Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

This investigation assessed the mechanisms of Tetrazepam action on spasticity using a battery of electromyographic methods. Thirty patients with post-stroke spastic hemiparesis treated with Tetrazepam took part in the investigation. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. The 5-point scales were used to assess muscle tone, muscle strength and tendon reflexes. A battery of electromyographic methods was used to analyse different mechanisms of spasticity: for alpha-motoneuron activity--the F-wave parameters; for gamma-motoneuron activity--the TA/H amplitude ratio; for presynaptic inhibition--the ratio of H-reflex maximal amplitudes before and after vibration on the Achilles tendon (Hvibr/Hmax); for common interneuron activity--the flexor reflex parameters. Our results revealed that Tetrazepam reduces tone in spastic muscles and has a slight effect on tendon hyperreflexia. It has no influence on muscle strength, Babinski sign and ankle clonus. Tetrazepam acts by decreasing motoneurone activity and increasing presynaptic inhibition.
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PMID:Mechanisms of tetrazepam action on spasticity. 134 69

This investigation estimated the mechanisms of baclofen action on spasticity using a battery of electromyographic methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with baclofen-mean daily dose 54.3 alpha 11.6 mg for a mean of 26.3 alpha 4.9 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of electromyographic methods was used to analyse different mechanisms of spasticity: for alpha motoneurone activity--the F wave parameters; for gamma motoneurone activity--the T/H reflex amplitude ratio; for presynaptic inhibition--the ratio of H reflex amplitudes before and after vibration on the achilles tendon (Hvibr./Hmax); for common interneurone activity--the flexor reflex parameters. Our results revealed that baclofen reduces spastically increased muscle tone and Babinski sign. It has no influence on muscle force, tendon reflexes and ankle clonus. Baclofen acts by normalizing the altered interneurone activity and decreasing of alpha motoneurone activity. When spasticity has altered interneurone activity and increased motoneurone activity, it is better to treat with baclofen.
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PMID:Mechanisms of baclofen action on spasticity. 162 92

Thirteen patients with post-stroke spastic hemiparesis underwent a percutaneous test trial of spinal cord stimulation (SCS) in order to modify their motor disturbances. Clinical evaluation based on Albert's motor scale and neurophysiological evaluation consisting of surface EMG during voluntary, involuntary, and reflex motor activity were performed before and during SCS. At the end of the test period, eight patients showed a significant improvement in their motor performance. The EMG analysis confirmed the clinical data. SCS was followed by a reduction or disappearance of synergic coactivation with better agonist-antagonist coordination, a decrease of clonus both in duration and spreading, and better endurance. The effect on motor control did not increase with time after the first month of SCS, but was long lasting (mean follow-up: 2 years). There was a correlation between sensory deficit and motor outcome suggesting that the enhancement of sensory input put into play by SCS and the consequent development of new sensory-motor integration might be responsible for the improvement in motor performance.
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PMID:Spinal cord stimulation (SCS) in spastic hemiparesis. 247 60

Spinal cord stimulation (SCS) was performed in 11 patients with stabilized spastic hemiparesis due to cerebrovascular ischaemic accident in order to improve their motor performances. The patients were studied before and after 5-7 days of stimulation of the cervical cord according to the following protocol: (1) clinical evaluation based on assessment of the neurological status and on Albert's motor scale and (2) neurophysiological evaluation of reflex voluntary and involuntary motor activity, obtained by means of surface electromyography. Improvement in motor performance following SCS occurred in 7 of the 11 patients. The effect appeared to be particularly evident during specific voluntary movements and gait. Analysis of the electromyography recordings showed that SCS mainly broke down pathological patterns of voluntary movement and reduced agonist-antagonist coactivation and clonus. A relationship between motor outcome and status of the sensory function was noticed as well. We conclude that SCS may play a role in the motor rehabilitation of post-stroke patients with spastic hemiparesis, provided that a careful selection be made before surgery.
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PMID:Effect of spinal cord stimulation on motor performances in hemiplegics. 278 8

Disruption of the upper motor neuron inhibitory pathways by stroke, brain trauma, or spinal cord injury leads to muscle spasticity. Spasticity is characterized by increased muscle tone, hyperactive reflexes, and possible clonus or rigidity. The increased muscle tone may result in loss of joint motion, leading to contractures. Treatment of established contractures is difficult. Prevention of contractures by joint mobilization is emphasized as a goal in the management of patients with spasticity.
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PMID:Spasticity and contracture. Physiologic aspects of formation. 304 37

Dantrolene sodium acts primarily by affecting calcium flux across the sarcoplasmic reticulum of skeletal muscle. Recently, dantrolene has been used very successfully in the treatment of several rare hypercatabolic syndromes which have previously been associated with high mortality rates. In malignant hyperthermia, where early diagnosis and treatment usually with intravenous dantrolene in association with other supportive measures (and often subsequent dantrolene therapy) is performed, recovery is seen in virtually 100% of patients. There is a rapid resolution of hyperthermia, dysrhythmias, muscle rigidity, tachycardia, hypercapnia, mottled or cyanotic skin, and metabolic acidosis, and a slower normalisation of myoglobinuria and elevated serum creatine phosphokinase levels. In patients with family history or previous episodes of malignant hyperthermia, prophylactic treatment with dantrolene prior to anaesthesia prevents the syndrome occurring in most cases. Where malignant hyperthermia has developed patients have been successfully treated with further dantrolene therapy. Dantrolene has also been used successfully in the treatment of a few cases of heat stroke and the neuroleptic malignant syndrome--both of which have many similarities to malignant hyperthermia. Dantrolene is well established in the treatment of patients with muscle spasticity where it generally improves at least some of the components of spasticity (i.e. hyper/hypotonia, clonus, muscle cramps and spasms, resistance to stretch and flexor reflexes, articular movement, neurological and motor functions and urinary control). However, in some patients, particularly those with multiple sclerosis, dantrolene may not be effective, and in many cases muscular strength may diminish. Long term dantrolene therapy has been associated with hepatic toxicity and may cause problems in patients treated for disorders of muscle spasticity. Thus, dantrolene offers a unique advance in the therapy available for the treatment of hypercatabolic disorders and is also useful in the treatment of muscle spasticity of various aetiology.
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PMID:Dantrolene. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in malignant hyperthermia, the neuroleptic malignant syndrome and an update of its use in muscle spasticity. 352 59

This investigation estimated the mechanisms of tizanidine action on spasticity using a battery of neurophysiological methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with tizanidine-mean daily dose 15.8 +/- 5.6 mg for a mean of 23.3 +/- 4.8 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of neurophysiological methods was used to analyze different mechanisms of spasticity: for alpha motoneuron excitability--the F wave parameters; for presynaptic inhibition--the ratio of H reflex amplitudes before and after vibration of the achilles tendon (Hvibr/Hmax); for common interneuron activity--the flexor reflex parameters. Our results revealed that tizanidine reduces spastically increased muscle tone, but has no influence on muscle force, tendon reflexes, Babinski sign and ankle clonus. Tizanidine is supposed to act by increasing the presynaptic inhibition and decreasing of alpha motoneuron excitability. When spasticity has decreased presynaptic inhibition and increased motoneuron excitability, it is better to treat with tizanidine.
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PMID:Mechanisms of tizanidine action on spasticity. 804 46

Locally acting treatments for spasticity such as nerve and motor point blocks have the advantage of reducing harmful spasticity in one area, while preserving useful spasticity in another area. This randomized, double-blind study is the first trial that was designed to find out whether botulinus toxin Type A and phenol relieves the signs and symptoms of ankle plantar flexor and foot invertor spasticity after stroke and if either of these methods offers any advantages and disadvantages over the other. Twenty patients who were included in this preliminary study were randomly assigned to receive a single treatment of 400 mouse units of botulinus toxin Type A injected into the calf muscles or to receive a tibial nerve blockade with 3 ml of 5% phenol. A combination of subjective and objective measures were used to assess functional change at baseline and at Weeks 2, 4, 8, and 12. At follow-up, significant improvement (P < 0.05) in the Ashworth score for dorsiflexion was observed in both groups. The change in the Ashworth score for eversion was significant in the group that received botulinus toxin Type A (P < 0.05) but not in the group that received phenol (P > 0.05). When those variables were compared between the two groups, the change in the Ashworth score at Weeks 2 and 4 was significantly better in the group that received botulinus toxin Type A (P < 0.05) but there was not a significant difference between the two groups at Weeks 8 and 12 (P > 0.05). The decrease in clonus duration that was detected by electromyography was significant in both groups at all visits, but the decrease in the group that received botulinus toxin Type A was significantly better at Weeks 2 and 4 (P < 0.05). It is concluded that both motor point injections with botulinus toxin Type A and tibial nerve blockade with phenol are effective in plantar flexor spasticity, but the changes were more significant in the group that received botulinus toxin Type A at Weeks 2 and 4, whereas there was not a significant difference between the two groups at Weeks 8 and 12. Future research should explore the long-term effect of these two treatment modalities.
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PMID:Comparison of phenol block and botulinus toxin type A in the treatment of spastic foot after stroke: a randomized, double-blind trial. 1049 61

Botulinum toxin A (BTX) injections have been used successfully in the treatment of post-stroke foot spasticity, but the optimal dose-response relationship for selected muscles has yet to be established. The aim of this study was to outline beneficial and unwanted effects of three different doses of BTX in the treatment of spastic foot. In this randomised, double-blind, dose-ranging study, 45 spastic feet were randomly allocated to one of three groups, each of which was treated with a different dosage of BTX. The doses were decided on the basis of suggestions in the literature. Outcome measures (Modified Ashworth Scale, Medical Research Council Scale, gait assessment, presence of Achilles tendon clonus, Visual Analogue Scales for Gait Function and Pain, Adverse Effects scale) were applied at baseline, 4 weeks and 4 months after treatment. All the groups showed significant scales scores improvements after treatment with BTX. Group II (mean BTX total dose: 322 U) and Group III (mean BTX total dose: 540 U) showed a greater and more prolonged response than Group I (mean BTX total dose: 167 U). Group III showed the highest rate of adverse effects 4 weeks post-treatment. BTX injections constitute a useful and safe method of improving post-stroke foot spasticity, associated pain, gait speed and function. In particular, the medium BTX dosages (320 UI spread over 2-5 muscles) were found to be both safe and effective in producing long-lasting improvement of spastic foot dysfunction.
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PMID:A randomised, double-blind, dose-ranging study to evaluate efficacy and safety of three doses of botulinum toxin type A (Botox) for the treatment of spastic foot. 1587 84


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