Neurology
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Randomized Controlled Trial Multicenter Study Clinical Trial
Efficacy and safety of tizanidine in the treatment of spasticity in patients with spinal cord injury. North American Tizanidine Study Group.
Tizanidine, an imidazoline that acts as an agonist at alpha 2-adrenergic receptors, has been shown to be effective in reducing spasticity caused by MS. This multicenter study (14 sites) assessed the efficacy and safety of oral tizanidine in patients who had spinal cord injury of > 12 months' duration. Of the 124 patients admitted to the study, 78 completed it. ⋯ No significant alterations in muscle strength or vital signs were noted in either treatment group. The most common adverse events during tizanidine treatment were somnolence, xerostomia, and fatigue. It was concluded that, overall, tizanidine is effective in reducing spasticity in patients with spinal cord injury.
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Randomized Controlled Trial Multicenter Study Clinical Trial
A double-blind, placebo-controlled trial of tizanidine in the treatment of spasticity caused by multiple sclerosis. United Kingdom Tizanidine Trial Group.
Tizanidine was evaluated in a prospective, double-blind, randomized, placebo-controlled trial in 187 patients with MS. Taken orally for 9 weeks and preceded by a titration phase for a period of 3 weeks starting at 2 mg daily, tizanidine produced a significant reduction in spastic muscle tone compared with placebo treatment. Within the effective dose range of 24 to 36 mg given daily in three doses, tizanidine achieved a 20% mean reduction in muscle tone. ⋯ Tizanidine achieved its maximum effect on spasticity within 1 week of the start of treatment; the benefit was maintained for at least 1 week after discontinuation of therapy. A variety of adverse events was recorded by patients taking tizanidine, but these were minor and reversible, and rarely limited treatment. Tizanidine is a well-tolerated and effective drug for symptomatic treatment of spasticity.
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Randomized Controlled Trial Clinical Trial
Phentolamine sympathetic block in painful polyneuropathies. II. Further questioning of the concept of 'sympathetically maintained pain'.
To test for the presence of "sympathetically maintained pain" (SMP), we administered placebo-controlled phentolamine sympathetic blocks to 14 patients with painful polyneuropathies. Six received i.v. infusion of saline for 30 minutes, followed by phentolamine (35 mg). In eight patients, the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 micrograms), a second saline phase, and then the other active drug. ⋯ Five patients reported significant diminution of pain (> 50%), all in response to placebo. Neither phentolamine nor phenylephrine provided relief, although all patients had signs of physiologic abnormalities reputed to be determinants or predictors of SMP. These results complement previous studies demonstrating the nonexistence of SMP among "reflex sympathetic dystrophy" patients and further question the concept of SMP.
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Randomized Controlled Trial Clinical Trial
Opioid responsiveness of cancer pain syndromes caused by neuropathic or nociceptive mechanisms: a combined analysis of controlled, single-dose studies.
We performed a combined analysis of the results from four controlled single-dose relative-potency studies to assess the impact of inferred pain mechanism on the response to an opioid drug. A total of 168 patients received 474 administrations of either morphine or heroin, and we assessed the analgesic response during a 6-hour period with visual analog scales. We summarized this as a total pain relief (TOTPAR) score. ⋯ We compared pain relief achieved by patients with different mechanisms, with TOTPAR adjusted for significant covariates (duration of prior opioid administration, doses of opioid administered in the previous 48 hours, pain intensity at the start of the study, BUN:creatinine ratio, and dose of administered opioid). The adjusted mean TOTPAR score of the group with any neuropathic pain was significantly lower than that of the group with nociceptive pain only (26.1 versus 20.4, p = 0.02). The score of the group with definite nociceptive pain alone (adjusted mean TOTPAR = 28.0) was significantly higher than scores of the groups with possible/probable nociceptive pain (TOTPAR = 19.9), mixed mechanisms (TOTPAR = 20.2), definite neuropathic pain alone (TOTPAR = 20.6), and possible/probable neuropathic pain alone (TOTPAR = 22.9).(ABSTRACT TRUNCATED AT 250 WORDS)
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Randomized Controlled Trial Comparative Study Clinical Trial
Sodium valproate has a prophylactic effect in migraine without aura: a triple-blind, placebo-controlled crossover study.
We included 43 patients with migraine without aura in a triple-blind, placebo- and dose-controlled, crossover study of the prophylactic effect of slow-release sodium valproate; 34 patients completed the trial. The number of days with migraine was 3.5 per 4 weeks during treatment with sodium valproate and 6.1 during placebo (p = 0.002). The severity and duration of the migraine attacks that did occur were not affected by sodium valproate when compared with placebo. ⋯ The number of responders increased during the trial to 65% in the last 4 weeks of the active treatment period. There were no serious side effects requiring withdrawal of patients from the study. We conclude that sodium valproate is an effective and well-tolerated prophylactic medication for migraine without aura.