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Carisoprodol: An effective abortive agent in migraine without aura
Abstract
Background: The early use of medications will often abort migraine headaches, but there is a limited availability of such medications. Objective: The efficacy of naproxen, a known effective drug in migraine, was compared to that of carisoprodol, a skeletal muscle relaxant, to see if the latter agent might be added to the drugs available for early migraine treatment. Design: Retrospective chart review of the treatment of 100 patients with migraine without aura, in a clinical headache practice. Results: Naproxen and carisoprodol both appeared to be very effective in the early treatment of migraine without aura. Naproxen was not superior to carisoprodol in any aspect. Conclusion: Carisoprodol appears to be very effective in the early treatment of migraine without aura. Further controlled, randomized, double-blinded studies are indicated to further evaluate carisoprodol's efficacy and safety in migraine treatment. Because of the apparent potential for abuse and/or habituation, cautious use of carisoprodol is recommended at this time.
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Carisoprodol (Soma) is a noncontrolled, skeletal-muscle relaxant whose active metabolite is meprobamate. Despite previous indications that the drug may be abused, it continues to be widely prescribed for musculoskeletal conditions involving muscle spasm. Presented here are three cases demonstrating patterns of carisoprodol abuse not previously reported. Carisoprodol usage should be limited to short-term treatment. Patients for whom carisoprodol is prescribed are at risk for meprobamate dependence.
A single-blind study to assess the analgesic and antipyretic effects of Stopayne was undertaken in a group of 37 patients suffering from influenza. Patients were instructed to take two tablets four-hourly over a period of 24 hours. Average period of headache relief lasted 4.1 hours and muscle pain was relieved for 3.7 hours. Ninety per cent of patients had satisfactory relief of muscle pain and a similar response was obtained for headache sufferers. A muscle-relaxant effect was noted in the group and an antipyretic effect was recorded in those patients with elevated temperatures.
The presence of acute or chronic muscle pain and muscle spasm is a common finding in the treatment of craniomandibular disorders. A review of the literature on the centrally acting oral skeletal muscle relaxants is presented to assist the practitioner in treating CMD. The pharmacology, pharmacokinetics, metabolism, adverse reactions and available dosage forms of the skeletal muscle relaxants are discussed. The agents reviewed are carisoprodol, methocarbamol, chlorphenesin carbamate, metaxalone, chloroxazone, orphenadrine citrate, diazepam, and cyclobenzaprine. Their mechanisms are not well defined. Most act via selective inhibition of polysynaptic pathways in the central nervous system. Most evidence for their efficacy is based on subjective responses and there is question as to the adequacy of the clinical studies to date. Based on the data all of the relaxants (possibly excepting diazepam) are better than placebo based on subjective analyses. Although combinations with analgesics provide better symptom relief, no superiority over analgesics exists. No skeletal relaxant has been shown to be superior over any other oral relaxant. Based on recent clinical suspicions, further study of multiple pharmacologic effects of newer agents is indicated.
Naproxen was compared with placebo in a double-blind, crossover trial in classic and common migraine. The trial was terminated at a fixed date; 37 patients had entered, 5 of whom were excluded. Naproxen was given as 750 mg at the first symptom of the attack, a total of 1250 mg per 24 h was allowed. Patients were followed for six attacks or three months in each phase, whichever came first. The severity of the headache was significantly less with naproxen in the first 2 h of the attack (p = 0.047), whereas there was no difference when the whole attack was considered. Significantly more patients preferred naproxen (p = 0.042). Side effects occurred in five patients, causing withdrawal of one patient while on naproxen.
SYNOPSISThe tolerability and efficacy of naproxen sodium and of ergotamine tartrate plus caffeine (ergotamine) were compared in the treatment of acute migraine attacks and associated symptoms. In this multicenter, double-blind, parallel study of up to six headaches over a 3-month period, patients took naproxen sodium 825 mg, ergotamine 2 mg, or placebo at the time of the first symptom of an attack; 30 minutes later, if necessary, patients repeated naproxen sodium 275 mg, ergotamine 1 mg or placebo, as appropriate. Rescue medication was allowed 30 minutes following the second dose if needed. Active drugs provided notably better relief of head pain than did placebo; 1 hour following the first dose the difference between naproxen sodium and placebo was statistically significant. Naproxen sodium was as efficacious as ergotamine in the relief of migraine attacks and associated symptoms. Relief of vomiting, nausea, photophobia, and motor symptoms favored naproxen sodium over ergotamine; these differences were statistically significant for nausea and motor symptoms. Ergotamine-treated patients reported more complaints and had more severe and longer-lasting complaints than patients on the other two regimens. Overall tolerance ratings by both investigators and patients indicated that naproxen sodium and placebo were tolerated significantly better than ergotamine.
An 8-month, double-blind, placebo-controlled, crossover trial of flunarizine in the prophylaxis of migraine has been performed in 70 children. After 4 weeks of medication-free base-line observation, 35 children (group A) received flunarizine (5 mg/day) and 35 (group B) received placebo over a 12-week period. After a 4-week washout they crossed treatments for another 12 weeks. Sixty-three patients completed the trial. In both groups flunarizine significantly reduced the frequency and average duration of headache attacks. In group A efficacy was maintained after placebo crossover for the last 4 months of the study. Five subjects in group B stopped placebo because of ineffectiveness; two children in group A discontinued flunarizine treatment, one because of excessive daytime sedation and the other because therapy was ineffective. The main side effects were daytime sedation and weight gain. It is concluded that flunarizine is an effective drug for the treatment of childhood migraine. In a study of this length no serious side effects were discovered.
Seventy patients with classical or common migraine were treated during their attacks with either naproxen sodium or placebo in a randomised, double-blind parallel group study. The initial dose of naproxen sodium was 825 mg followed one hour later by a further 550 mg, if symptoms were the same or had improved. If the migraine symptoms had worsened, patients were offered an escape analgesic combination of 1000 mg paracetamol and 10 mg metoclopramide. Patients were assessed at monthly intervals for changes in the severity and duration of headache, premonitory symptoms (mainly visual disturbances) and photophobia, nausea and vomiting associated with migraine attacks that had occurred since the previous visit. Patients were studied for a maximum of ten attacks and significant improvement was observed in the severity and duration of headache when the patients were on naproxen sodium. Also the premonitory symptoms and photophobia improved significantly on naproxen sodium and significantly less rescue analgesics were required. Patients suffering from common migraine had less severe headaches and photophobia when taking naproxen sodium than when taking placebo and the headaches were shorter in duration and patients took less rescue analgesic. No significant difference was observed between the treatment groups in patients with classical migraine. Ten patients in the placebo group and six in the naproxen sodium group reported side-effects but these were possibly related to the use of rescue medication. Naproxen sodium proved safe and effective in common migraine attacks, but in this study efficacy was not established for classical migraine.
A double-blind, cross-over, randomized study of acute migraine attack compared treatment results of naproxen with that of placebo. Each treatment period continued for either three months or six migraine attacks, whichever occurred first. The initial dose of naproxen was 750 mg, with additional 250-500 mg doses taken if and when required, to a maximum of five 250 mg tablets within a period of 24 h in each migraine attack. Forty-one patients were enrolled in the study; they had all experienced at least two but not more than eight migraine attacks a month during the preceding year. Thirty-two patients completed the two treatment periods. Naproxen was statistically significantly superior to placebo in reducing the severity of head pain, nausea, and photophobia; in shortening the duration of head pain, nausea, vomiting, photophobia, and lightheadedness; in diminishing the frequency of vomiting; and in decreasing the need for escape medication. Both patient and physician treatment preferences significantly favoured naproxen. Nine side effects were experienced by seven patients while receiving placebo and seven by five patients during naproxen treatment. Mild gastrointestinal discomfort was the main complaint. Only one patient withdrew from treatment because of a side effect, which occurred while receiving placebo.
The elimination of the muscle relaxant drug, carisoprodol, was examined in 10 healthy volunteers after an oral dose of 700 mg. In nine subjects, carisoprodol was rapidly eliminated, with a mean half-life of 99 +/- 46 min, and extensively converted to meprobamate. Within 2.5 h after carisoprodol intake, meprobamate serum concentrations exceeded those of carisoprodol. Serum levels of meprobamate recorded (15-25 mumol/L) indicate that meprobamate might contribute to the effect(s) of carisoprodol. One subject eliminated carisoprodol with an overall half-life of 376 min, and only small amounts of meprobamate were recorded. This subject was found to be a poor metabolizer of mephenytoin. In spiked human sera, protein binding of carisoprodol was in the range of 41-67%, whereas meprobamate was bound to a lesser extent, 14-24%.
Carisoprodol (available as Soma and in other commercial forms) is a commonly prescribed muscle relaxant. A small group of patients was recently discovered colluding to obtain the drug under false pretenses for the purposes of substance abuse. Animal and human studies have previously shown limited potential for tolerance or abuse, while the evidence for therapeutic efficacy is inadequate. There are two previous case reports of human carisoprodol abuse or dependence, one in which a patient showed signs of a true withdrawal syndrome. A third case involved a fatality linked to carisoprodol abuse. Data from the National Institute on Drug Abuse reveal that overdose and abuse of carisoprodol may be more common than previously suspected. Carisoprodol use should be limited to short-term treatment of acute musculoskeletal conditions involving significant muscle spasm. Suspicions of abuse should be raised by patients requesting the drug by name, "losing" prescriptions, using carisoprodol chronically, or denying the efficacy of less mind-altering alternatives.
Carisoprodol (Soma, others) is a commonly prescribed, noncontrolled, skeletal muscle relaxant whose active metabolite is meprobamate. Patients for whom carisoprodol is prescribed are at risk for meprobamate dependence; several such cases have been reported. Toxicity and withdrawal associated with the use of meprobamate is high and has led to abandonment of this agent in clinical practice. Because carisoprodol possesses the same risks it should be avoided when possible, and it should be given schedule IV controlled substance status.