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The misuse and abuse of meprobamate and other muscle relaxing drugs was an item of great concern in the 1950s and 1960s 11. Carisoprodol was developed in the 1950s by Dr. Frank M. Berger at Wallace laboratories on the basis of meprobamate, hoping that it would have better muscle-relaxing properties, less abuse potential, and less risk of overdose than meprobamate 12. The substitution of one hydrogen atom with an isopropyl group on one of the carbamyl nitrogens was intended to yield a molecule with new pharmacological properties.

Initial pharmacokinetic studies using a canine model indicated that carisoprodol was metabolized to hydroxy-carisoprodol. The metabolism of carisoprodol to meprobamate was described in mice in 1969. But it was only after a description of a carisoprodol intoxication in 1976 13 that it was acknowledged that carisoprodol was mostly metabolized to meprobamate in humans 14.

Carisoprodol is sold in most countries. Some countries like Spain sell it over-the-counter, but in most countries a prescription is required.

Carisoprodol was approved for marketing before the FDA required that safety and efficacy be proved in clinical studies.

• As an adjunct to rest, physical therapy, and other measures for the relief of discomfort associated with acute, painful musculoskeletal conditions.

• fibromyalgia 2
• back pain 3, 4

Lower back pain
Carisoprodol is a centrally acting muscle relaxant commonly used for back pain. In several studies it was found to be superior to placebo in relieving stiffness, increasing movement, and leading to general improvement. In comparative study carisoprodol was better than propoxyphene in relieving stiffness and increasing movement 7. In the other comparative study carisoprodol was superior to diazepam for relieving the symptoms of acute lower back pain 8.

The results of a double-blind study that compared carisoprodol, butabarbital, and placebo, have shown the effectiveness of carisoprodol in the treatment of the low back pain syndrome 4. Carisoprodol was found to be significantly more effective in providing both subjective pain relief and objective improvements in range of motion when evaluated by finger to floor testing. The results of this study suggest that the effects of carisoprodol are not secondary to its sedative effects alone, but are also related to its muscle relaxant activity.

Fibromyalgia
In a study of patients with fibromyalgia, carisoprodol compound (carisoprodol/paracetamol/caffeine) was found to be superior to placebo in alleviating pain, inducing sleep, and minimizing the general feeling of being sick 2.

• Advantages:
• potent muscle relaxant
• relatively inexpensive
• Disadvantages:
• potential for drug abuse and dependence 15
• potential for withdrawal syndrome 5
• may impair the mental and physical abilities required for the performance of potentially hazardous tasks such as driving

Carisoprodol is a muscle relaxant that does not directly relax tense skeletal muscles in man 1. Although not well understood, the mechanism of action of carisoprodol in humans may be related to its sedative properties, either directly or indirectly, via the effects of meprobamate.

In animals, carisoprodol produces muscle relaxation by blocking interneuronal activity in the descending reticular formation and spinal cord. However, it is unknown if this mechanism of action is also present in humans 1. Carisoprodol's primary metabolite, meprobamate, has barbiturate like modulatory effects on GABA-A receptors 9. However, it is unclear whether the GABA-A receptor-like effects are from carisoprodol itself or its metabolite meprobamate.

The pharmacological effects of carisoprodol appear to be due to the combination of the effects of carisoprodol and meprobamate. In addition to the desired skeletal muscle-relaxing effects, carisoprodol also produces weak anticholinergic, antipyretic, and analgesic effects. High doses of carisoprodol may induce symptoms that are similar to the symptoms associated with serotonin syndrome 10.

Muscle relaxant action. It produces muscle relaxation by affecting the central nervous system. It is possible that carisoprodol induced muscle relaxation results from a slight depression of all neurons at synaptic junctions within the central nervous system. It is noteworthy that this agent has a marked depressant effect on hyperactive spinal reflexes in doses that do not affect normal reflexes.

Analgesic action. The pain-relieving properties of carisoprodol are distinctive and in certain respects are different from the actions of either the opium alkaloids, or the antipyretic-analgesics such as aspirin and paracetamol. The analgesic action of any drug may be due to its effect on:

• peripheral pain receptors
• the sensory pain pathways and their synapses
• the centers concerned with pain receptors or sensory pain pathways and that it probably acts upon centers concerned with pain perception.

Case reports have established carisoprodol as a drug of abuse, but no systematic studies have been published about the extent of abuse.

It is suggested that abuse and dependence potential of carisoprodol are due to carisoprodol’s metabolite meprobamate (federally controlled substance) 6, 15, 16. Carisoprodol undergoes hepatic biotransformation to three primary metabolites: hydroxycarisoprodol, hydroxymeprobamate, and meprobamate. The significant serum levels of meprobamate after chronic use of carisoprodol may lead to meprobarnate dependency. Withdrawal from meprobamate may result in severe reactions including seizures and coma.

One study evaluated abuse risk in patients taking carisoprodol. This study enrolled 40 patients taking carisoprodol for more than 3 months. It assessed the potential for abuse using an unvalidated six-item questionnaire and found that 20% of patients with no history of substance abuse and 65% with a history of substance abuse responded yes to one or more questions, which the authors suggested indicated a tendency towards possible abuse 6.

Carisoprodol elimination half-life is 2.44 ± 0.93 hours. So, it may take 3-4 days to clear out of the system.

The onset of action is rapid (30 min.) and lasts four to six hours.

• Carisoprodol (Soma) versus Other Medications

• 1. Physicians’ Desk Reference, 54th ed; Medical Economics, Thomson Healthcare: Montvale, NJ; 2000.
• 2. Vaeroy H, Abrahamsen A, Forre O, Kass E. Treatment of fibromyalgia (fibrositis syndrome): a parallel double blind trial with carisoprodol, paracetamol and caffeine (Somadril comp) versus placebo. Clin Rheumatol. 1989 Jun;8(2):245-50. PubMed
• 3. Toth PP, Urtis J. Commonly used muscle relaxant therapies for acute low back pain: a review of carisoprodol, cyclobenzaprine hydrochloride, and metaxalone. Clin Ther. 2004 Sep;26(9):1355-67. PumMed
• 4. Hindle TH 3rd. Comparison of carisoprodol, butabarbital, and placebo in treatment of the low back syndrome. Calif Med. 1972 Aug;117(2):7-11. PubMed
• 5. Reeves RR, Parker JD. Somatic dysfunction during carisoprodol cessation: evidence for a carisoprodol withdrawal syndrome. J Am Osteopath Assoc. 2003 Feb;103(2):75-80.
• 6. Reeves R, Carter O, Pinkofsky H. Carisoprodol (Soma): abuse potential and physician unawareness. J Addict Dis. 1999;18:51-56.
• 7. Baratta RR. A double-blind comparative study of carisoprodol, propoxyphene, and placebo in the management of low back syndrome. Curr Ther Res Clin Exp. Sep 1976;20(3):233-240.
• 8. Boyles W, Glassmann J, Soyka J. Management of acute muskuloskeletal conditions: thoracolumbar strain and sprain. A double-blind evaluation comparing the efficacy and safety of carisoprodol with diazepam. Today's Ther Trends. 1983;1:1-16.
• 9. Rho JM, Donevan SD, Rogawski MA Barbiturate-like actions of the propanediol dicarbamates felbamate and meprobamate. J Pharmacol Exp Ther. 1997 Mar;280(3):1383-91.
• 10. Bramness JG, M?rland J, S?rlid HK, Rudberg N, Jacobsen D Carisoprodol intoxications and serotonergic features. Clin Toxicol (Phila). 2005;43(1):39-45. PubMed
• 11. Kamin I, Shaskan D. Death due to massive overdose of meprobamate. Am J Psychiatry. 1959;115(12):1123-1124.
• 12. Berger F, Kletzkin M, Ludwig B, Margolin S. The history, chemistry, and pharmacology of carisoprodol. Annals of the New York Academy of Sciences. 1959;86:90-107.
• 13. Brandslund I. A case of acute carisoprodol poisoning. Symptoms and metabolism. Ugeskr Laeger. Jan 26 1976;138(5):281-283
• 14. Beermann B, O"hman B. Meprobamat - huvudmetabolit tilll karisoprodol. La"kartidn. 1978;75(39):1962.
• 15. Littrell RA, Sage T, Miller W. Meprobamate dependence secondary to carisoprodol (Soma) use. Am J Drug Alcohol Abuse. 1993;19(1):133-134
• 16. Reeves RR, Beddingfield JJ, Mack JE. Carisoprodol withdrawal syndrome. Pharmacother. 2004;24(12):1804-1806

Published: March 31, 2008
Last updated: January 07, 2010