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)

A young epileptic presented with spasticity as well as ataxia, diplopia and nystagmus; his serum phenytoin level was very high. All the abnormal signs disappeared after withdrawal of phenytoin. Spasticity, hyperreflexia, and clonus are features of phenytoin intoxication, present in this case, which are not commonly seen, and which have rarely been mentioned previously in the literature.
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PMID:Spasticity due to phenytoin toxicity. 10 44

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

A double-blind, five-week, multicenter trial was conducted to compare the effect of baclofen, a unique amino acid derivative, with that of placebo in the treatment of 106 patients with spasticity secondary to multiple sclerosis. A spasticity assessment method that included a neurological examination, physicians' clinical impressions of changes during treatment, and a patient's self-evaluation was used to determine efficacy. This method showed baclofen (70 to 80 mg daily maximum, titrated) is effective relative to placebo in relieving symptoms of spasticity, such as flexor spasms, pain and stiffness, resistance to passive joint movements, and tendon stretch reflexes. Patient self-evaluation results also showed a significant reduction in clonus. Side effects were generally mild and transient.
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PMID:Baclofen, a new antispastic drug. A controlled, multicenter trial in patients with multiple sclerosis. 32 87

Baclofen is a safe and effective means for treating spasticity associated with multiple sclerosis. We found no toxic effects on hepatologic, hematopoietic, or renal function, acutely or for over 3 years of follow-up. A statistically significant reduction was noted in frequency of spasms, and clonus, and there was improved range of joint movement, which enabled patients to maintain functional status for prolonged periods. For the more disabled patients, treatment with baclofen gave symptomatic relief of painful spasms and made immobility more tolerable. Optimum effect was achieved when baclofen was administered in the early stages of disease, before major disabilities became permanent.
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PMID:Baclofen for spasticity in multiple sclerosis. Double-blind crossover and three-year study. 36 34

Using the clinical quantification of the neurologic symptomatology the authors made observations and avaliated the action of Ciba 34.647-Ba, a GABA derivative, in 12 patients suffering from spasticity and motor incapacity due to spinal cord lesions. The results are reported emphasizing the effects of the drug on the main components of spasticity (hypertonus, hyperactivity of the deep reflexes, clonus and automatisms). Some theories explaining the mechanism of action of the drug are mentioned. References are made about doses, duration of action, tolerance and side-effects.
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PMID:[Clinico-quatitative evaluation of the action of Ciba 34.647-Ba on spasticity]. 58 90

Baclofen (a gamma aminobutylic acid derivative) and a placebo were compared for their efficacy in relieving certain symptoms in patients with long-standing spinal cord lesions and "spinal spasticity." In a double-blind, cross-over clinical investigation, 22 patients with chronic spinal cord disease were studied. Baclofen regularly alleviated involuntary flexor or extensor spasms and increased resistance to passive movement of the legs but did not alter strength, gait, stretch reflexes, or clonus. Side effects were mild and transient. This study demonstrates that (1) baclofen is useful for the treatment of flexor spasms and (2) in evaluating a new mode of therapy, one must consider selectively the response of individual components of such global syndromes as "spasticity."
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PMID:An evaluation of baclofen treatment for certain symptoms in patients with spinal cord lesions. A double-blind, cross-over study. 77 61

Seventy-seven patients with muscle spasticity secondary to central nervous system pathology were treated with dantrolene sodium for periods of up to two years. The drug was effective in reducing muscle spasms, clonus, muscle tone, and the force of muscle contraction elicited by Achilles tendon tap and tibial nerve stimulation, but improvement of function was seen less often. The incidence of side-effects was considerable, and poses a problem regarding patient acceptance of drug treatment.
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PMID:Dantrolene sodium: long-term effects in patients with muscle spasticity. 77 22

The effects of dantrolene sodium and diazepam were compared in a double crossover study of 42 patients with spasticity due to stable multiple sclerosis. Both drugs reduced the findings of spasticity, clonus, and hyperreflexia, and the complaints of muscle stiffness and cramping. Each drug had different side effects which suggest indications and contraindications for its use in spastic patients.
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PMID:Comparison of dantrolene sodium and diazepam in the treatment of spasticity. 77 44

The results of the present electrophysiological investigation have shed some light on the mechanisms underlying many clinical signs, at least, in patients with capsular hemiplegia. A tentative interpretation of them is given below. Cerebral lesions due to haemorrhage or infarction in the area of the middle cerebral artery interrupt an extensive part of the corticospinal tract and disturb many other descending pathways involved in voluntary performance. In consequence, a marked reduction in the ability to drive the spinal motor apparatus occurs, resulting in weakness of motor power. Here, we refer only to muscle power but not to performance. For example, the disturbance of voluntary contraction by clonus is disregarded (cf. fig. 8). On the other hand, the same lesions also release the spinal reflexes from inhibition by the higher levels of the brain and cause increased excitability in flexors and extensors. In the lower extremity, this is much more makred in extensors and extensor spasticity becomes a dominant sign clinically. Any release effect on the flexor system is largely cancelled by the high activity of the reciprocal Ia inhibitory pathway from extensors and only a fragment of it is occasionally revealed in some patients as an H-reflex in pre-tibial muscles or as weak Ia inhibition of the triceps surae. Reduced driving power of the brain may be compensated by raised excitability in the spinal cord and spastic extensors are thus naturally in a better condition to preserve motor power. Flexor muscles are doubly crippled by reduced descending impulses and strong reciprocal inhibition by the Ia impulses from the spindles of the extensor muscles.
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PMID:Reciprocal Ia inhibition in spastic hemiplegia of man. 100 Feb 87


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