ArticlePDF AvailableLiterature Review

Carisoprodol: Update on Abuse Potential and Legal Status

Authors:

Abstract and Figures

Carisoprodol is a centrally acting skeletal muscle relaxant of which meprobamate, a controlled substance, is the primary active metabolite. The abuse of carisoprodol has increased dramatically in the last several years. A withdrawal syndrome occurs in some patients who abruptly cease carisoprodol intake. The symptoms of this syndrome are similar to those seen with meprobamate withdrawal, suggesting that they may result from withdrawal from meprobamate accumulated with intake of excessive carisoprodol; however, carisoprodol is capable of modulating GABAA function, which may contribute to its abuse potential.There has been considerable debate about whether carisoprodol should be considered a controlled substance. Carisoprodol was removed from the market in Norway on May 1, 2008, but may still be used by specially approved patients. Carisoprodol was classified as a controlled substance in several US states, and effective January 11, 2012, became a schedule IV controlled substance at the US federal level. This article updates the literature on abuse potential and examines recent developments regarding the legal status of carisoprodol.
Content may be subject to copyright.
Carisoprodol: Update on Abuse Potential
and Legal Status
Roy R. Reeves, DO, PhD, Randy S. Burke, PhD, and Samet Kose, MD, PhD
Abstract: Carisoprodol is a centrally acting skeletal muscle relaxant
of which meprobamate, a controlled substance, is the primary active
metabolite. The abuse of carisoprodol has increased dramatically in
the last several years. Awithdrawal syndrome occurs in some patients
who abruptly cease carisoprodol intake. The symptoms of this syn-
drome are similar to those seen with meprobamate withdrawal, sug-
gesting that they may result from withdrawal from meprobamate
accumulated with intake of excessive carisoprodol; however, car-
isoprodol is capable of modulating GABA
A
function, which may
contribute to its abuse potential.
There has been considerable debate about whether carisoprodol
should be considered a controlled substance. Carisoprodol was re-
moved from the market in Norway on May 1, 2008, but may still be
used by specially approved patients. Carisoprodol was classified as a
controlled substance in several US states, and effective January 11,
2012, became a schedule IV controlled substance at the US federal
level. This article updates the literature on abuse potential and ex-
amines recent developments regarding the legal status of carisoprodol.
Key Words: carisoprodol, controlled substances, substance abuse
Carisoprodol (N-isopropyl-2 methyl-2-propyl-1,3-propanediol
dicarbamate; N-isopropylmeprobamate; C
12
H
24
N
2
O
4
,mo-
lecular weight 260.33) is a skeletal muscle relaxant available as
250- and 350-mg tablets with a recommended dosage of one
tablet three to four times daily for both strengths. Carisoprodol
is marketed in the United States under the brand name Soma
(MedPointe Healthcare, Somerset, NJ), in the United Kingdom
under the brand name Carisoma (Forest Laboratories UK Ltd,
Kent, UK), and in other countries under the brand names Sonoma,
Somadril, Somacid, Scutamil C, Relacton-C, Mio Relax and
Relaxibys. Carisoprodol has been distributed in the United
States under the brand names Rela and Soridol.
1
Carisoprodol is
commonly prescribed for relief of pain associated with mus-
culoskeletal conditions. A search of Intercontinental Marketing
Services data from January 2003 to January 2004 showed that
carisoprodol, cyclobenzaprine, and metaxalone represented
more than 45% of all prescriptions for the management of
musculoskeletal pain.
2
There has been concern and debate about whether car-
isoprodol should be classified as a controlled substance
because the drug acts centrally, causing sedation.
1
It is me-
tabolized to meprobamate, which activates barbiturate-like
GABA
A
receptors and is itself a schedule IV controlled sub-
stance at the US federal level. Meprobamate was shown to have
a risk of addiction similar to that of benzodiazepines, which are
well known to be drugs of abuse.
3
Meprobamate is a carbamate derivative that is pharma-
cologically similar to barbiturates, which was introduced as an
antianxiety agent in 1955 and marketed under the brand names
Miltown and Equanil. The drug was popular as a sedative-
hypnotic, but was replaced by benzodiazepines. The potential
for abuse and addiction related to meprobamate was quickly
Key Points
&Carisoprodol has potential for abuse for multiple reasons. The
drug is metabolized to meprobamate, a controlled substance
with proven abuse potential. Carisoprodol itself is capable of
modulating GABA
A
function, which also may contribute to
its potential for abuse.
&Numerous case reports of carisoprodol abuse have been
published. Some patients who abruptly cease intake of large
amounts of carisoprodol have experienced a withdrawal
syndrome consisting of insomnia, vomiting, tremors, muscle
twitching, anxiety, ataxia, and sometimes hallucinations and
delusions.
&Carisoprodol has been withdrawn from the market in Norway,
but may still be used in speciallyapproved patients. The European
Medicines Agency has recommended that carisoprodol-
containing products be removed from the market in other
European countries . Effective January 11, 2012, carisoprodol
was classified as a schedule IV controlled substance at the
federal level in the United States.
&Clinicians should exercise appropriate caution when pre-
scribing carisoprodol.
Review Article
Southern Medical Journal &Volume 105, Number 11, November 2012 619
From the G.V. (Sonny) Montgomery VA Medical Center, Mental Health Ser-
vice, and the Department of Psychiatry, University of Mississippi School of
Medicine, Jackson, Mississippi.
Reprint requests to Dr Roy R. Reeves, Chief of Psychiatry (11M), VA Medical
Center, 1500 E. Woodrow Wilson Dr, Jackson, MS 29216. Email:
roy.reeves@va.gov
The authors have no financial relationships to disclose and no conflicts of
interest to report.
Accepted June 8, 2012.
Copyright *2012 by The Southern Medical Association
0038-4348/0Y2000/105-619
DOI: 10.1097/SMJ.0b013e31826f5310
Copyright © 2012 The Southern Medical Association. Unauthorized reproduction of this article is prohibited.
recognized because reports of misuse appeared in the literature
within 2 years of being placed on the market.
4
The chemical
nomenclature suggests that carisoprodol is structurally related
to meprobamate. Meprobamate and carisoprodol differ only by
the substitution of a hydrogen atom for an isopropyl group on
one of the carbamyl nitrogens. Carisoprodol itself may also
activate GABA
A
receptors
5
; therefore, carisoprodol has po-
tential for being abused.
Carisoprodol has been scheduled as a controlled substance
in several US states. In 1996, the US Drug Enforcement Ad-
ministration (DEA) recommended scheduling at the federal
level, but the US Food and Drug Administration (FDA) Drug
Advisory Committee concluded that there was insufficient
evidence
6
; however, since that time, additional information led
the DEA to alter this conclusion.
Carisoprodol Abuse
Numerous reports describe more than 30 individuals abusing
carisoprodol under various conditions.
7Y19
Carisoprodol has been
abused (usually in amounts much larger than the recommended
daily dosage) for its sedative and relaxant effects. It has been used
to augment or alter the effects of other drugs (eg, to increase the
sedating effects of benzodiazepines or alcohol, prevent jitteriness
during cocaine consumption, and help calm individuals after an
episode of cocaine use). Some patients have substituted car-
isoprodol for opiates or benzodiazepines when those substances
were not available. Others have combined carisoprodol with other
drugs to intentionally produce a synergistic effect, resulting in
significant relaxation and euphoria. Abuse has involved the
planned procurement of carisoprodol and other noncontrolled
medications because of the ease (as compared with controlled
substances) of obtaining prescriptions. A concise overview of
reports of carisoprodol abuse and withdrawal is available.
20
Reeves and colleagues surveyed 40 carisoprodol users
and found that among those with a history of substance abuse
(n = 20), 40% used carisoprodol in larger than prescribed
amounts: 30% to obtain an effect other than that for which it
was prescribed, 10% to augment the effect of another drug, and 5%
to counteract another medication.
21
Twenty percent attempted to
obtain extra carisoprodol by prescription and 10% obtained it by
means other than a legal prescription. Owens and colleagues
reviewed 2005 Idaho Medicaid claims and surveyed pharmacies
filling prescriptions for long-term carisoprodolusers (N = 340).
22
Patients prescribed carisoprodol used opioids and other drugs
more frequently, and 80% of patients continued to pay out of
pocket for carisoprodol when Medicaid coverage ended.
Prisoners in Norway taking 700 to 2100 mg/day of car-
isoprodol for at least 9 months and then withdrawing from the
drug reported anxiety, insomnia, irritability, cranial and mus-
cular pain, and anergy.
23
Withdrawal symptoms occurred in 2
patients following cessation of doses as low as 4 to 8 tablets
daily.
16
More severe symptoms occurred in 5 patients who
stopped daily intake of 2100 to 4200 mg.
24
Carisoprodol withdrawal syndrome was described in
2004
25
by a 43-year-old man taking more than thirty 350-mg
carisoprodol tablets per day. Within 48 hours of cessation he
developed anxiety, tremors, muscle twitching, insomnia, hal-
lucinations, and bizarre behavior, peaking on the fourth day. He
was treated with olanzapine and lorazepam. Four other cases
were subsequently described.
26Y28
They shared similar char-
acteristics: cessation from daily intake of 12 to 25 carisoprodol
tablets followed by anxiety, tremulousness, insomnia, psy-
chomotor agitation, hallucinations (auditory and/or visual),
and paranoia. Treatment involved benzodiazepines and/or
antipsychotics until withdrawal symptoms resolved, typically
within 4 to 6 days. The likely mechanism for carisoprodol
withdrawal syndrome is withdrawal from meprobamate accu-
mulated with intake of excessive carisoprodol, although the
capacity of carisoprodol to modulate GABA
A
function also
may contribute to withdrawal symptoms.
26Y28
It is not known
whether carisoprodol has cross-tolerance with other sedative
drugs, although case reports of patients substituting car-
isoprodol for benzodiazepines and opiates suggest the possi-
bility of this substitution. Another case report noted that the
benzodiazepine antidote flumazenil reversed carisoprodol in-
toxication in a 52-year-old woman,
29
suggesting similarities in
the actions of carisoprodol and benzodiazepines.
Animal studies support the development of tolerance and
withdrawal from meprobamate and carisoprodol. Hyperexcit-
ability was shown to be detectable in mice 4 to 8 hours after
drug withdrawal following chronic administration of mepro-
bamate. This excitation subsides within 28 hours.
30
In another
study, mice were administered carisoprodol (0, 100, 200, 300,
or 500 mg/kg) for 4 days.
31
The loss of righting reflex (a mea-
sure of coordination) was measured 20 to 30 minutes following
each administration. On day 4, 20 mg/kg bemegride (a drug
not used clinically in humans that antagonizes the effects of
barbiturates), 20 mg/kg flumazenil, or vehicle was administered
following carisoprodol, after which withdrawal signs were
measured. Separate groups of mice receiving the same treatment
were tested for spontaneous withdrawal at 6, 12, and 24 hours
following the last dose of carisoprodol. The first administration
of carisoprodol produced a substantial dose-dependent loss of
motor coordination as measured by the loss of righting score. A
75% to 100% decrease in the impairment of the righting reflex
occurred during the 4 days of exposure, indicating the devel-
opment of tolerance to carisoprodol. Withdrawal signs were not
observed with carisoprodol cessation; however, bemegride and
flumazenil each precipitated withdrawal within 15 to 30 minutes
of administration. Carisoprodol administration resulted in tol-
erance and antagonist precipitated withdrawal, suggesting sig-
nificant potential for addiction.
Carisoprodol and Public Safety
Carisoprodol may impair a person’s ability to drive, as
reported by Logan and colleagues, who investigated drivers in
whom carisoprodol or meprobamate was detected following
Reeves et al &Carisoprodol: Update on Abuse Potential and Legal Status
620 *2012 Southern Medical Association
Copyright © 2012 The Southern Medical Association. Unauthorized reproduction of this article is prohibited.
accidents or arrests for impaired driving.
32
In 21 cases, no other
drugs were detected. Signs of intoxication occurred in some
patients, even when combined serum concentrations of car-
isoprodol and meprobamate were within the therapeutic range.
Bramness and colleagues reviewed 62 cases of drivers in whom
carisoprodol and meprobamate were the only drugs identi-
fied.
33
Impaired drivers (73%) had higher blood carisoprodol
concentrations than unimpaired drivers, but no difference in
blood meprobamate concentration was found for all drivers
reviewed together. Thus, carisoprodol alone can have an
impairing effect at higher blood levels. An obvious concern is
the degree of impairment that could occur when carisoprodol
and alcohol are combined; however, the impact of combining
alcohol and carisoprodol on driver performance has not been
formally investigated.
Hoiseth and colleagues assessed the impact of the
scheduling of carisoprodol in Norway.
34
Driving under the
influence cases involving carisoprodol dropped 7% to 8% from
2004 to 2006, 5% in 2007, and 1% in 2008. Detection of the
drug during autopsies dropped 3% from 2004 to 2006, 2.5% in
2007, and 0.6% in 2008. Poison control contacts regarding
carisoprodol decreased from 1% between 2004 and 2006, to
0.8% in 2007, and 0.3% in 2008. Zacny and colleagues ad-
ministered subjects 0, 350, and 700 mg of carisoprodol. For the
next 6 hours they administered a battery of tests at fixed
intervals to assess subjective and psychomotor effects.
35
The
therapeutic dose (350 mg), although producing few or mild
subjective effects, still produced psychomotor impairment,
leading to concern that patients prescribed carisoprodol may
feel normal and engage in tasks such as driving that could place
themselves and others at risk. The same researchers showed
that the administration of oxycodone and carisoprodol within
60 minutes of each other produced effects that are of concern
for abuse liability and public safety.
36
Evidence of Increasing Carisoprodol Misuse
The Drug Abuse Warning Network reports a steady in-
crease in emergency department visits involving carisoprodol.
Carisoprodol-related visits more than doubled, from 6569 visits
in 1994 to 14,376 in 2004 and more than doubled to 29,980 by
2009 (Fig.).
37,38
National Survey on Drug Use and Health data
from 2002Y2005 demonstrated that incidences of misuse of
carisoprodol were approximately equal to those of clonaze-
pam.
39
The 2008 annual report of the American Association of
Poison Control Centers reported 2632 intentional carisoprodol
exposures requiring medical treatment.
40
The 2009 Monitoring
the Future national survey on drug use showed an annual
prevalence of carisoprodol abuse by high school seniors of
1.3% in 2007 and 1.4% in 2008; these rates are higher than
those for lorazepam and clonazepam.
41
Carisoprodol abuse is common in the southern United
States, and in 1991 the Mississippi Board of Pharmacy issued a
warning that carisoprodol abuse was increasing. Two phar-
macists in the state were fined and given probation after 71,000
doses of the drug were discovered missing. An investigation
showed that certain patients may have taken Q20 carisoprodol
tablets daily.
42
Theft or loss of carisoprodol also was reported in
neighboring Louisiana and Alabama. In Alabama, pharmacists
were sanctioned by their licensing boards for personal misuse
of the drug.
42
Davis and Alexander performed a retrospective
study on deceased individuals who were examined at the Jef-
ferson County (Alabama) medical examiner’s office from
January 1, 1986 to October 31, 1997 and reported that car-
isoprodol was detected in 24 cases.
43
They concluded that
carisoprodol was ‘‘probably responsible, in part, for those
deaths.’’ Texas poison control centers received 936 car-
isoprodol-related calls from 1998 to 2003.
44
It was reported
that for many years carisoprodol distributed under the brand
name Somacid could be obtained easily in large quantities (up
to several thousand pills at a time) in Mexican pharmacies near
the US border and transported into the United States.
45
A study of the Norwegian Prescription Database revealed
that in 2004, 83,713 individuals were prescribed car-
isoprodol.
46
Many patients used more carisoprodol than was
recommended in treatment guidelines. High carisoprodol use
was associated with high benzodiazepine and opiate use.
Patients abusing carisoprodol often received prescriptions from
doctors widely known to overprescribe. In Norway, the com-
pany that distributed carisoprodol agreed to withdraw mar-
keting authorization for carisoprodol-containing products.
47
Legal Status of Carisoprodol
Although evidence of abuse is widespread, legal action to
declare carisoprodol a controlled substance has occurred pri-
marily in Norway and the United States. In August 2007,
Norway reclassified carisoprodol to class A (their highest
scheduling level, in which opiates and amphetamines also are
classified). Carisoprodol was withdrawn from the market in
Norway on May 1, 2008, but, after application to the Norwe-
gian Medication Agency, could still be used by patients for
whom there were no alternative therapies.
34
In September
Fig. Emergency department (ED) visits related to carisoprodol
reported by the Drug Abuse Warning Network.
Review Article
Southern Medical Journal &Volume 105, Number 11, November 2012 621
Copyright © 2012 The Southern Medical Association. Unauthorized reproduction of this article is prohibited.
2007, the European Medicines Agency’s Committee for Me-
dicinal Products for Human Use concluded that carisoprodol’s
risks outweighed its benefits and recommended the suspension
of marketing authorization for carisoprodol-containing pro-
ducts in European Union member states.
48
To the best of the
authors’ knowledge, this action occurred only in Norway.
Abuse concerns have resulted in carisoprodol being
classified as a controlled substance in several US states. As
early as 1998, the drug was classified a schedule IV substance
in Alabama.
43
Fass showed that carisoprodol was classified a
schedule IV substance in 18 states (Alabama, Arizona, Arkansas,
Florida, Georgia, Hawaii, Indiana, Kentucky, Louisiana,
Massachusetts, Minnesota, Nevada, New Mexico, Oklahoma,
Oregon, Texas, Washington, and West Virginia) and was under
monitoring programs in North Dakota and Ohio.
6
Since then,
Tennessee (April 7, 2011),
49
Wyoming (July 1, 2011),
50
and
Mississippi (July 1, 2011)
51
have classified carisoprodol as
schedule IV.
After considerable debate, significant activity has occurred
at the federal level, including a ruling by the DEA to clas-
sify carisoprodol as a schedule IV controlled substance. The
December 12, 2011, issue of the Federal Register examines this
decision in detail.
52
Pertinent considerations included ‘‘car-
isoprodol possesses sedative properties that may underlie its
therapeutic usefulness and potential for abuse’’; ‘‘recent in vitro
studies demonstrated that carisoprodol possesses barbiturate-
like effects;’’ ‘‘carisoprodol’s discriminative stimulus effects
are similar to other Schedule IV drugs such as barbital, mep-
robamate, and chlordiazepoxide;’’ and ‘‘the record demon-
strates that excessive carisoprodol use creates toxicity and
withdrawal symptoms similar to other Schedule IV drugs.’’ The
FDA stated, ‘An evaluation of published case reports and case
series, the FDA Adverse Event Reporting System and the
SAMHSA DAWN databases, show that carisoprodol as cur-
rently used, raises concerns not only for the health and safety of
the users but also for the public because of exposure to those
who use carisoprodol.’
With this ruling, the DEA placed carisoprodol, its salts,
isomers, and salts of its isomers into schedule IV of the Con-
trolled Substances Act, effective January 11, 2012. ‘Thereafter
any person who engages in the manufacture, distribution,
dispensing, importing, exporting, as well as any person who
possesses the drug will be subject to the provisions of the Act
and DEA regulations, including the Act’s administrative, civil,
and criminal sanctions which are applicable to Schedule IV
controlled substances,’’ including registration, disposal of
stocks, security, labeling and packaging, inventory, records,
and prescriptions. There is no definite gauge or way to predict
the impact that classifying carisoprodol as schedule IV at the
federal level will have on the use of the drug. Meprobamate was
used as a sedative hypnotic for many years after being
scheduled a controlled substance and is still available but
typically not prescribed. The decrease in use may have been the
result of concern about abuse and the drug’s essentially being
replaced by the increased use of benzodiazepines. What is
likely to happen with carisoprodol use in the United States is
uncertain, although the authors propose that some decrease in
both legal and illicit consumption as was seen in Norway may
be the most likely scenario.
In conclusion, carisoprodol is a schedule IV controlled
substance at the federal level in the United States, creating
applicable regulations, regardless of scheduling in individual
states. Carisoprodol has been classified as schedule A in
Norway and was removed from the market, but may still be
used by specially approved patients. The European Medicines
Agency has recommended similar actions by other European
countries, with action by these countries to be determined.
Clearly, clinicians should be aware of the abuse potential of
carisoprodol and exercise appropriate caution when prescrib-
ing the drug.
References
1. Littrell RA, Hayes LR, Stillner V. Carisoprodol (Soma): a new and
cautious perspective on an old agent. South Med J 1993;86:753Y756.
2. 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;26:1355Y1367.
3. Rho JM, Donevan SD, Rogawski MA. Barbiturate-like actions of the
propanediol dicarbamates felbamate and meprobamate. J Pharmacol
Exp Ther 1997;280:1383Y1391.
4. Ewing JA, Fullilove RE. Addiction to meprobamate. NEnglJMed
1957;257:76Y77.
5. Gonzalez LA, Gatch MB, Forster MJ, et al. Abuse potential of Soma: the
GABA(A) receptor as a target. Mol Cell Pharmacol 2009;1:180Y186.
6. Fass JA. Carisoprodol legal status and patterns of abuse. Ann Pharmacother
2010; 44:1 962Y1967.
7. Morse RM, Chua L. Carisoprodol dependence: a case report. Am J Drug
Alcohol Abuse 1978;5:527Y530.
8. Luehr JG, Meyerle KA, Larson EW.Mail-order (veterinar y) drug dependence.
JAMA 1990;263:657.
9. Elder NC. Abuse of skeletal muscle relaxants. Am Fam Physician 1991;44:
1223Y1226.
10. Rust GS, Hatch R, Gums JG. Carisoprodol as a drug of abuse. Arch Fam
Med 1993;429Y432.
11. Sikdar S, Basu D, Malhotra AK, et al. Carisoprodol abuse: a report from
India. Acta Psychiatr Scand 1993;88:302Y303.
12. Dougherty RJ. Carisoprodol should be a controlled substance. Arch Fam
Med 1995;4:582.
13. Heacock C, Bauer MS. Tolerance and dependence risk wi th the use of
carisoprodol. Am Fam Physician 2004;69:1622Y1623.
14. Reeves RR, Mack JE. Possible dangerous interaction of oxycontin and
carisoprodol. Am Fam Physician 2003;67:941Y942.
15. Littrell RA, Sage T, Miller W. Meprobamate dependence secondary to
carisoprodol (Soma) use. Am J Drug Alcohol Abuse 1993;19:133Y134.
16. Reeves RR, Pinkofsky HB, Carter OS. Carisoprodol: a drug of continuing
abuse. J Am Osteopath Assoc 1997;97:723Y724.
17. Reeves RR, Carter OS, Pinkofsky HB. Use of carisoprodol by substance
abusers to modify the effects of illicit drugs. South Med J 1999;92:441.
18. Reeves RR, Liberto V. Abuse of combinations of carisoprodol and
tramadol. South Med J 2001;94:512Y514.
19. Reeves RR,Henderson RH, Ladner MD. Carisoprodol abuse in Mississippi.
J Miss State Med Assoc 2007;363Y365.
20. Reeves RR, Burke RS. Carisoprodol: abuse potential and withdrawal
syndrome. Curr Drug Abuse Reviews 2010;3:33Y38.
Reeves et al &Carisoprodol: Update on Abuse Potential and Legal Status
622 *2012 Southern Medical Association
Copyright © 2012 The Southern Medical Association. Unauthorized reproduction of this article is prohibited.
21. Reeves RR, Carter OS, Pinkofsky HB, et al. Carisoprodol (soma): abuse
potential and physician unawareness. J Addict Dis 1999;18:51Y56.
22. Owens C, Pugmire B, Salness T, et al. Abuse potential of carisoprodol: a
retrospective reviewof Idaho Medicaid pharmacy and medical claims data.
Clin Ther 2007;29:2222Y2225.
23. Wyller TB, Korsmo G, Gadeholt G. Dependence on carisoprodol (Somadril)?
A prospective study among prisoners. Tidsskr Nor Laegeforen 1991;111:
193Y195.
24. Reeves RR, Parker JD. Somatic dysfunction during carisoprodol withdrawal
syndrome. J Am Osteopath Assoc 2003;103:75Y80.
25. Reeves RR, Beddingfield JJ, Mack JE. Carisoprodol withdrawal syndrome.
Pharmacotherapy 2004;24:1804Y1806.
26. Rohatgi G, Rissmiller DJ, Gorman JM. Treatment of carisoprodol
dependence: a case report. J Psychiatr Pract 2005;11:347Y352.
27. Reeves RR, Hammer JS, Pendarvis RO. Is the frequency of carisoprodol
withdrawal syndrome increasing? Pharmacotherapy 2007;27:1462Y1466.
28. Eleid MF, Krahn LE, Agrwal N, et al. Carisoprodol withdrawal after
internet purchase. Neurologist 2010;16:262Y264.
29. Roberge RJ, Lin E, Krenzelok EP. Flumazenil reversal of carisoprodol
(Soma) intoxication. J Emerg Med 2000;18:61Y64.
30. Swinyard EA, Chin L, Fingl E. Withdrawal hyperexcitability following
chronic administration of meprobamate to mice. Science 1957;125:
739Y741.
31. Gatch MB, Nguyen JD, Carbonaro T, et al. Carisoprodol tolerance and
precipitated withdrawal. Drug Alcohol Depend 2012;123:29Y34.
32. Logan BK, Case GA, Gordon AM. Carisoprodol, meprobamate, and
driving impairment. J Forensic Sci 2000;45:619Y623.
33. Bramness JG, Skurtveit S, Morland J. Impairment due to intake of
carisoprodol. Drug Alcohol Depend 2004;74:311Y318.
34. Hoiseth G, Karinen R, Sorlid HK, et al. The effect of scheduling and
withdrawal of carisoprodol on the prevalence of intoxications with the
drug. Basic Clin Pharmacol Toxicol 2009;105:345Y349.
35. Zacny JP, Paice JA, Coalson DW. Characterizing the subjective and
psychomotor effects of carisoprodol in healthy volunteers. Pharmacol
Biochem Behav 2011;100:138Y143.
36. Zacny JP, Paice JA, Coalson DW. Subjective and psychomotor effects of
carisoprodol in combination with oxycodone in healthy volunteers.
Drug Alcohol Depend 2012;120:229Y232.
37. Department of Health and Human Services. Emergency department
trends from the Drug Abuse Warning Network, final estimates 1994Y2001.
http://www.oas.samhsa.gov/DAWN/Final2k1EDtrends/text/EDtrend
2001v6.pdf. Published August 2002. Accessed December 12, 2011.
38. Substance Abuse and Mental Health Services Administration, Drug Abuse
Warning Network. National Estimates of Drug-Related Emergency
Department Visits. HHS Publication No. (SMA) 11-4659, DAWN Ser
D-35. Rockville, MD: Substance Abuse and Mental Health Services
Administration; 2011.
39. Office of Applied Studies, Substance Abuse and Mental Health Services.
National survey on drug use and health. www.oas.samhsa.gov/nsduh.htm.
Accessed December 12, 2011.
40. Bronstein AC, Spyker DA, Cantilena LR, et al. 2008 Annual Report of
the American Association of Poison Control Centers’ National Poison
Data System (NPDS): 26th annual report. Clin Toxicol (Phila) 2009;47:
911Y1084.
41. Deleted in proof.
42. Ukens C. Carisoprodol abuse on rise, warns Mississippi board. Drug
Topics 1992;19:13.
43. Davis GG, Alexander CB. A review of carisoprodol deaths in Jefferson
County, Alabama. South Med J 1998;91:726Y730.
44. Forrester MB. Carisoprodol abuse in Texas, 1998Y2003. J Med Toxicol
2006;2:8Y13.
45. Deleted in proof.
46. Bramness JG, Furu K, Engeland A, et al. Carisoprodol use and abuse in
Norway. A pharmacoepidemiological study. Br J Clin Pharmacol
2007;64:210Y218.
47. European Medicines Agency. Questions and answers on the rec-
ommendation to suspend the marketing authorizations for carisoprodol-
containing medicines. Doc. ref. EMEA/520140/2007, November 15, 2007.
48. European Medicines Agency. European Medicines Agency recommends
suspension of marketing authorizations for carisoprodol-containing
medicinal products. Doc. ref. EMEA/520463/2007, November 16, 2007.
49. Tennessee Board of Pharmacy. Tramadol and carisoprodol now classified
schedule IV. Tennessee Board Pharm News 2011;13:1.
50. Wyoming Board of Pharmacy. Tramadol and carisoprodol to become
Schedule IV in Wyoming. Wyoming State Board Pharm Newsl 2011;20:1.
51. Mississippi Board of Pharmacy. Annual controlled substance inventory.
Mississippi Board Pharm Newsl May 2011.
52. Drug Enforcement Administration. Schedule of controlled substances:
placement of carisoprodol into Schedule IV. Fe d Re g 2011;76:
77330Y77360.
Review Article
Southern Medical Journal &Volume 105, Number 11, November 2012 623
Copyright © 2012 The Southern Medical Association. Unauthorized reproduction of this article is prohibited.
... Meningkatnya popularitas carisoprodol pada anak SMA menjadi perhatian, Mengacu kepada Monitoring the Future National Survey on Drug Use (2009) melaporkan penggunaan carisoprodol selain untuk pengobatan terjadi peningkatan pada remaja SMA masing-masing 1,3% dan 1,4% pada tahun 2007 dan 2008. Angka penyalahgunaan obat ini lebih tinggi daripada obat yang lainya seperti chlordiazepoxide (0,2%) dan sebanding dengan Clonazepam (1,3%) 9 . ...
Article
Full-text available
Penggunaan obat yang rasional (POR), sangat penting bagi para konsumen obat, yang diperlukan agar tidak terjadi penyalahgunaan obat atau pengguunaan obat yang tidak sesuai anjuran. Walaupun namanya tidak sepopuler obat-obatan yang lain, obat zenith cukup dikenal terutama di antara mereka yang sering stress atau banyak bekerja keras. Namun, sayangnya obat zenith Carnophen seringkali disalahgunakan oleh sebagian orang penggunaannya sebagai obat pengganti narkoba. Sama seperti obat lainnya, obat ini memiliki efek samping kalau dikonsumsi secara berlebihan. Berdasarkan hal tersebut maka perlu dilakukannya kegiatan pemberian informasi kepada masyarakat terutama para remaja mengenai bahaya penggunaak pil Zenith. Tujuan kegiatan pengabdian masyarakat ini adalah untuk meningkatkan wawasan mengenai penyalahgunaan obat / pil Zenith di kalangan remaja. Kegiatan pangabdian dilakukan dengan metode daring (online) via Zoom. Penyuluhan berlangsung sangat baik dan lancar, dibuktikan dengan antusiasme peserta yang aktif saat tanya jawab dan hasil kuis. PENDAHULUAN Penggunaan obat yang rasional, sangat penting bagi para konsumen obat. POR (Penggunaan Obat Rasional) diperlukan agar tidak terjadi penyalahgunaan obat atau pengguunaan obat yang tidak sesuai anjuran. Walaupun namanya tidak sepopuler obat-obatan yang lain, obat zenith (Carnophen) cukup dikenal terutama di antara mereka yang sering stress atau banyak bekerja keras. Kandungan dalam obat ini memang dikenal bisa membantu dua kondisi tersebut. Namun, sayangnya obat zenith (Carnophen) seringkali disalahgunakan oleh sebagian orang penggunaannya sebagai obat pengganti narkoba. Dalam dosis dan penggunaan yang tepat, obat ini jelas membawa banyak manfaat positif. Sayangnya obat ini sering kali disalahgunakan justru karena manfaat yang diberikan. Apabila diminum secara berlebihan melebihi Dosis yang dianjurkan, obat ini bisa menimbulkan efek memabukan. Konsumen menjadi tidak sadar dan mengalami perasaan senang yang luar
... 59 In an acute overdose of carisoprodol and meprobamate symptoms including sedation, coma, cardiovascular collapse, and in rare cases, pulmonary edema and myoclonic jerks have been noted. 60,61 Overdoses with chloral hydrate often occur with coingestion of ethanol, and the overall toxicologic effects include coma, cardiac instability (including ventricular dysrhythmias), decreased cardiac contractility, sensitivity to catecholamines, gastrointestinal issues, and hemorrhagic gastritis. 51 The toxicologic effects of GHB, sodium oxybate, g-butyrolactone, and 1,4-butanediol include CNS depression, euphoria, seizures, anterograde amnesia, and hypothermia. ...
Article
Over the last 2 decades, prescription and nonprescription substance use has significantly increased. In this article, 3 particular drug classes-opioids, sedatives, and hypnotics-are discussed. For each class, a brief history of the agent, a description of relevant pharmacology, the clinical presentation of overdose, the management of specific drug overdoses, and a summary of salient points are presented. The intent is to provide a clinically relevant and comprehensive approach to understanding these potential substance exposures in order to provide a framework for management of opioid, sedative, and hypnotic overdoses.
... 182 of the year 1960. The drug is found in markets by diversity names (Soma, Sodol, Somalgit, Vanadam, Sonoma, Scutamil, Carisoma, Somacid, Mio Relax, Relacton-C, Relaxibys, Rela and Soridol) (3) , Skeletal muscle relaxants contain a diverse mixture of proxies with different buildings and instrument of achievement. These proxies are categorized as antispasticity or antispasmodic proxies; one of them is carisoprodol drug (4) .It essentially acts as a skeletal muscle relaxant and it is thought to slab inter-neuron action by stimulating GABA-A receptors in descendent reticular creation and spinal rope (5) . ...
... The side effects of carisoprodol are drowsiness and sedation when taken in excess. Due to the risk of physical and psychological dependence, the Food and Drug Administration (FDA) recommends only using carisoprodol for two to three weeks [3]. Patients that abuse carisoprodol may experience blurred vision, dizziness, drowsiness, and loss of coordination. ...
... Meprobamate is partially removed by ozonation, so its suitability as a GAC PBI may depend in part on the upstream ozone dosage. Furthermore, meprobamate has been phased out as a pharmaceutical in response to its risk of addiction (Reeves, Burke, & Kose, 2012). Meprobamate may also be present in reclaimed water as a metabolite of carisoprodol (Lewandowski, 2017), but carisoprodol prescription is also declining due to addiction concerns (Y. ...
Article
Full-text available
Many organic chemicals occur in reclaimed water at higher concentrations than in conventional drinking water sources. Some of these chemicals are known to occur at concentrations that pose chronic health risks. The toxicity or occurrence of other chemicals may not yet be known. Thus, potable reuse systems should achieve robust removal of known and unknown chemicals to ensure public health protection. Here, criteria were proposed for performance-based indicators that could cost-effectively verify this robust removal. The selection process was then demonstrated for a hypothetical system using ozon-ation, granular activated carbon, and direct ultraviolet photolysis. A set of indicators (e.g., acesulfame, meprobamate, perfluoroheptanoic acid, sucralose, iopromide, benzotriazole, and iohexol) was recommended on the basis of original and literature review data. However, the concentrations of some of these indicators are sufficient at certain locations only or decrease over time. Thus, indicators should be site-specific, periodically reevaluated, and the topic of further research.
... Moreover, carisoprodol drug is available as somadril compound which contains paracetamol 160mg, caffeine 32mg and carisoprodol 200mg (Bramness et al. 2008). The drug is found in markets by a diversity names (Soma, Sodol, Somalgit, Vanadam, Sonoma, Scutamil, Carisoma, Somacid, Mio Relax, Relacton-C, Relaxibys, Rela and Soridol) as reported with Reeves et al. (2012). Soma is a neutral crystalline powder with white color and it is a chemical derivative of meprobamate with an aliphatic dicarbamate. ...
Article
Full-text available
Carisoprodol is a common muscle relaxant indicated as adjunctive therapy in acute, painful musculoskeletal cases. This current study aimed to investigate the histopathological, histochemical and immunohistochemical effects in the lung tissue of the pregnant rats and their fetuses after carisoprodol treatment. The present study was applied on twenty seven pregnant female rats and they were randomly divided into three groups (nine pregnant female rats in each group). Rats of the first (control) group were administered oral doses of distilled water. Rats of the second (S1) and third groups (S2) were administered oral doses of carisoprodol in the distilled water equivalent to 10.8 mg and 21.6 mg/100g body weight/day respectively for fifteen days from the six to the twenty day of gestation. Several histopathological, histochemical and some immunohistochemical changes were studied to detect the pathological changes. Maternal and fetal pulmonary tissues of both treated groups showed numerous degenerative changes post-treatment with carisoprodol, the severity of these changes was more obvious in the fetal lung tissue of both groups. Also, carisoprodol treated rats showed a marked increase in caspase-3 content in the maternal and fetal pulmonary tissues. Treatment of pregnant rats with carisoprodol drug led to numerous dystrophic changes in both maternal and fetal lung tissues.
Article
Background: Educational outreach programs that focus on safe opioid prescribing and awareness of state prescription monitoring programs may modify clinicians’ prescribing behavior. The objective of this study was to evaluate the secondary effects of an opioid-focused academic detailing (AD) program on non-opioid controlled substance prescribing in primary care. Methods: A quasi-experimental pre-post study of primary care clinicians exposed and unexposed to the AD program was conducted using data from the Illinois Prescription Monitoring Program from December 2017 to February 2019. Outcomes were mean monthly prescriptions for benzodiazepines (BZD), non-BZD sedative-hypnotics, and carisoprodol, per clinician. A difference-in-differences (DID) approach utilizing repeated-measures mixed-effects linear regression models was used to compare changes in outcomes six-months before and after the program. Results: Mean monthly BZD prescriptions declined in both groups of clinicians (AD-exposed n = 151; controls n = 399) after implementation of the AD program. Although the mean monthly number of BZD prescriptions decreased in both groups after the AD program, BZD prescribing in the AD-exposed group declined at a slower rate following the AD program (DID = 0.73; 95% CI: 0.14, 1.31). The AD-exposed group had a 0.06 (95% CI: −0.11, −0.01) lower rate of mean monthly carisoprodol prescriptions compared to the control group following the AD program. There was no change in the rate of mean monthly non-BZD sedative-hypnotic prescriptions between the two groups. Conclusions: The higher relative rate of BZD prescribing in the AD-exposed group compared to the control group following the AD program may be reflective of an unintended consequence of opioid-focused AD programs as clinicians learn to be cautious about opioid prescribing. Our findings may suggest the need for incorporation of targeted education on appropriate BZD prescribing into opioid-focused AD programs as a featured component. These findings warrant further consideration and investigation before large-scale implementation of opioid-focused educational outreach programs.
Chapter
Abuse of and dependence on prescription drugs is an increasing problem and is closely related to the increasing use of prescription drugs worldwide. The problem of prescription drug abuse includes both weak and strong opioids for pain management; sedating drugs like benzodiazepines, barbiturates, and newer hypnotics; and stimulant drugs used for the treatment of narcolepsy and attention-deficit/hyperactivity disorder (ADHD). Several other prescription drugs also have the potential for abuse. This chapter focuses on the epidemiology, the diagnostics, the treatment, and the prevention of prescription drug abuse.
Article
Background: Tolerance and dependence of centrally acting muscle relaxants have been reported in the medical literature for nearly 50 years. Meprobamate, which is one of the best-known examples, had been a controlled substance after studies indicating its addictive effects, shortly after its introduction in the 1950 s. Phenprobamate, which has been reported to be similar to meprobamate in terms of effects, side effects, and toxicity, is not a controlled substance and is frequently prescribed as a centrally acting 10 muscle relaxant. To our knowledge, there is only one case report regarding phenprobamate dependence, which is known for its similar mechanism of action to meprobamate. Methods and Results: Here a case study, who is taking 12 grams a day (30 tablets/day), is presented about phenprobamate, which could have an addictive effect similar to some centrally acting muscle relaxants that were reported in the literature. Conclusions: Physicians should investigate non-phenprobamate muscle relaxant options in those with a history of 15 alcohol and substance use disorders, and health policy should prevent over-the-counter drug sales and prevent possible addictions.
Article
Full-text available
Soma(®) (carisoprodol) is an increasingly abused, centrally-acting muscle relaxant. Despite the prevalence of carisoprodol abuse, its mechanism of action remains unclear. Its sedative effects, which contribute to its therapeutic and recreational use, are generally attributed to the actions of its primary metabolite, meprobamate, at GABA(A) receptors (GABA(A)R). Meprobamate is a controlled substance at the federal level; ironically, carisoprodol is not currently classified as such. Using behavioral and molecular pharmacological approaches, we recently demonstrated carisoprodol, itself, is capable of modulating GABA(A)R function in a manner similar to central nervous system depressants. Its functional similarities with this highly addictive class of drugs may contribute to the abuse potential of carisoprodol. The site of action of carisoprodol has not been identified; based on our studies, interaction with benzodiazepine or barbiturate sites is unlikely. These recent findings, when coupled with numerous reports in the literature, support the contention that the non-controlled status of carisoprodol should be reevaluated.
Article
Full-text available
This is the 26th Annual Report of the American Association of Poison Control Centers (AAPCC; http://www. aapcc.org ) National Poison Data System (NPDS). During 2008, 60 of the nation's 61 US poison centers uploaded case data automatically. The median upload time was 24 [7.2, 112] (median [25%, 75%]) minutes creating a real-time national exposure and information database and surveillance system. We analyzed the case data tabulating specific indices from NPDS. The methodology was similar to that of previous years. Where changes were introduced, the differences are identified. Poison center cases with medical outcomes of death were evaluated by a team of 28 medical and clinical toxicologist reviewers using an ordinal scale of 1-6 to determine Relative Contribution to Fatality (RCF) from the exposure to the death. In 2008, 4,333,012 calls were captured by NPDS: 2,491,049 closed human exposure cases, 130,495 animal exposures, 1,703,762 information calls, 7,336 human confirmed nonexposures, and 370 animal confirmed nonexposures. The top five substances most frequently involved in all human exposures were analgesics (13.3%), cosmetics/personal care products (9.0%), household cleaning substances (8.6%), sedatives/hypnotics/antipsychotics (6.6%), and foreign bodies/toys/miscellaneous (5.2%). The top five most common exposures in children age 5 or less were cosmetics/personal care products (13.5%), analgesics (9.7%), household cleaning substances (9.7%), foreign bodies/toys/miscellaneous (7.5%), and topical preparations (6.9%). Drug identification requests comprised 66.8% of all information calls. NPDS documented 1,756 human exposures resulting in death with 1,315 human fatalities deemed related with an RCF of at least contributory (1, 2, or 3). Poisoning continues to be a significant cause of morbidity and mortality in the US. The near real-time, always current status of NPDS represents a national resource to collect and monitor US poisoning exposure cases and information calls. NPDS continues its mission as one of the few real-time national surveillance systems in existence, providing a model public health surveillance system for all types of exposures, public health event identification, resilience response and situational awareness tracking.
Article
With the issuance of this final rule, the Deputy Administrator of the Drug Enforcement Administration places the substance 2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol (tramadol), including its salts, isomers, and salts of isomers, into schedule IV of the Controlled Substances Act. This scheduling action is pursuant to the Controlled Substances Act which requires that such actions be made on the record after opportunity for a hearing through formal rulemaking. This action imposes the regulatory controls and administrative, civil, and criminal sanctions applicable to schedule IV controlled substances on persons who handle (manufacture, distribute, dispense, import, export, engage in research, conduct instructional activities with, or possess) or propose to handle tramadol.
Article
Carisoprodol is a muscle relaxant that acts at the GABA(A) receptor. Concerns about the abuse liability of carisoprodol are increasing, but evidence that carisoprodol produces tolerance and a significant withdrawal syndrome has yet to be established. The purpose of the current study was to determine if repeated administration of carisoprodol produces tolerance and withdrawal signs in a mouse model. Carisoprodol (0, 100, 200, 300, or 500 mg/kg bid, i.p.) was administered to Swiss-Webster mice for 4 days and loss-of-righting reflex was measured 20-30 min following each administration. On the fourth day, bemegride (20 mg/kg), flumazenil (20 mg/kg), or vehicle was administered following carisoprodol and withdrawal signs were measured. Separate groups of mice receiving the same treatment regimen and dose range were tested for spontaneous withdrawal at 6, 12 and 24 h after the last dose of carisoprodol. The righting reflex was dose-dependently impaired following the first administration of carisoprodol. A 75-100% decrease in the magnitude of the impairment occurred over the four days of exposure, indicating the development of tolerance to the carisoprodol-elicited loss-of-righting reflex. Withdrawal signs were not observed within 24h following spontaneous withdrawal; however, bemegride and flumazenil each precipitated withdrawal within 15-30 min of administration. Carisoprodol treatment resulted in tolerance and antagonist-precipitated withdrawal, suggesting it may have an addiction potential similar to that of other long-acting benzodiazepine or barbiturate compounds.
Article
Carisoprodol is a centrally acting drug used to relieve skeletal muscle spasms and associated pain in acute musculoskeletal conditions. There is evidence from different sources that this oral muscle relaxant is abused and that it is associated with impairment leading to arrests for "driving under the influence" as well as increased risk of automobile accidents. Its subjective and psychomotor effects in healthy volunteers at therapeutic and supratherapeutic doses have not been well-characterized, and form the basis of this report. Fifteen healthy volunteers (8 males, 7 females) were administered 0, 350, and 700 mg of carisoprodol in separate sessions and for 6h afterwards they completed a battery of tests at fixed time intervals so as to assess the subjective and psychomotor effects of the drug. The supratherapeutic dose, 700 mg, increased visual analog scale ratings of terms that were more reflective of sedation (e.g., "sleepy," "heavy, sluggish feeling") than those of abuse liability, and produced impaired performance on several psychomotor tests. The therapeutic dose, 350 mg, while producing few and mild subjective effects, still produced psychomotor impairment. The fact that the therapeutic dose of carisoprodol produced minimal subjective effects while adversely affecting performance is of concern in that patients prescribed this drug may feel relatively normal and engage in tasks (driving) that could put themselves and others at risk.
Article
Some chronic pain patients on long-term opioid therapy also take centrally active skeletal muscle relaxants. One of those muscle relaxants is carisoprodol, a drug that is abused and capable of producing impairment. It would be of relevance to characterize the effects of an opioid and carisoprodol when taken together to determine if abuse liability-related measures and psychomotor impairment are increased compared to when the drugs are taken alone. As part of a larger crossover, randomized, double-blind study, we examined the subjective and psychomotor responses of 15 healthy volunteers to four experimental conditions: placebo, 350 mg carisoprodol, 10mg oxycodone, and 350 mg carisoprodol followed 60 min later by 10mg oxycodone (intended to test the interaction of the two drugs when they were producing their maximal effects). Preliminary data analyses indicated that some of carisoprodol's effects were declining when we tested for drug interactions. Despite this, on some outcome measures in which the drugs alone did not differ from placebo, when tested together subjective effects were increased, including those that were abuse liability-related, and psychomotor performance decreased, relative to placebo. This is the first study that we are aware of that has shown that carisoprodol and oxycodone, two drugs that are sometimes co-prescribed for relief of pain, produce effects when administered "together" (i.e., separated by 60 min) that are of greater magnitude than when they are administered alone. Some of the effects were not benign, and are of concern from both abuse liability and public safety standpoints.
Article
Low back pain is a leading reason for primary care visits. Many treatment options are available, but some lack scientific support. The aim of this review was to discuss the etiology of low back pain and the relative risks and benefits of muscle relaxants commonly prescribed for the management of back pain. We searched Intercontinental Marketing Services data for January 2003 through January 2004 to determine the most commonly prescribed agents for the management of musculoskeletal pain. Carisoprodol, cyclobenzaprine hydrochloride, and metaxalone represented >45% of all such prescriptions. Cochrane Library, MEDLINE, and EMBASE databases were searched (time frame: 1960 through January 2004; search terms: back pain, carisoprodol, cyclobenzaprine, metaxalone, muscle relaxants, and pharmacotherapy) and reference lists of identified articles were hand-searched. Three trials of carisoprodol (N = 197) were located in the Cochrane Library database. Two double-blind, randomized, placebo-controlled trials evaluating the safety and efficacy of cyclobenzaprine hydrochloride (N = 1405) were identified in the literature. Three double-blind, placebo-controlled trials were identified for metaxalone (N = 428) in 2 reports. The types of adverse events seen with these agents involved the central nervous system, including drowsiness/sedation, fatigue, and dizziness. However, the efficacy of cyclobenzaprine hydrochloride was shown to be independent of its sedative effects, which were dose related. The potential for abuse with carisoprodol is of growing concern. Analgesic pain management for low back pain due to muscle spasm may be combined with a muscle relaxant. Cyclobenzaprine hydrochloride has the most recent and largest clinical trials demonstrating its benefit, but carisoprodol and metaxalone also appear to be effective. However, carisoprodol's usefulness is mitigated by its potential for abuse.
Article
To review the current legal status and patterns of abuse of carisoprodol. A literature search was conducted through MEDLINE (1950-August 2010), PubMed (1966-August 2010), EMBASE (1966-August 2010), and International Pharmaceutical Abstracts (1970-August 2010) using the search terms carisoprodol and abuse. In addition, reference citations from publications identified were reviewed. State laws and regulations were accessed through NABPLAW Online (2010) using the search term carisoprodol. Federal proposed rules were accessed through the Federal Register (1995 Volume 59-2010 Volume 75) using the search term carisoprodol. State laws and federal proposed rules regarding carisoprodol were examined. Case reports and studies involving carisoprodol abuse were evaluated. Carisoprodol is not federally scheduled under the Controlled Substances Act (CSA). However, carisoprodol is scheduled in 36% (n = 18) of states of the US. The Drug Enforcement Administration issued a Notice of Proposed Rulemaking in the Federal Register on November 17, 2009, to place carisoprodol into schedule IV of the CSA, with a deadline to submit written comments by December 17, 2009. Case reports, retrospective studies, and national reports, including reports from the American Association of Poison Control Centers and results from the Monitoring the Future national survey on drug use, have identified carisoprodol's abuse potential. Carisoprodol should be placed in schedule IV of the CSA based on its abuse potential and current state laws and regulations. Federally scheduling carisoprodol would lead to uniformity among the states and hopefully assist in preventing prescription drug abuse. Larger, well-designed studies evaluating carisoprodol abuse should be performed.
Article
Carisoprodol is a centrally acting muscle relaxant used in the treatment of various musculoskeletal disorders whose main metabolite, meprobamate, is a controlled substance in the United States due to its sedative properties and potential for abuse. We report a case of a 51-year-old man with cognitive impairment and tremor who developed worsening tremor, anxiety, myoclonus, ataxia, and psychosis on abrupt cessation of carisoprodol. At hospital discharge, his cognitive function significantly improved compared with when he was on carisoprodol. Carisoprodol withdrawal is an important and under-recognized syndrome that should be considered in patients presenting with neurologic symptoms who are taking the medication. Carisoprodol withdrawal can be successfully treated with the use of benzodiazepines, although further studies are needed to identify the most appropriate treatment protocol.
Article
Carisoprodol (N-isopropyl-2 methyl-2-propyl-1,3-propanediol dicarbamate; N-isopropylmeprobamate) is a centrally acting skeletal muscle relaxant whose primary active metabolite is meprobamate, a substance with well established abuse potential similar to that of benzodiazepines. A number of reports show that carisoprodol has been abused for its sedative and relaxant effects, to augment or alter the effects of other drugs, and by the intentional combination of carisoprodol and other noncontrolled medications because of the relative ease (as compared to controlled substances) of obtaining prescriptions. The diversion and abuse of carisoprodol and its adverse health effects appear to have dramatically increased over the last several years. Clinicians have begun to see a withdrawal syndrome consisting of insomnia, vomiting, tremors, muscle twitching, anxiety, and ataxia in patients who abruptly cease intake of large doses of carisoprodol. Hallucinations and delusions may also occur. The withdrawal symptoms are very similar to those previously described for meprobamate withdrawal, suggesting that what may actually be occurring is withdrawal from meprobamate accumulated as a result of intake of excessive amounts of carisoprodol. However carisoprodol itself is capable of modulating GABA(A) function, and this may contribute both to the drugs abuse potential and to the occurrence of a withdrawal syndrome with abrupt cessation of intake. Carisoprodol has been classified as a controlled substance in several states in the US and restrictions on the use of the drug have been imposed in some European countries. Carisoprodol is metabolized to a controlled substance, has clear evidence of abuse potential and increasing incidence of abuse, and has shown evidence of a withdrawal syndrome with abrupt cessation from intake. This article will discuss the abuse potential of carisoprodol and the associated withdrawal syndrome, and consider implications for future use of the drug.