VA Class:MS200
Carisoprodol is a centrally acting skeletal muscle relaxant.
Carisoprodol is used for the short-term relief of discomfort associated with acute, painful musculoskeletal conditions.29, 100, 101, 102 The drug is indicated for short-term use only (i.e., up to 2-3 weeks) because adequate evidence of efficacy for more prolonged use has not been established and because acute, painful musculoskeletal conditions generally are of short duration.100 In addition, long-term use of carisoprodol may increase the risk of abuse, dependence, and tolerance.100, 113, 114, 117
Evidence supporting the efficacy of skeletal muscle relaxants is generally low to moderate in quality; while these agents appear to be more effective than placebo in providing short-term relief of acute low back pain, they are associated with a high incidence of adverse effects (e.g., sedation).103, 104, 106, 209, 210, 211, 212 Although comparative studies are limited, available data suggest that various skeletal muscle relaxants generally have similar efficacy for such use.103, 104, 106, 108 Acute low back pain usually is a benign and self-limiting condition that improves spontaneously over time;105, 106, 108 therefore, nonpharmacologic treatment strategies (e.g., heat, massage) are recommended.209 If pharmacologic therapy is required, experts state that a nonsteroidal anti-inflammatory agent (NSAIA) or a skeletal muscle relaxant may be used; however, these drugs have been shown to result in only small improvements in pain relief and can increase the risk of adverse effects.104, 106, 107, 108, 209 In general, skeletal muscle relaxants should be used with caution after weighing the potential risks against the benefits in individual patients.104, 106, 107, 108 Although skeletal muscle relaxants are often used in combination with NSAIAs for the treatment of acute low back pain, randomized controlled studies generally have not demonstrated any additional improvement in pain or functional outcomes with such combination therapy compared with use of an NSAIA alone.210, 212, 213
Efficacy of carisoprodol for the relief of acute, painful musculoskeletal conditions was evaluated in 2 randomized, placebo-controlled studies in adults 18-65 years of age with acute, idiopathic low back pain of no more than 3 days' duration.100, 101, 102 In these studies, patients were randomized to receive carisoprodol (250 or 350 mg) or placebo 3 times daily and at bedtime for 7 days.100, 101, 102 In both studies, carisoprodol was found to be more effective than placebo, as measured by patient-rated relief from starting backache and patient-rated global impression of change.100, 101, 102 The 250-mg dosage of carisoprodol was similar in efficacy to the 350-mg dosage, but was associated with a lower incidence of adverse events.100, 101 Patients receiving carisoprodol in these studies also experienced an improvement in functional status compared with those receiving placebo (as measured by the Roland-Morris Disability Questionnaire score), and clinical improvement was observed regardless of whether patients reported sedation.100, 101, 102
It is unclear whether relief of musculoskeletal pain by carisoprodol results from skeletal muscle relaxant effects, sedative effects, or a placebo effect of the drug. Most authorities attribute the beneficial effects of skeletal muscle relaxants to their sedative properties.
Carisoprodol is ineffective in the treatment of skeletal muscle hyperactivity secondary to chronic neurologic disorders such as cerebral palsy and other dyskinesias.25, 29
Carisoprodol is administered orally with or without food.100
The recommended dosage of carisoprodol in adults is 250-350 mg 3 times daily and at bedtime.100 Treatment should be limited to short periods (i.e., up to 2-3 weeks) because adequate evidence of efficacy for more prolonged periods has not been established and because acute, painful musculoskeletal conditions generally are of short duration.100
The most frequent adverse effects of carisoprodol are drowsiness, dizziness, and headache.100 In clinical studies of carisoprodol in patients with acute low back pain, sedation was reported in 13-17% of patients receiving the drug compared with 6% of those receiving placebo.100 Other adverse CNS effects include vertigo, ataxia, tremor, agitation, irritability, headache, depressive reactions, syncope, and insomnia.100 In addition, seizures have been reported during postmarketing experience in patients receiving carisoprodol, mostly in the setting of multiple-drug overdoses (including drugs of abuse, illicit drugs, and alcohol).100 Use of carisoprodol also has been implicated as a factor in motor vehicle accidents.100, 114
Allergic or idiosyncratic reactions have been reported in patients receiving meprobamate, a metabolite of carisoprodol.109 These events have ranged from mild (e.g., pruritus, urticaria, erythematous maculopapular rash) to more severe hypersensitivity reactions, including hyperpyrexia, chills, angioedema, bronchospasm, anaphylaxis, stomatitis, proctitis, oliguria, anuria, exfoliative dermatitis, erythema multiforme, Stevens-Johnson syndrome, and bullous dermatitis.109 Leukopenia, acute nonthrombocytopenic purpura, petechiae, ecchymoses, eosinophilia, adenopathy, peripheral edema, fever, and fixed drug eruptions with a cross-reaction to carisoprodol also have occurred in association with meprobamate use.109
Adverse GI effects of carisoprodol include nausea, vomiting, and epigastric distress. Adverse cardiovascular effects include tachycardia, postural hypotension, and facial flushing. Although a causal relationship to carisoprodol has not been established, leukopenia and pancytopenia have occurred rarely in patients receiving carisoprodol along with other drugs.
Precautions and Contraindications
Because carisoprodol is metabolized by the liver and excreted by the kidneys, the drug should be used with caution in patients with impaired hepatic or renal function. Patients should be warned that carisoprodol may impair their ability to perform hazardous activities requiring mental alertness or physical coordination such as operating machinery or driving a motor vehicle. In addition, the possibility of additive sedative effects should be considered in patients receiving other CNS depressants (e.g., alcohol, benzodiazepines, opiate agonists, tricyclic antidepressants) concomitantly.100, 122
Carisoprodol is contraindicated in patients with a history of acute intermittent porphyria and in patients with known hypersensitivity to carisoprodol or other carbamate derivatives (e.g., meprobamate).100
Abuse, Dependence, and Withdrawal
Carisoprodol is subject to control as a schedule IV drug.100 The drug has been associated with dependence, abuse, misuse, and diversion.100, 108, 113, 114, 117, 118 (See Chronic Toxicity.) The risk of abuse should be assessed in individual patients prior to prescribing carisoprodol and special precautions should be taken during treatment to reduce this risk; such precautions include limiting use to short periods (i.e., up to 3 weeks), maintaining careful prescription records, monitoring for signs of abuse and overdosage, and educating patients and their family members on abuse and proper storage and disposal of the drug.100
Pharmacogenomics and Effects of CYP2C19 Polymorphism
Carisoprodol should be used with caution in patients with reduced cytochrome P-450 (CYP) 2C19 activity (i.e., poor metabolizers) because such patients may have higher than expected concentrations of the drug.100, 120 (See Pharmacokinetics: Elimination.)
Safety and efficacy of carisoprodol in children younger than 16 years of age have not been established.100
Safety and efficacy of carisoprodol in patients older than 65 years of age have not been established.100
Because of the risk of injury, skeletal muscle relaxants should generally be avoided in geriatric patients.111
A drug-associated risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes has not been identified to date with use of carisoprodol or meprobamate (an active metabolite) in pregnant women.100 In an animal reproduction study, reduced fetal weights, postnatal weight gain, and postnatal survival were observed when pregnant mice were exposed to carisoprodol from gestation through weaning.100 Some experts recommend that the drug be avoided, if possible, during the first trimester of pregnancy.125
Limited data indicate that carisoprodol is distributed into human milk and may reach concentrations that are 2-4 times maternal plasma concentrations.100, 110, 125 Other than mild sedation, no adverse effects have been observed in nursing infants exposed to carisoprodol; while the effects of the drug on milk production are not known, insufficient maternal milk production has been described in several case reports.100, 110, 111, 125 The known benefits of breastfeeding should be considered along with the mother's clinical need for carisoprodol and any potential adverse effects on the breastfed infant from the drug or underlying maternal condition.100 The nursing infant should be monitored for signs of sedation during breastfeeding.100
Drugs Affecting Hepatic Microsomal Enzymes
Carisoprodol is metabolized by cytochrome P-450 (CYP) isoenzyme 2C19; pharmacokinetic interactions are possible with drugs that affect this isoenzyme.100 CYP2C19 inhibitors (e.g., fluvoxamine, omeprazole) may increase exposure to carisoprodol and decrease exposure to meprobamate; conversely, CYP2C19 inducers (e.g., rifampin, St. John's wort [ Hypericum perforatum ]) may decrease exposure to carisoprodol and increase exposure to meprobamate.100 Low-dose aspirin also may have some CYP2C19-inducing effects.100 The clinical importance of these potential pharmacokinetic interactions is not known.100
Additive CNS depression may occur when carisoprodol is used concomitantly with other CNS depressants, including alcohol, benzodiazepines, opiate agonists, sedating antihistamines, and tricyclic antidepressants.100, 122 If carisoprodol is used concomitantly with other CNS depressant drugs, caution should be exercised.100, 122 Concomitant use of carisoprodol and meprobamate (a metabolite of carisoprodol) is not recommended.100
Carisoprodol overdosage generally produces symptoms of CNS depression.100 Manifestations have included headache, rigidity, muscular incoordination, euphoria, mydriasis, blurred vision, nystagmus, dystonic reactions, hallucinations, delirium, seizures, hypotension, respiratory depression, coma, and death.100, 114 One man who ingested 8.4 g of carisoprodol and another who ingested 9.45 g had maximum plasma concentrations of 37 and 38 mcg/mL, respectively. In these patients, drowsiness, dizziness, headache, diplopia, and nystagmus on lateral gaze occurred. Treatment consisted of supportive therapy, gastric lavage, and emesis; recovery was uneventful. Many cases of carisoprodol overdosage have occurred in the setting of multiple-drug overdoses, including drugs of abuse, illicit drugs, and alcohol.100, 122 Fatalities have been reported following accidental or intentional overdosage of carisoprodol administered alone or in combination with other CNS depressants.100
Management of carisoprodol overdosage should include basic life support measures (e.g., maintenance of an adequate airway, respiratory and circulatory support) as dictated by the clinical presentation.100 Induced emesis is not recommended because of the potential for CNS and respiratory depression, which may increase the risk of aspiration pneumonia.100 If circulatory support is necessary, IV fluids and vasopressor agents should be administered.100 Seizures should be treated initially with IV benzodiazepines; if seizures recur, phenobarbital may be used.100 In patients who experience severe CNS depression, tracheal intubation should be considered for airway protection and respiratory support.100 Activated charcoal should be considered in a hospital setting in patients experiencing a large overdosage who present early and do not have CNS depression or airway compromise.100
Cases of abuse, tolerance, and dependence have been reported with prolonged use of carisoprodol.100, 108, 112, 113, 114, 117, 118 While most reported cases have occurred in patients with a history of drug abuse or who were receiving carisoprodol in combination with other drugs with abuse potential (e.g., opiate analgesics, benzodiazepines, illicit drugs),100, 108, 112, 114, 115, 118 there were some instances where carisoprodol was the primary or sole drug of abuse.100, 114, 118 Abrupt cessation of carisoprodol following prolonged administration has resulted in withdrawal symptoms, including hallucinations, tremors, anxiety, muscle twitching, and insomnia; in most cases, excessive dosages of carisoprodol were used.100, 113, 117
In vitro studies demonstrate that carisoprodol elicits barbiturate-like effects, which may contribute to its potential for abuse.100, 114, 119 Results of animal studies indicate that carisoprodol has positive reinforcing and discriminative effects similar to those of certain other schedule IV drugs (e.g., barbital [not commercially available in the US], meprobamate, chlordiazepoxide).100, 114, 119 In addition, because carisoprodol is metabolized to meprobamate, a drug that is associated with abuse and dependence,100, 103, 104, 106, 109, 120 accumulation of this active metabolite also may contribute to the abuse potential of carisoprodol.100, 106, 112, 113, 117, 118, 119 Withdrawal symptoms reported with carisoprodol are similar to those described in patients who abruptly discontinue meprobamate.112, 113
Carisoprodol is a CNS depressant that has sedative and skeletal muscle relaxant effects. The precise mechanism of action of the drug is not known. The skeletal muscle relaxant effects of orally administered carisoprodol are minimal and probably are related to its sedative effect. In animal studies, carisoprodol-induced muscle relaxation was associated with altered interneuronal activity in the spinal cord and in the descending reticular formation of the brain.100 The drug does not directly relax skeletal muscle and, unlike neuromuscular blocking agents, does not depress neuronal conduction, neuromuscular transmission, or muscle excitability. In animals, carisoprodol appears to modify central perception of pain without abolishing peripheral pain reflexes and to have slight antipyretic activity, but these effects have not been demonstrated in clinical studies.25, 27
Plasma concentrations of carisoprodol required for sedative, skeletal muscle relaxant, or toxic effects are not known. Peak plasma concentrations of approximately 1.2 and 1.8 mcg/mL were attained following oral administration of single doses of 250 and 350 mg of carisoprodol, respectively, to healthy adults.100, 121 Peak plasma concentrations were achieved in approximately 1.5-2 hours.100, 121 Administration of a high-fat meal had no effect on the pharmacokinetics of the drug.100 Following usual therapeutic dosages, the onset of action is usually within 30 minutes and the duration of action is 4-6 hours.
Animal studies indicate that carisoprodol crosses the placenta.100 The drug distributes into milk in concentrations 2-4 times higher than concurrent maternal plasma concentrations.100, 110, 125
Carisoprodol is metabolized in the liver by cytochrome P-450 (CYP) isoenzyme 2C19; several metabolites (meprobamate, hydroxycarisoprodol, hydroxymeprobamate) have been identified, among which meprobamate is the main active metabolite.100, 112, 117 Carisoprodol is eliminated via both renal and nonrenal routes; the mean elimination half-life of carisoprodol is approximately 2 hours and the mean elimination half-life of meprobamate is approximately 10 hours.100, 121 Carisoprodol may be removed by hemodialysis and peritoneal dialysis.100
Pharmacogenomics: Genetic polymorphism of the CYP2C19 isoenzyme may affect the pharmacokinetics of carisoprodol.100, 120 Studies have shown that exposure to carisoprodol is increased (by fourfold) and exposure to meprobamate is decreased (by 50%) in individuals with genetic deficiency of the CYP2C19 isoenzyme (i.e., poor metabolizers) compared with those with normal CYP2C19 function.100, 120 Approximately 15-20% of Asians and approximately 3-5% of Caucasians and African Americans exhibit the CYP2C19 poor metabolizer phenotype.100
Carisoprodol, a centrally acting skeletal muscle relaxant, is structurally and pharmacologically related to meprobamate. Carisoprodol occurs as a white, crystalline powder with a bitter taste and a mild characteristic odor. The drug is slightly soluble in water and freely soluble in alcohol, chloroform, and acetone.
Carisoprodol tablets should be stored at a controlled room temperature of 20-25°C in tight containers.100 The fixed combination preparation containing carisoprodol, aspirin, and codeine phosphate should be stored in tight, light-resistant containers at 20-25°C and protected from moisture.123 The fixed combination preparation containing carisoprodol and aspirin also should be stored in tight, light-resistant containers at 20-25°C and protected from moisture.124
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Carisoprodol is subject to control under the Federal Controlled Substances Act of 1970 as a schedule IV (C-IV) drug.100 Preparations containing the drug in combination with codeine phosphate are subject to control under the Federal Controlled Substances Act of 1970 as schedule III (C-III) drugs.123
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets | 250 mg* | Carisoprodol Tablets (C-IV) | |
Soma® (C-IV) | ||||
350 mg* | Carisoprodol Tablets (C-IV) | |||
Soma® (C-IV) | Meda |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets | 200 mg with Aspirin 325 mg* | Carisoprodol and Aspirin Tablets (C-IV) | |
200 mg with Aspirin 325 mg and Codeine Phosphate 16 mg* |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
AHFS® Drug Information. © Copyright, 1959-2025, Selected Revisions February 24, 2020. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
Only references cited for selected revisions after 1984 are available electronically.
25. Drug efficacy study, Soma®, Rela®, Soma® Compound, and Soma® Compound with Codeine, National Academy of Sciences-National Research Council
27. BERGER FM, KLETZKIN M, LUDWIG BJ et al. Unusual muscle relaxant and analgesic properties of N-isopropyl-2-propyl-1,3-propanediol dicarbamate (carisoprodol). J Pharmacol Exp Ther . 1959; 127:66-74. [PubMed 13799301]
29. SCHWAB RS. MUSCLE RELAXANTS. Practitioner . 1964; 192:104-8. [PubMed 14106636]
100. Meda Pharmaceuticals Inc. Soma® (carisoprodol) tablets prescribing information. Somerset, NJ; 2018 May.
101. Serfer GT, Wheeler WJ, Sacks HJ. Randomized, double-blind trial of carisoprodol 250 mg compared with placebo and carisoprodol 350 mg for the treatment of low back spasm. Curr Med Res Opin . 2010; 26:91-9. [PubMed 19908948]
102. Ralph L, Look M, Wheeler W. Double-blind, placebo-controlled trial of carisoprodol 250-mg tablets in the treatment of acute lower-back spasm. Curr Med Res Opin . 2008; 24:551-8. [PubMed 18194591]
103. See S, Ginzburg R. Skeletal muscle relaxants. Pharmacotherapy . 2008; 28:207-13. [PubMed 18225966]
104. van Tulder MW, Touray T, Furlan AD et al. Muscle relaxants for non-specific low back pain. Cochrane Database Syst Rev . 2003; :CD004252. [PubMed 12804507]
105. Roelofs PD, Deyo RA, Koes BW et al. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev . 2008; :CD000396. [PubMed 18253976]
106. Chou R, Qaseem A, Snow V et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med . 2007; 147:478-91. [PubMed 17909209]
107. Institute for Clinical Systems Improvement. Health care guideline: adult acute and subacute low back pain. 15th ed. Bloomington, MN; 2012 Jan. From the ICSI website [Web]
108. 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; 26:1355-67. [PubMed 15530999]
109. Watson Laboratories, Inc. Meprobamate tablets prescribing information. Corona, CA; 2004 Apr.
110. Nordeng H, Zahlsen K, Spigset O. Transfer of carisoprodol to breast milk. Ther Drug Monit . 2001; 23:298-300. [PubMed 11360042]
111. Briggs GG, Ambrose PJ, Nageotte MP et al. High-dose carisoprodol during pregnancy and lactation. Ann Pharmacother . 2008; 42:898-901. [PubMed 18460586]
112. Reeves RR, Beddingfield JJ, Mack JE. Carisoprodol withdrawal syndrome. Pharmacotherapy . 2004; 24:1804-6. [PubMed 15585447]
113. Reeves RR, Hammer JS, Pendarvis RO. Is the frequency of carisoprodol withdrawal syndrome increasing?. Pharmacotherapy . 2007; 27:1462-6. [PubMed 17896902]
114. Drug Enforcement Administration (DEA), Department of Justice. Schedules of controlled substances: placement of carisoprodol into schedule IV. 21 CFR Part 1308. Final Rule. [Docket No. DEA-333]. Fed Regist . 2011; 76: 77330-60.
115. Owens C, Pugmire B, Salness T et al. Abuse potential of carisprodol: a retrospective review of Idaho Medicaid pharmacy and medical claims data. Clin Ther . 2007; 29:2222-5. [PubMed 18042478]
116. Fass JA. Carisoprodol legal status and patterns of abuse. Ann Pharmacother . 2010; 44:1962-7. [PubMed 21062909]
117. Boothby LA, Doering PL, Hatton RC. Carisoprodol: a marginally effective skeletal muscle relaxant with serious abuse potential. Hosp Pharm . 2003; 38:337-45.
118. US Department of Health and Human Services, Substance Abuse and Mental Health Services Administration (SAMHSA), Center for Behavioral Health Statistics and Quality. DAWN report: ED visits involving the muscle relaxant carisoprodol. 2011 Oct 27. From the SAMHSA website. [Web]
119. Gonzalez LA, Gatch MB, Taylor CM et al. Carisoprodol-mediated modulation of GABAA receptors: in vitro and in vivo studies. J Pharmacol Exp Ther . 2009; 329:827-37. [PubMedCentral][PubMed 19244096]
120. Dalén P, Alvan G, Wakelkamp M et al. Formation of meprobamate from carisoprodol is catalysed by CYP2C19. Pharmacogenetics . 1996; 6:387-94. [PubMed 8946470]
121. Simon S, D'Andrea C, Wheeler WJ et al. Bioavailability of oral carisoprodol 250 and 350 mg and metabolism to meprobamate: a single-dose crossover study. Curr Ther Res . 2010; 71:50-9. [PubMedCentral][PubMed 24683250]
122. Reeves RR, Mack JE. Possible dangerous interaction of oxycontin and carisoprodol. Am Fam Physician . 2003; 67:2273. [PubMed 12800958]
123. Sandoz. Carisoprodol, aspirin, and codeine phosphate tablets prescribing information. Princeton, NJ; 2018 Aug.
124. Sandoz. Carisoprodol and aspirin tablets prescribing information. Princeton, NJ; 2013 Mar.
125. Carisoprodol. In: Briggs GG, Freeman RK, Yaffe SJ. Drugs in pregnancy and lactation: a reference guide to fetal and neonatal risk. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2011:210-11
209. Qaseem A, Wilt TJ, McLean RM et al. Noninvasive Treatments for Acute, Subacute, and Chronic Low Back Pain: A Clinical Practice Guideline From the American College of Physicians. Ann Intern Med . 2017; 166:514-530. [PubMed 28192789]
210. Friedman BW, Cisewski D, Irizarry E et al. A Randomized, Double-Blind, Placebo-Controlled Trial of Naproxen With or Without Orphenadrine or Methocarbamol for Acute Low Back Pain. Ann Emerg Med . 2018; 71:348-356.e5. [PubMed 29089169]
211. Spence MM, Shin PJ, Lee EA et al. Risk of injury associated with skeletal muscle relaxant use in older adults. Ann Pharmacother . 2013 Jul-Aug; 47:993-8. [PubMed 23821610]
212. Friedman BW, Irizarry E, Solorzano C et al. A Randomized, Placebo-Controlled Trial of Ibuprofen Plus Metaxalone, Tizanidine, or Baclofen for Acute Low Back Pain. Ann Emerg Med . 2019; [PubMed 30955985]
213. Friedman BW, Dym AA, Davitt M et al. Naproxen With Cyclobenzaprine, Oxycodone/Acetaminophen, or Placebo for Treating Acute Low Back Pain: A Randomized Clinical Trial. JAMA . 2015; 314:1572-80. [PubMed 26501533]