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)

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

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

Dantrium and Valium were compared in 22 children manifesting various degrees of spasticity. Treatment brought definite improvement in spasticity and in activities of daily living in 20 of the 22 patients. The two-part double-blind study showed that Dantrium was most effective in nine and Valium in seven cases. In four cases the drugs appeared to be equally beneficial. The combination of Dantrium and Valium appeared to be more effective in eight patients than either medication along, the greatest effect being seen in the upper extremities and about the hip joints. Patients on placebo showed no significant change. Side effects of lethargy and drowsiness on the combination were not bothersome after a short period of acclimation. The results indicate that the spasticity of cerebral palsy can be relieved significantly, and that the combination of peripherally and centrally acting agents is more beneficial than either medication alone.
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PMID:Medical treatment for spasticity in children with cerebral palsy. 79 60

Dantrolene sodium has been given to 45 patients suffering from dyskinetic syndromes: 33 were suffering from spastic syndromes, either secondary to cerebral lesions at birth, or to other cerebral lesions, or to cord lesions; 9 were affected by infantile dystonic syndromes; 1 by dystonia muscolorum deformans and the last 2 patients were suffering from parkinsonism. The best dosage schedule was individual and ranged from 50 mg to 300 mg a day. In this range, the majority of the spastic patients showed reduction of spasticity, unrelated with the site of pathology: a slight one in 12 patients, a moderate one in 9 and a marked one in 2. On the contrary, slight improvement has been noticed in only two of the patients suffering from dystonic syndromes. In no case side effects has been noticed. In all patients who underwent slight or moderate improvement only, we tried to obtain better results on spasticity by growing the dosage schedules; but we have always noticed side effects, that is weakness or drowsiness and, sometimes, urinary uncontinence. Moreover 2 patients showed evidence of transitory metabolic side effects. Therefore our experience shows that dantrolene sodium is an useful drug into the therapy of spasticity, even if often a slight of moderate improvement only is achieved. Slow increase in dosage schedule, repeated laboratory controls and alternate periods of treatment and suspended treatment should be observed.
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PMID:[Clinical study of dantrolene sodium in the treatment of spastic and dystonic syndromes]. 102 44

In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
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PMID:Phencyclidine. Nine cases of poisoning. 124 71

Seventeen patients with congenital spastic cerebral palsy and six patients with other forms of spasticity were injected intrathecally with doses of placebo or baclofen, 25 micrograms, 50 micrograms, or 100 micrograms, in a randomized, double-blind manner. Muscle tone in the upper and lower extremities was assessed by Ashworth scores both before the injections and every 2 hours afterward for 8 hours. Function of the upper extremities was evaluated before the injections and 4 hours afterward. Muscle tone in the lower extremities was significantly decreased within 2 hours after baclofen injection and remained lower than baseline 8 hours afterward. Upper extremity tone and function were not significantly affected by these single doses. Confusion and drowsiness occurred in two of the youngest children in the study after the 50-micrograms dose, but cleared within 2 hours. Our findings indicate that intrathecal baclofen reduces spasticity in children with cerebral palsy, as it does in adults with spasticity of spinal origin.
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PMID:Intrathecal baclofen for spasticity in cerebral palsy. 204 30

We studied the effect of the intrathecal infusion of baclofen, an agonist of gamma-aminobutyric acid, on abnormal muscle tone and spasms associated with spinal spasticity, in a randomized double-blind crossover study. Twenty patients with spinal spasticity caused by multiple sclerosis or spinal-cord injury who had had no response to treatment with oral baclofen received an intrathecal infusion of baclofen or saline for three days. The infusions were administered by means of a programmable pump implanted in the lumbar subarachnoid space. Muscle tone decreased in all 20 patients (mean [+/- SD] Ashworth score for rigidity, from 4.0 +/- 1.0 to 1.2 +/- 0.4; P less than 0.0001), and spasms were decreased in 18 of the 19 patients who had spasms (mean [+/- SD] score for spasm frequency, from 3.3 +/- 1.2 to 0.4 +/- 0.8; P less than 0.0005). Tests for motor function, neurologic examination, and assessments by the patients correctly indicated when baclofen was being infused in all cases. All patients were then entered in an open long-term trial of continuous infusion of intrathecal baclofen. During a mean follow-up period of 19.2 months (range, 10 to 33), muscle tone has been maintained within the normal range (mean Ashworth score, 1.0 +/- 0.1) and spasms have been reduced to a level that does not interfere with activities of daily living (mean spasm score, 0.3 +/- 0.6). No drowsiness or confusion occurred, one pump failed, and two catheters became dislodged and had to be replaced. No infections were observed. Our observations suggest that intrathecal baclofen is an effective long-term treatment for spinal spasticity that has not responded to oral baclofen.
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PMID:Intrathecal baclofen for severe spinal spasticity. 265 24

The expanding use of intrathecal baclofen for spasticity has raised a concern about the treatment of overdose in these patients, since no specific baclofen antagonist is available. Since physostigmine has been reported to reverse the respiratory depression and somnolence due to opiates, the drug was tried for the treatment of baclofen overdose. In three cases, intravenous physostigmine (2 mg) completely reversed the respiratory depression and coma caused by boluses of 80 to 800 micrograms of lumbar intrathecal baclofen. Physostigmine, although not a specific antagonist, should provide increased safety for patients receiving intrathecal baclofen.
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PMID:Physostigmine in the treatment of intrathecal baclofen overdose. Report of three cases. 274 50

The effect on increased myotatic reflexes of desmethyldiazepam, formed from its precursor clorazepate, was assessed in a double-blind cross-over study of 27 days duration. Eight patients with spasticity or rigidity were given placebo or active substance; first in loading doses for 2 days, then 5 mg every 12 h for a total of 10 days. A wash-out period of 7 days was interposed between the 2 10-day periods. Desmethyldiazepam had a normalizing effect on the increased phasic ankle reflexes seen in spasticity, but not on the increased tonic reflex seen in rigidity. The mean concentration of desmethyldiazepam in the steady state was 1227 nmol/l (range 600-1990 nmol/l). The plasma concentration of desmethyldiazepam tended to correlate with the percent decrease in phasic reflex activity (P = 0.08, 2-tailed). A slight drowsiness in 2 patients was the only side-effect seen. In conclusion, desmethyldiazepam given as clorazepate seems to be a suitable medicament in the treatment of spasticity.
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PMID:Effect of clorazepate in spasticity and rigidity: a quantitative study of reflexes and plasma concentrations. 285 28

The previously described anti-spastic effect of oxcarbazepine and 10,11-dihydro-10-hydroxycarbamazepine was found accidentally in 2 patients undergoing a double-blind comparative study for evaluation of antiepileptic effect. In this study oxcarbazepine was given orally in doses of 300-2700 mg daily to one patient with transverse myelitis and to two patients with multiple sclerosis, all of whom had clinically disabling spasticity in the form of difficulty in walking, lower limb rigidity, spastic contractions of the lower limbs and ankle clonus. Anti-spastic effect was observed at doses between 600-1200 mg daily and consisted in a substantial decrease in the above symptoms of spasticity. The anti-spastic effect appears at a dose immediately below that which produces nausea, dizziness and somnolence.
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PMID:Oxcarbazepine and spasticity: further observations. 307 37


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