Carisoprodol, sold under the brand name Soma among others, is an oral medication used for musculoskeletal pain.
Effects generally begin within half an hour and last for up to six hours.
Routes of administration By mouth
Muscle relaxant
Protein binding 60%
Metabolism Liver (CYP2C19-mediated)
Metabolites-Meprobamate
Onset of action
Rapid (30 minutes) Elimination half-life 2.5 hours Excretion Kidney
Common side effects include headache, dizziness, and sleepiness.
Serious side effect may include addiction, allergic reactions, and seizures.
Safety during pregnancy and breastfeeding is not clear.
Some of its effects are believed to occur following being converted into meprobamate.
It is a Schedule IV controlled substance.
It comes in tablet format and is taken by the mouth three times a day and before bed.
The usual dose of 350 mg is unlikely to engender prominent side effects other than somnolence, and mild to significant euphoria or dysphoria, but the euphoria is generally short-lived due to the fast metabolism of carisoprodol into meprobamate and other metabolites.
Carisoprodol’s potent anxiolytic effects are far stronger than those produced by its primary metabolite, meprobamate, which is often misblamed for the drug-seeking associated with carisoprodol, as carisoprodol itself is responsible for the significantly more intense central nervous system effects than meprobamate alone.
The medication is well tolerated and without adverse effects in the majority of patients for whom it is indicated.
In some patients it can have sedative side effects and can impair the patient’s ability to operate a firearm, motor vehicles, and other machinery of various types, especially when taken with medications containing alcohol, in which case an alternative medication would be considered.
The intensity of the side effects of carisoprodol tends to lessen as therapy continues.
Other side effects include: dizziness, clumsiness, headache, fast heart rate, upset stomach, vomiting and skin rash.
There are 368 drugs known to interact with carisoprodol including 28 major drug interactions.
The interaction of carisoprodol with essentially all opioids, and other centrally acting analgesics, but especially codeine, those of the codeine-derived subgroups of the semisynthetic class allows the use of a smaller dose of the opioid to have a given effect, is useful in general and especially where skeletal muscle injury and/or spasm is a large part of the problem.
This potentiation effect is also useful in other pain situations and is also especially useful with opioids such as methadone, and others.
In recreational drug users, deaths have resulted from combining doses of hydrocodone and carisoprodol.
The misuse of carisoprodol and opiates has the potential to asphyxiate while unconscious.
Carisoprodol is metabolized by the liver and excreted by the kidneys, so this drug must be used with caution with patients that have impaired hepatic or renal function.
This drug is on the list to avoid for elderly people.
Carisoprodol, meprobamate, and related drugs have the potential to produce physical dependence of the barbiturate type following periods of prolonged use.
Withdrawal of the drug after extensive use may require hospitalization in medically compromised patients.
In severe cases the withdrawal can mimic the symptoms of alcohol withdrawal including the potentially lethal status epilepticus.
Psychological dependence is linked to carisoprodol use although this is much less severe than with meprobamate itself,
Psychological dependence is more common in those who use carisoprodol non-medically and those with a history of substance abuse.
Psychological dependence may reach clinical significance before physiological tolerance.
Discontinuation of carisoprodol, can result in cognitive changes which persist for weeks, months, or rarely even years.
Changes include greatly increased anxiety and depression, social withdrawal, hair-trigger aggression, chronic insomnia, new or aggravated phobias, reduced IQ, short term and long-term memory loss, and dozens of other sequelae.
The effects, severity, and duration appear dose-dependent, patients pattern of use, genetic predisposition to substance use, and a history of substance use all increase the patients risk of persistent discontinuation syndrome symptoms.
Treatment for physical withdrawal generally involves switching the patient to a long-acting benzodiazepine, and slowly titrating them off the replacement drug completely.
Psychotherapy and cognitive behavioral therapy have demonstrated moderate success in reducing the rebound anxiety which results upon discontinuation.
Carisoprodol withdrawal can be life-threatening.
Combining a muscle relaxant like carisoprodol with opioids and benzodiazepines potentiates the effects.
Recreational users of carisoprodol usually seek its potentially heavy sedating, relaxant, and anxiolytic effects.
Because of its potentiating effects on narcotics, it is often used in conjunction with many opioid drugs.
As with other GABAergic drugs, combination with other drugs that depress the respiratory system, such as alcohol, sedatives and opioids possess a significant risk to the user in the form of overdose.
Overdose symptoms are similar to those of other GABAergics including excessive sedation and unresponsiveness to stimuli, severe ataxia, amnesia, confusion, agitation, intoxication and inappropriate behavior.
Severe overdoses may present with respiratory depression, subsequent pulmonary aspiration, coma, and death.
Carisoprodol is not detected on all toxicology tests.
Overdose symptoms distinguished from opioids by the presentation of normal or pinpoint pupils, which are generally unresponsive to light.
Carisoprodol, as with its metabolite meprobamate, is dangerous in combination with alcohol.
Flumazenil (the benzodiazepine antidote) is not effective in the management of carisoprodol overdose as carisoprodol acts at the barbiturate binding site.
Treatment of overdose is generally supportive, including the administration of mechanical respiration and pressors as indicated and.
Total amnesia of the experience is not uncommon following recovery.
Carisoprodol’s structural similarity to meprobamate indicates GABAergic activity, including GABAA agonism, similar to the mechanism of benzodiazepines.
Carisoprodol has a rapid, 30-minute onset of action, with the effects lasting about two to six hours.
It is metabolized in the liver via the cytochrome P450 oxidase isozyme CYP2C19, excreted by the kidneys and has about an eight-hour half-life.
A considerable proportion of carisoprodol is metabolized to meprobamate.
Meprobamate is a known addictive substance, and accounts for the addictive potential of carisoprodol.
Carisoprodol possesses stronger muscle relaxant and analgesic than meprobamate.
Crisoprodol has addictive potential[ as a prodrug of meprobamate and/or potentiator of hydrocodone, oxycodone, codeine, and similar drugs.
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