulant patients, particularly in those with multiple sclerosis, and therapy could be hazardous in patients with pre-existing bulbar or respiratory weakness. The dosage of dantrolene has been fixed in most controlled trials, though long-term studies have indicated the need for individualisation of dosage. The initial dose is usually 25mg once daily, increasing to 25mg two, three or four times daily, and then by increments of 25mg up to as high as 100mg two, three or four times daily. The lowest dose compatible with optimal response is recommended.
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PMID:Dantrolene sodium: a review of its pharmacological properties and therapeutic efficacy in spasticity. 31 89

Baclofen was used in a double-blind crossover placebo-controlled trial to treat spasticity in patients with multiple sclerosis (MS). While on Baclofen, patients obtained a significant (p less than 0.001) reduction in spasticity compared to controls. The drug was particularly effective in alleviating flexor and extensors spasms, as well as their associated pain. Side effects were common in this study, but were usually well tolerated by the patients. The commonest side effects were sedation, nausea and vomiting. There were no changes in hepatic, renal, or hematological function in any patients. Increase weakness due to loss of spasticity for support was also a fairly common complaint. The drug seems best indicated in patients in whom spasticity is not required for support or other activities of daily living. Careful monitoring of the patient is essential for effective use of this drug.
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PMID:The use of baclofen in treatment of spasticity in multiple sclerosis. 38 32

Clinical studies of members of a six-generation kindred of familial spastic paraplegia support the diagnostic distinction of a pure form of this autosomal dominant disease. Onset was in the fourth decade or later and symptoms were those of progressive gait difficulties with lower limb spasticity and weakness. Sensor, cerebellar and cranial nerve changes were absent. Pathologic changes in one member were confined to the lateral corticospinal tracts and in the fasciculus gracilis.
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PMID:Familial spastic paraplegia-clinical and pathologic studies in a large kindred. 70 33

Three patients are presented, each showing clinical and electrophysiological findings indicative of the anterior spinal artery syndrome: sudden onset of nonprogressive weakness and spasticity of one or both legs, associated in one patient with pain and in all three patients with selective impairment of temperature sensation, radiological evidence of aortic calcification, normal sensory and motor conduction velocities and normal amplitude of sensory potentials, but diminished amplitude of evoked motor responses. Electromyography showed widespread fibrillation in muscles of the leg in two patients and evidence of marked loss of motor units in all three patients.
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PMID:Anterior spinal artery syndrome. 70 36

Facial nerve cable autografts were performed on 20 cats with 10 animals receiving 6,000 Rads of postoperative irradiation over six weeks. Testing by clinical appearance, pontograms, and axon counts showed no statistical difference in the operated only and the operated plus irradiated groups. Pontograms illustrated the clinical observance of spasticity, delay and weakness often seen after grafting. This animal work tends to verify the clinical impression that in patients requiring postoperative irradiation for a malignancy necessitating excision and grafting of the facial nerve, anticipated results should be equivalent to the facial nerve cable autografts without postoperative irradiation.
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PMID:Effect of radiation therapy on facial nerve cable autografts. 83 35

A 21-year-old man had progressive symmetric, distal muscle atrophy and weakness, as well as spasticity of the limbs. Histologic examination of the sural nerve disclosed swollen axons containing membranous tubular profiles, ring tubules, large mitochondria with abnormal cristae, and glycogen like granules. Peripheral sensory nerve fibers also were affected. The pathologic features of the peripheral nerves were similar to those of infantile neuroaxonal dystrophy. Sural nerve biopsy may be useful in the study of pathologic processes in spastic paraplegia.
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PMID:Spastic paraplegia with neurogenic amyotrophy manifesting ballooned axons in sural nerve. 89 37

A systematic search for cases of adult-onset hereditary ataxia was conducted on location in Scotland. The investigation resulted in the discovery of eight pedigrees with 42 patients of whom 16 were alive in 1975. Nine patients were examined by the authors and recent hospital records were available on the remaining seven. The clinical features were quite variable. In declining order of frequency, findings were gait and limb ataxia, dysarthria, hyperreflexia, extrapyramidal motor disturbances, impaired vibratory sense, spasticity, defects of extraocular movements and nystagmus, reflex depression, Babinski signs, impaired joint position sense, muscle weakness, optic atrophy, and mental abnormalities. Foot deformity occurred only once. Inheritance was compatible with autosomal dominant transmission, but complicated by consanguinity in two families. The minimum prevalence was calculated as 0.31/100,000. Autopsy in two members in one family revealed olivopontocerebellar degeneration.
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PMID:Adult-onset hereditary ataxia in Scotland. 90 33


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