1. How Many Soma To Overdose 5
2. How Many Soma To Overdose In Children
3. How Many Soma To Overdose Drugs

In very large doses, Soma will produce a meprobamate overdose, which can include coma. With long-term use, you may also develop tolerance and experience mild withdrawal symptoms that can last for 2 to 4 days after your last dose.

Yes, you can overdose on muscle relaxers. It is alwaysrecommended that you follow the dosage recommended on the bottle,these dosages aren't guidline..they're lifelines becauseoverdosing on any drug can be lethal. Muscle relaxers when takencorrectly can relieve a person from pain..either from tension orsome other injury. Taking more than recommended however, puts yourbody in serious danger. Breathing is done through a person'sdiaphragm (the muscles between the ribs and the abdominal muscles),heart and lungs. Since the diaphragm is a muscle (as well as theheart and the lungs) overdosing on muscle relaxers (of anykind) can relax these very important muscles to the point wherethey are no longer working or no longer working hard enough to meetthe body's needs. This is why it's very important to pay attentionto what your exact dosage is and any side effects you mayhave while on it (difficulty breathing, chest pain extremedrowsiness or dizziness etc.) If a person suspected of musclerelaxer overdose is admitted to the ER it is considered a veryserious thing (as with any other drug OD). Blood will be takenimmediately to determine how much the person took and how much ofthe drug is in the blood stream. Breathing and heart rate will beclosely monitored and oxygen will be given to make sure enough isgetting to the brain. Since it takes 24-48 hours for the drugs toexit your system (though it relies a lot on how much was taken, howclose together and when) hospitals will want to admit the patientto the ICU so that they can carefully monitor them for the durationrecommended by the attending physician Large overdoses can cause aperson to go into a coma and/or leave them with permanent brain,heart or liver damage. It is a very serious thing. We are fortunateto be able to buy and use these drugs to help us when we need themhowever, we need to remember that we also have a responsibility totake any form of drug.

Can too much muscle relaxants stop the heart?

Definitely. Your heart is a muscle, and muscle relaxers do exactly what they sound like: relax your muscles. An overdose of muscle relaxers can also relax your diaphragm (the muscle beneath you lungs that contracts and expands, allowing you to breathe). Relaxation of the diaphragm would inhibit contraction and, therefore, breathing.

Can you mix muscle relaxers with pain pills?

can you take muscle relaxers with the pain medication oxycodone?

How long does it take for muscle relaxers to leave your system?

It could take days for certain muscle relaxers to leave your system. Most muscle relaxers will leave your system within 24 hours.

Will muscle relaxers show in urine drug test?

Muscle relaxers like Soma and Flexaril do Not show up in drug tests

Can you take barbiturates and muscle relaxers together?

You sure can. In fact both drugs are, often times, more effective when taken together. Just be sure to monitor intake, and not overdose. -Doc-

Is lortab a muscle relaxer?

No, it's a pain pill. To explain: Lortab is a combination of hydrocodone and Tylenol, which helps to relieve pain. Muscle relaxers are usually more like Advil but stronger. Lortabs will help with muscle pain but not as well as muscle relaxers. Muscle relaxers will only help with pain relating to muscles or inflammation.

Can you mix steroids and muscle relaxers?

yes I feel you can but it depends on what kind of muscle relaxer

Can i die from taking muscle relaxers and smoking pot?

'dont know about the muscle relaxer part, but you can from smoking pot.' What the hell? No you can't die from smoking Pot. It's one of those drugs you just can't overdose on. Anyway, if you're asking if you can die from taking a muscle relaxer and then smoking a bowl, that's still definitely a no.

Do muscle relaxers make you fat?

no, there is no correlation between weight gain and muscle relaxers. However, they relax both body and mind, which may lead a user to make unwise food choices.

Can you die from overdosing on muscle relaxers?

you can faint or have seizures. but mostly it CAN lead to death. any overdose of medicine can have its consequences. Absolutely yes. The effects depend upon what the chemicals are in the 'muscle relaxer'. Even acetaminophen ( one Brand Name being Tylenol) can be fatal if taken in a too large a quantity.

Do muscle relaxers affect high blood pressure?

Muscle relaxers may have an effect on high blood pressure. It is important to use only those prescribed to you by a doctor so you get the correct medication and dosage.

What is a twitch in electromyography?

electromyography is about muscle relaxers and contractions testing devise.

How Many Soma To Overdose 5

What muscle relaxers can you give to a dog?

Dogs can not have muscle relaxers if you give them muscle relaxers Cats can't either If you do take them to the Nearest vet ---- Dogs should not be given any human-intended drugs or medicinal substances. Please consult a trained veterinarian for suitable medications. If you have experience with positive results and/or are trained, you could try a gentle massage. However, you should be careful with that.

Can you take muscle relaxers and dilautin?

no, because 'dilautin' is not an actual marketed drug

What helps a pull muscle?

Vicodin or another pain reliever and muscle relaxers. You will want to rest the muscle as well. I would consult a doctor, they can be painful.

Can you take 600 mg ibuprofen with muscle relaxers?

depends on the muscle relaxer one of the most common is tizaniden and yes with that

Can you take muscle relaxers with metoprolol?

Metoprolol is a BP medication. There should be no ill effects of also taking a muscle relaxer.

What contains barbiturate?

Answer muscle relaxants: flrxeril etc. Barbitutes are most often found in drugs like Firorecet and Seconal. Not muscle relaxers. Barbiturates are very addictive and very few muscle relaxers have that time of drug in them. yes it is a barbituate Phentermine is in the amphetamine and phenethylamine class of drugs.

Can you take hydrocodne with muscle relaxers?

depends how much MG the Hydrocodone and how much MG the muscle relaxers, just like if someone had a beer n took a benzo or such they may just get a lil more 'inebreiated' but depends on person, but it generally a no no

How Many Soma To Overdose In Children

How long can muscle relaxers be detected in urine laboratory testing?

Most muscle relaxers are non narcotic and aren't tested for. Valium is the only medication that I can think of that is sometimes used as a muscle relaxer that may show up on a test (it is a benzodiazapine). It usually stays in the system for 5-7 days.

Can you die from mixing a muscle relaxer with marijuana?

hell no I'd only gonna die if u taketoo many muscle relaxers

Is soma and norflex the same type of muscle relaxer?

i just want to know if soma and norflex are the same type of muscle relaxers.

Can you drink beer while taking muscle relaxers?

can you? of course! Should you? should be on the label

Can you snort muscle relaxers?

Well, yes. BUT! I do not advise it because it WILL BURN your nose and sinuses.

Can you take muscle relaxants with Fentanyl patches?

It depends on each patients, but for most Fentanyl patients, using muscle relaxers such as Flexeril is not uncommon.

Are soma and norflex the same type of muscle relaxer?

I just want to know if the 2 muscle relaxers called Soma and Norflex the same or not.

Can you take suboxone while taking somas?

Yes. Muscle relaxers are fine to take with Suboxone

Can you mix muscle relaxers?

NO to many muscle relaxers can do harm to your body you should only take one at a time, if your taking flexerall stay with it and don't change unless your doctor tells you to again always ask your pharmacist they know what drugs interact with each other.

How Many Soma To Overdose Drugs

Can you take muscle relaxers and ibuprofen together?

Yes, there is no problem in taking those 2 drugs together.

Can you take pain medication and muscle relaxers together?

depends on how strong they are and also what other medications ur on

Are all muscle relaxers narcotics?

No, few if any of them are. Some narcotics can certainly have a muscle relaxant effect, but muscle relaxants - an important therapeutic part of medicine - are completely different kinds of compounds.

Carisoprodol, marketed under the brand name Soma among others, is a medication used for musculoskeletal pain.^[2] Use is only approved for up to three weeks.^[2] Effects generally begin within half an hour and last for up to six hours.^[2] It is taken by mouth.^[2]

Common side effects include headache, dizziness, and sleepiness.^[2] Serious side effect may include addiction, allergic reactions, and seizures.^[2] In people with a sulfa allergy certain formulations may result in problems.^[2] Safety during pregnancy and breastfeeding is not clear.^[3][2] How it works is not clear.^[2] Some of its effects are believed to occur following being converted into meprobamate.^[2]

Carisoprodol was approved for medical use in the United States in 1959.^[2] Its approval in Europe was withdrawn in 2008.^[4] It is available as a generic medication.^[2] In the United States the wholesale costs is less than 0.10 USD per dose.^[5] In 2016 it was the 181st most prescribed medication in the United States with more than 3 million prescriptions.^[6] In the United States, it is a Schedule IV controlled substance.^[2]

• 2Side effects
• 4Pharmacology
• 6Usage and legal status

Medical uses[edit]

Carisprodol is meant to be used along with rest, physical therapy and other measure to relax muscles after strains, sprains and muscle injuries.^[7] It comes in tablet format and is taken by the mouth three times a day and before bed.^[7]

Side effects[edit]

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; the euphoria derived is, according to new research, most likely due to carisoprodol's inherent, potent anxiolytic effects that 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 CNS effects than meprobamate alone. Carisoprodol has a unique mechanism of action, qualitatively different from that of meprobamate (Miltown). The medication is well-tolerated and without adverse effects in the majority of patients for whom it is indicated. In some patients, however, and/or early in therapy, carisoprodol can have the full spectrum of 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, as is the case with many other drugs. Other side effects include: dizziness, clumsiness, headache, fast heart rate, upset stomach, vomiting and skin rash.^[7]

The interaction of carisoprodol with essentially all opioids, and other centrally acting analgesics, but especially^{[citation needed]}codeine, those of the codeine-derived subgroup of the semisynthetic class (ethylmorphine, dihydrocodeine, hydrocodone, oxycodone, nicocodeine, benzylmorphine, the various acetylated codeine derivatives including acetyldihydrocodeine, dihydroisocodeine, nicodicodeine and others)^{[citation needed]} which allows the use of a smaller dose of the opioid to have a given effect,^{[citation needed]} is useful in general and especially where skeletal muscle injury and/or spasm is a large part of the problem. The potentiation effect is also useful in other pain situations and is also especially useful with opioids of the open-chain class, such as methadone, levomethadone, ketobemidone, phenadoxone and others. In recreational drug users, deaths have resulted from carelessly combining overdoses of hydrocodone and carisoprodol. Another danger of misuse of carisoprodol and opiates is the potential to aspirate while unconscious.

Meprobamate and other muscle-relaxing drugs often were subjects of misuse in the 1950s and 60s.^[8][9] Overdose cases were reported as early as 1957, and have been reported on several occasions since then.^{[10][11][12][13][14][15][16]}

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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.^[17] Because of potential for more severe side effects, this drug is on the list to avoid for elderly people.^[18]

Withdrawal[edit]

Carisoprodol, meprobamate, and related drugs such as tybamate, 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 has also been linked to carisoprodol use although this is much less severe than with meprobamate itself (presumably due to the slower onset of effects). Psychological dependence is more common in those who abuse carisoprodol and those who have a history of drug abuse (particularly sedatives or alcohol). It may reach clinical significance before physiological tolerance and dependence have occurred and (as with benzodiazepines) has been demonstrated to persist to varying degrees of severity for months or years after discontinuation.

Discontinuation of carisoprodol, as with all GABA-ergics, can result in cognitive changes which persist for weeks, months, or rarely even years including greatly increased anxiety and depression, social withdrawal, hair-trigger agitation/aggression, chronic insomnia, new or aggravated (often illogical) phobias, reduced IQ, short term and long term memory loss, and dozens of other sequelae.^[19] The effects, severity, and duration appear to be slightly dose-dependent but are mainly determined by the patients pattern of use (taken as prescribed, taken in bulk doses, mixed with other drugs, a combination of the above, etc.), genetic predisposition to drug abuse, and a history of substance abuse all increase the patients risk of persistent discontinuation syndrome symptoms.

Treatment for physical withdrawal generally involves switching the patient to a long-acting benzodiazepine such as diazepam or clonazepam then slowly titrating them off the replacement drug completely at a rate which is both reasonably comfortable for the patient but rapid enough for the managing physician to consider the rate of progress acceptable (overly rapid dose reduction greatly increases the risk of patient non-compliance such as the abuse of illicitly obtained alternative sedatives and/or alcohol). Psychotherapy and cognitive behavioral therapy have demonstrated moderate success in reducing the rebound anxiety which results upon carisoprodol discontinuation but only when combined with regular and active attendance to a substance abuse support group.

Carisoprodol withdrawal can be life-threatening (especially in high dose users and those who attempt to quit 'cold turkey'). Medical supervision is recommended, with gradual reduction of dose of carisoprodol or a substituted medication, typical of other depressant drugs.

Abuse[edit]

Combining a muscle relaxant like carisoprodol with opioids and benzodiazepines is referred to as 'The Holy Trinity' as it has been reported to increase the power of the 'high'.^[20]

Recreational users of carisoprodol usually seek its potentially heavy sedating, relaxant, and anxiolytic effects.^[21] Also, because of its potentiating effects on narcotics, it is often abused in conjunction with many opioid drugs. Also it is not detected on standard drug testing screens. On 26 March 2010 the DEA issued a Notice of Hearing on proposed rule making in respect to the placement of carisoprodol in schedule IV of the Controlled Substances Act.^[22] Carisoprodol is sometimes mixed with date rape drugs.^[23]

Many overdoses have resulted from recreational users combining these drugs to combine their individual effects without being aware of the enzyme-induction induced potentiation.^{[medical citation needed]}

Overdose[edit]

As with other GABAergic drugs, combination with other GABAergic drugs, including alcohol, as well as with sedatives in general, 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 (potentially violent) behavior. Severe overdoses may present with respiratory depression (and subsequent pulmonary aspiration), coma, and death.^{[citation needed]}

Carisoprodol is not detected on all toxicology tests which may delay diagnosis of overdose. Overdose symptoms in combination with opiates are similar but are distinguished by the presentation of normal or pinpoint pupils, which are generally unresponsive to light. Carisoprodol (as with its metabolite meprobamate) is particularly 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 mirrors that of barbiturate overdoses and is generally supportive, including the administration of mechanical respiration and pressors as implicated (and in rare cases, bemegride). Total amnesia of the experience is not uncommon following recovery.^{[citation needed]}

Pharmacology[edit]

Carisoprodol is a GABAergic drug^{[citation needed]}.

Pharmacokinetics[edit]

Carisoprodol has a rapid, 30-minute onset of action, with the aforementioned effects lasting about two to six hours. It is metabolized in the liver via the cytochrome P450 oxidaseisozymeCYP2C19, excreted by the kidneys and has about an eight-hour half-life. A considerable proportion of carisoprodol is metabolized to meprobamate, which is a known drug of abuse and dependence; this could account for the abuse potential of carisoprodol (meprobamate levels reach higher peak plasma levels than carisoprodol itself following administration). Meprobamate is believed to play a significant role in the effects of carisoprodol and meprobamates long half-life results in bioaccumulation following extended periods of carisoprodol administration.

It is slightly soluble in water and freely soluble in ethanol, chloroform and acetone. The drug's solubility is practically independent of pH.

History[edit]

On 1 June 1959 several American pharmacologists convened at Wayne State University in Detroit, Michigan to discuss a new drug. The drug, originally thought to have antiseptic properties, was found to have central muscle-relaxing properties.^[24] It had been developed by Frank Berger at Wallace Laboratories and was named carisoprodol.

Carisoprodol was a modification of meprobamate, intended to have better muscle relaxing properties, less potential for abuse, and less risk of overdose.^[25] The substitution of one hydrogenatom with an isopropyl group on one of the carbamyl nitrogens was intended to yield a molecule with new pharmacological properties.

Usage and legal status[edit]

Norway[edit]

Reports from Norway have shown carisoprodol has abuse potential^[26] as a prodrug of meprobamate and/or potentiator of hydrocodone, oxycodone, codeine, and similar drugs. In May 2008 it was taken off the market in Norway.^[27]

European Union[edit]

In the EU, the European Medicines Agency issued a release recommending member states suspend marketing authorization for this product in the treatment of acute (not chronic) back pain.^[28]

As of November 2007, carisoprodol has been taken off the market in Sweden due to problems with dependence and side effects. The agency overseeing pharmaceuticals considered other drugs used with the same indications as carisoprodol to have the same or better effects without the risks of the drug.^[29]

United States[edit]

Until 12 December 2011, when the Administrator of the Drug Enforcement Administration (DEA) issued the final ruling placing the substance carisoprodol into Schedule IV of the Controlled Substances Act (CSA), carisoprodol was not a controlled substance. The placement of carisoprodol into Schedule IV was effective 11 January 2012.^[30]

Carisoprodol is available generically as 350 mg and, more recently, 250 mg tablets. Compounded tablets with acetaminophen and codeine are also available.^[31]

Canada[edit]

Federally, carisoprodol is a Prescription Drug (Schedule I, sub-schedule F1).^[32] Provincial regulations vary.^[33] It is no longer readily available.^{[medical citation needed]}

Indonesia[edit]

• In September 2013, carisoprodol has been taken off the market due to problems with diversion, dependence and side effects.
• In September 2017, one child died and 50 suffered seizures when PCC, which stands for 'Paracetamol Caffeine Carisoprodol' was mixed (probably illicit) into children's drinks in elementary and junior high schools in Kendari.^[34]

Notes[edit]

1. ^'Carisoprodol'. drugs.com. Retrieved 16 April 2017.
2. ^ ^{abcdefghijklm}'Carisoprodol Monograph for Professionals'. Drugs.com. American Society of Health-System Pharmacists. Retrieved 8 April 2019.
3. ^'DailyMed - carisoprodol tablet'. dailymed.nlm.nih.gov. Retrieved 8 April 2019.
4. ^'Carisoprodol'. European Medicines Agency. 15 November 2007. Retrieved 8 April 2019.
5. ^'NADAC as of 2019-02-27 Data.Medicaid.gov'. Centers for Medicare and Medicaid Services. Retrieved 8 April 2019.
6. ^'The Top 300 of 2019'. clincalc.com. Retrieved 22 December 2018.
7. ^ ^abc'Carisoprodol'. MedlinePlus. National Library of Medicine. Retrieved 6 May 2019.
8. ^Kamin I, Shaskan D (1959). 'Death due to massive overdose of meprobamate'. Am J Psychiatry. 115 (12): 1123–1124. doi:10.1176/ajp.115.12.1123-a. PMID13649976.
9. ^Hollister LE (1983). 'The pre-benzodiazepine era'. J Psychoactive Drugs. 15 (1–2): 9–13. doi:10.1080/02791072.1983.10472117. PMID6350551.
10. ^Gaillard Y, Billault F, Pepin G (1997). 'Meprobamate overdosage: a continuing problem. Sensitive GC-MS quantitation after solid phase extraction in 19 fatal cases'. Forensic Sci. Int. 86 (3): 173–180. doi:10.1016/S0379-0738(97)02128-2. PMID9180026.
11. ^Allen MD, Greenblatt DJ, Noel BJ (1977). 'Meprobamate overdosage: a continuing problem'. Clin Toxicol. 11 (5): 501–515. doi:10.3109/15563657708988216. PMID608316.
12. ^Kintz P, Tracqui A, Mangin P, Lugnier AA (1988). 'Fatal meprobamate self-poisoning'. Am J Forensic Med Pathol. 9 (2): 139–140. doi:10.1097/00000433-198806000-00009. PMID3381792.
13. ^Eeckhout E, Huyghens L, Loef B, Maes V, Sennesael J (1988). 'Meprobamate poisoning, hypotension and the Swan-Ganz catheter'. Intensive Care Med. 14 (4): 437–438. doi:10.1007/BF00262904. PMID3403779.
14. ^Lhoste F, Lemaire F, Rapin M (1977). 'Treatment of hypotension in meprobamate poisoning'. N Engl J Med. 296 (17): 1004. doi:10.1056/NEJM197704282961717. PMID846530.
15. ^Bedson H (1959). 'Coma due to meprobamate intoxication. Report of a case confirmed by chemical analysis'. Lancet. 273 (1): 288–290. doi:10.1016/S0140-6736(59)90209-0. PMID13632000.
16. ^Blumberg A, Rosett H, Dobrow A (1959). 'Severe hypotension reactions following meprobamate overdosage'. Ann Intern Med. 51 (3): 607–612. doi:10.7326/0003-4819-51-3-607. PMID13801701.
17. ^'CARISOPRODOL'. TOXNET. National Library of Medicine. Retrieved 6 May 2019.
18. ^NCQA’s HEDIS Measure: Use of High Risk Medications in the ElderlyArchived 1 February 2010 at the Wayback Machine
19. ^Melinda J Barker; Kenneth M Greenwood; Martin Jackson; Simon F Crowe (April 2004). 'Persistence of cognitive effects after withdrawal from long-term Archives of Clinical Neuropsychology'. Archives of Clinical Neuropsychology. 19 (3): 437–454. doi:10.1016/S0887-6177(03)00096-9. PMID15033227.
20. ^Horsfall, JT; Sprague, JE (February 2017). 'The Pharmacology and Toxicology of the 'Holy Trinity''. Basic & clinical pharmacology & toxicology. 120 (2): 115-119. doi:10.1111/bcpt.12655. PMID27550152. access-date= requires url= (help)
21. ^'DEA Drugs & Chemicals of Concern 'Carisoprodol''. Archived from the original on 17 April 2011. Retrieved 29 April 2011.
22. ^'Archived copy'. Archived from the original on 15 July 2011. Retrieved 19 April 2010.CS1 maint: Archived copy as title (link)
23. ^Madea B, Musshoff F (May 2009). 'Knock-out drugs: their prevalence, modes of action, and means of detection'. Dtsch Arztebl Int. 106 (20): 341–7. doi:10.3238/arztebl.2009.0341. PMC2689633. PMID19547737.
24. ^Miller JG, ed. The pharmacology and clinical usefulness of carisoprodol. Detroit:Wayne State University; 1959.
25. ^Berger, F; Kletzkin, M; Ludwig, B; Margolin, S (1959). 'The history, chemistry, and pharmacology of carisoprodol'. Annals of the New York Academy of Sciences. 86: 90–107. doi:10.1111/j.1749-6632.1960.tb42792.x. PMID13799302.
26. ^Bramness JG, Furu K, Engeland A (2007). 'Carisoprodol use and abuse in Norway. A pharmacoepidemiological study'. Br J Clin Pharmacol. 64 (2): 210–218. doi:10.1111/j.1365-2125.2007.02847.x. PMC2000626. PMID17298482.
27. ^'Somadril trekkes fra markedet'. 20 April 2008. Archived from the original on 16 July 2011. Retrieved 12 March 2010.
28. ^'Carisprodol press release'(PDF). EMEA. Archived from the original(PDF) on 18 July 2009. Retrieved 12 May 2008.
29. ^'Marknadsföringen av Somadril och Somadril comp rekommenderas upphöra tillfälligt' [Marketing of Somadril and Somadril is recommended to cease temporarily] (in Swedish). 16 November 2007. Archived from the original on 23 July 2014. Retrieved 9 May 2009.
30. ^US Department of Justice (2011). 'Schedules of Controlled Substances: Placement of Carisoprodol into Schedule IV'(PDF). Federal Register. 76 (238): 77330–77360. Retrieved 1 February 2012.
31. ^'High Cost, No Benefit – The Rheumatologist'. the-rheumatologist.org. Archived from the original on 7 May 2015. Retrieved 31 August 2017.
32. ^'NAPRA – Search National Drug Schedule'. National Association of Pharmacy Regulatory Authorities. 2009. Archived from the original(ASP) on 1 February 2014. Retrieved 7 January 2014.
33. ^For British Columbia, see library.bcpharmacists.org/D-Legislation_StandardsArchived 17 December 2013 at the Wayback Machine
34. ^'One Schoolchild Dies, More Than 50 Suffer Seizures After Consuming Pills in Southeast Sulawesi'. 14 September 2017.

External links[edit]