Club Drugs: MDMA, Gamma-Hydroxybutyrate (GHB), Rohypnol, and Ketamine
Am Fam Physician. 2004 Jun 1;69(11):2619-2627.
Club drugs are substances commonly used at nightclubs, music festivals, raves, and dance parties to enhance social intimacy and sensory stimulation. The most widely used club drugs are 3,4-methylenedioxymetham-phetamine (MDMA), also known as ecstasy; gamma-hydroxybutyrate (GHB); flunitrazepam (Rohypnol); and ketamine (Ketalar). These drugs are popular because of their low cost and convenient distribution as small pills, powders, or liquids. Club drugs usually are taken orally and may be taken in combination with each other, with alcohol, or with other drugs. Club drugs often are adulterated or misrepresented. Any club drug overdose should therefore be suspected as polydrug use with the actual substance and dose unknown. Persons who have adverse reactions to these club drugs are likely to consult a family physician. Toxicologic screening generally is not available for club drugs. The primary management is supportive care, with symptomatic control of excess central nervous system stimulation or depression. There are no specific antidotes except for flunitrazepam, a benzodiazepine that responds to flumazenil. Special care must be taken for immediate control of hyperthermia, hypertension, rhabdomyolysis, and serotonin syndrome. Severe drug reactions can occur even with a small dose and may require critical care. Club drug overdose usually resolves with full recovery within seven hours. Education of the patient and family is essential.
Although alcohol remains the primary “social lubricant,” it has been joined by many newer psychoactive drugs that are used to intensify social ex-eriences. Because of the prevalence of these drugs at dance parties, raves, and nightclubs, they often are referred to as “club drugs.” The most prominent club drugs are MDMA (3,4-methylenedioxymethamphetamine), also known as ecstasy; gamma-hydroxybutyrate (GHB); flunitrazepam (Rohypnol); and ketamine (Ketalar). Table 11 lists the various street names for these agents.
Club drugs are favored over other recreational drugs, such as marijuana, lysergic acid diethylamide (LSD), methamphetamine, and opiates, because they are believed to enhance social interaction. They often are described as “entactogens,” giving a sense of physical closeness, empathy, and euphoria. MDMA is structurally similar to amphetamine and mescaline, which is a hallucinogen. However, it is not as stimulating or addictive as amphetamine, and is considered much less likely to cause psychosis than LSD and other potent hallucinogens.2 GHB and Rohypnol are powerful sedative/hypnotic agents. Ketamine is a dissociative anesthetic that produces a dreamy tranquility and disinhibition in small doses. Unlike opiates, these sedatives encourage sociability and seldom cause nausea.
TABLE 1 Street Names for “Club Drugs”
Street Names for “Club Drugs”
Ecstasy, X, M, E, XTC, rolls, beans, Clarity, Adam, lover's speed, hug drug
G, liquid ecstasy, Grievous Bodily Harm, gib, soap, scoop, nitro
Blue Nitro, GH Revitalizer, Gamma G
Weight Belt Cleaner, Serenity, Thunder Nectar, Revitalize Plus
Mexican valium, circles, roofies, la rocha, roche, rophies, R2, rope, forget-me pill
K, special K, super K, vitamin K, kit-kat, keets, super acid, jet, cat valiums
MDMA = 3,4-methylenedioxymethamphetamine; GHB = gamma-hydroxybutyrate; GBL = gamma butyrolactone; BD = 1,4-butanediol.
*—Chemical precursors of GHB.
Information from Gahlinger PM. Illegal drugs: a complete guide to their history, chemistry, use and abuse. New York: Plume, 2004:169–72.
The popularity of these club drugs is due to their low cost and convenient distribution as small pills, powders, or liquids that can be taken orally. Consequently, these drugs are popular among young persons who have been educated about the hazards of drug injection and the dangers of heroin, cocaine, and methamphetamine. However, most users are unaware that MDMA is a type of methamphetamine, and incorrectly assume that substances that appear as pharmaceuticals are safe to use.
Club drugs often are taken together, with alcohol, or with other drugs to enhance their effect. Often, they are misrepresented, adulterated, or entirely substituted for another substance without the users' knowledge. These actions result in an extraordinarily high risk of unanticipated effects and overdose.3
In the past 10 years, there has been a generalized decrease in the use of marijuana, cocaine, and heroin in the United States, according to statistics from the Drug Enforcement Administration, the University of Michigan Monitoring the Future Study, the Columbia University National Survey of American Attitudes on Substance Abuse, the Community Epidemiology Working Group, and the Partnership for a Drug-Free America.4 However, during this same period, the use of club drugs has dramatically increased.5 A 2001–2002 Chicago household survey6 of 18-to 40-year-old persons showed that 38 percent had attended a rave, and 49 percent of these had a taken a club drug. One Australian study7 showed that only 8 percent of club-goers had not consumed any psychoactive substance.
MDMA was developed in 1914 as an appetite suppressant, but animal tests were unimpressive, and it was never tested in humans. In 1965, psychiatrists prescribed the drug to break through psychologic defenses as an “empathy agent.” By 1985, illegal laboratories were producing the drug for recreational use, and it was classified as a schedule I controlled substance.
MDMA has become the most common stimulant found in dance clubs and is available at 70 percent of raves.8 MDMA usually is sold as small tablets of variable colors imprinted with popular icons or words. A high proportion of MDMA pills are adulterated with substances such as caffeine, dextromethorphan,9 pseudoephedrine,10 or potent hallucinogens such as LSD, paramethoxyamphetamine (PMA), methylenedioxyamphetamine (MDA), N-ethyl-3,4-methylenedioxyamphetamine (MDEA), and 4-bromo-2,5-dimethoxyam-phetamine (2-CB).11 Many of these substances are “designer drugs” that are illicitly manufactured variants of pharmaceuticals and have intentional and unintentional effects. For example, MDEA (“Eve”), 2-CB, and PMA (“death”) are substituted amphetamines but have primarily hallucinogenic, and often unpleasant, effects.1
MDMA ingestion increases the release of serotonin, dopamine, and norepinephrine from presynaptic neurons and prevents their metabolism by inhibiting monoamine oxidase. Effects of an oral dose appear within 30 to 60 minutes and last up to eight hours.12 A quicker onset of action can be achieved by snorting the powder of a crushed tablet. Users of MDMA describe initial feelings of agitation, a distorted sense of time, and diminished hunger and thirst, followed by euphoria with a sense of profound insight, intimacy, and well-being.13 To further enhance the sensory effects, users often wear fluorescent necklaces, bracelets, and other accessories, and apply mentholated ointment on their lips or spray menthol inhalant on a surgical mask. Unpleasant side effects of MDMA include trismus and bruxism, which can be reduced by sucking on a pacifier or lollipop.14
Adverse effects of MDMA ingestion result from sympathetic overload and include tachycardia, mydriasis, diaphoresis, tremor, hypertension,15 arrhythmias,16 parkinsonism,17 esophoria (tendency for eyes to turn inward), and urinary retention.18 However, the most troublesome potential outcome of MDMA ingestion is hyperthermia19 and the associated “serotonin syndrome.” Serotonin syndrome is manifested by grossly elevated core body temperature, rigidity, myoclonus, and autonomic instability;20 it results in end-organ damage, rhabdomyolysis and acute renal failure, hepatic failure, adult respiratory distress syndrome, and coagulopathy.21
MDMA ingestion directly causes a rise in antidiuretic hormone.22 Heat from the exertion of dancing in a crowded room coupled with the MDMA-induced hyperthermia can lead easily to excessive water intake and severe hyponatremia.23 Neurologic effects include confusion, delirium, paranoia, headache, anorexia, depression, insomnia, irritability, and nystagmus, all of which may continue for several weeks.
Two days after ingestion of MDMA, users typically experience depression consistent with serotonin depletion,24 which may be severe.25 One study26 showed that, compared with alcohol withdrawal, persons who are withdrawing from MDMA were more depressed, irritable, and unsociable. Repeated use of MDMA has been associated with cognitive deficits in animals and humans, with potentially permanent memory impairment.27,28
A number of products are sold legally as “herbal ecstasy.” These products, available in health food stores or on the Internet, contain stimulants such as ephedra, caffeine, and guarana, with variable additions of common herbs or vitamins.29 Users of these products may believe they are safe alternatives to MDMA, but several cases of toxic overdose have been reported from the intense stimulation of ephedrine or excessive caffeine.30
GHB is a derivative of the inhibitory neurotransmitter γ-aminobutyric acid and occurs naturally in the central nervous system, where it is believed to mediate sleep cycles, body temperature, cerebral glucose metabolism, and memory.31
GHB was first synthesized in France in 1960 as an anesthetic. It later achieved popularity as a recreational drug and a nutritional supplement marketed to bodybuilders.32 Nonprescription sales in the United States were banned in 1990 because of adverse effects, including uncontrolled movements and depression of the respiratory and central nervous systems (CNS).33,34 In 2000, with 60 deaths reported from overdose and concern over its use as a “date rape” drug, GHB was reclassified as a schedule I controlled substance.35 In 2002, sodium oxybate, a formulation of GHB, was approved for the treatment of narcolepsy and classified as schedule III. Recently, sodium oxybate has been studied as a treatment for alcohol withdrawal.36,37
GHB is easily manufactured from industrial chemicals. Internet Web sites offer instructions for home production and sell kits with the requisite materials. GHB is chemically related to gamma butyrolactone and 1,4-butanediol, which are metabolized in the body to GHB.38
The salty powder usually is dissolved in water and sold at $5 to $10 per dose. Overdose is common because the strength of the solution is often unknown. The unpleasant salty or soapy taste may be masked in flavored or alcoholic beverages.39 Effects of GHB appear within 15 to 30 minutes of oral ingestion and peak at 20 to 60 minutes, depending on whether it is mixed with food. Toxicity is increased if taken with alcohol or other CNS depressants.40
GHB produces euphoria, progressing with higher doses to dizziness, hypersalivation, hypotonia, and amnesia.41 Overdose may result in Cheyne-Stokes respiration, seizures, coma, and death. Coma may be interrupted by agitation, with flailing activity described similar to a drowning swimmer fighting for air.42 Bradycardia and hypothermia are reported in about one third of patients admitted to a hospital for using GHB and appear to be correlated with the level of consciousness.43 Chronic use of GHB may produce dependence and a withdrawal syndrome that includes anxiety, insomnia, tremor, and in severe cases, treatment-resistant psychoses.44
Flunitrazepam, marketed as Rohypnol, is a potent benzodiazepine with a rapid onset. Manufactured by Roche Laboratories, it is available in more than 60 countries in Europe and Latin America for preoperative anesthesia, sedation, and treatment of insomnia. In the United States, imported Rohypnol came to prominence in the 1990s as an inexpensive recreational sedative and a “date rape” drug.45 The tablets are sold on the street for $0.50 to $5 a piece.
In a single 1- or 2-mg dose, Rohypnol reduces anxiety, inhibition, and muscular tension with a potency that is approximately 10 times that of diazepam (Valium). Higher doses produce anterograde amnesia, lack of muscular control, and loss of consciousness. Effects occur about 30 minutes after ingestion, peak at two hours, and may last up to eight to 12 hours. The effects are much greater with the concurrent ingestion of alcohol or other sedating drugs. Some users experience hypotension, dizziness, confusion, visual disturbances, urinary retention, or aggressive behavior.46
Like other benzodiazepines, chronic use of Rohypnol can produce dependence. The withdrawal syndrome includes headache, tension, anxiety, restlessness, muscle pain, photosensitivity, numbness and tingling of the extremities, and increased seizure potential.47
Ketamine was derived from phencyclidine (PCP) in the 1960s for use as a dissociative anesthetic.48 It causes anesthesia without respiratory depression by inhibiting the neuronal uptake of norepinephrine, dopamine, serotonin, and glutamate activation in the N-methyl-D-aspartate receptor channel.49 This agent can cause bizarre ideations and hallucinations—side effects that limited its medical use but appealed to recreational drug users.
Ketamine is difficult to manufacture; therefore, most of the illicit supply is diverted from human and veterinary anesthesia products. As a pharmaceutical, ketamine is distributed in a liquid form that can be ingested or injected. In clubs, it usually has been dried to a powder and is smoked in a mixture of marijuana or tobacco, or is taken intranasally. A typical method uses a nasal inhaler, called a “bullet” or “bumper”; an inhalation is called a “bump”. Ketamine often is taken in “trail mixes” of methamphetamine, cocaine, sildenafil citrate (Viagra), or heroin.50
Effects of ketamine ingestion appear rapidly and last about 30 to 45 minutes, with sensations of floating outside the body, visual hallucinations, and a dream-like state.51 Along with these “desired” effects, users also commonly experience confusion, anterograde amnesia, and delirium. They also may experience tachycardia, palpitations, hypertension, and respiratory depression with apnea. “Flashbacks” or visual disturbances can be experienced days or weeks after ingestion.32 Some chronic users become addicted and exhibit severe withdrawal symptoms that require detoxification.
Because club drugs are illicitly obtained and often are adulterated or substituted, they must be considered as unknown substances. In the ever-changing world of illegal drug distribution, Internet Web sites can be helpful in identifying the rapidly changing appearances of these substances (Table 2).
The immediate concern with the use of club drugs is cardiorespiratory maintenance. Users often present with multiple drug ingestions, which may include stimulant and depressant drugs (e.g., MDMA combined with GHB or alcohol). When the predominant symptoms are controlled, the symptoms of a second underlying drug may surface. Most hallucinogens are CNS stimulants; in overdose, patients may exhibit hyperthermia, hypertension, tachycardia, anxiety, and agitation. The risk of escape or self-injury also should be considered.
No standard treatment regimen has been identified for club drug overdose. Basic management should include cardiac monitoring, pulse oximetry, urinalysis, and performance of a comprehensive chemistry panel to check for electrolyte imbalance, renal toxicity, and possible underlying disorders (Figure 1). Precautions should be taken to prevent seizures.19
Gastrointestinal decontamination with activated charcoal and a cathartic may be useful in acute exposures if the drug was taken orally within the previous 60 minutes. Otherwise, unless a massive dose was taken, inducing emesis is seldom effective and may increase psychologic distress. Hypertension and tachycardia generally will resolve with the management of anxiety or agitation. Severe hypertension can be treated with labetalol (Normodyne), phentolamine (Regitine), nitroprusside (Nipride), or similar agents. For agitation, benzodiazepines such as diazepam, lorazepam (Ativan), or midazolam (Versed) may be used.52
Algorithm for the management and treatment of ingestion of a ”club drug.” (MDMA = 3,4-methylenedioxymethamphetamine; LSD = lysergic acid diethylamide; 2-CB = 4-bromo-2,5-dimethoxyamphetamine; GHB = gamma-hydroxybutyrate; IV = intravenous)
Hyperthermia should be treated immediately with tepid water bathing and fanning. One study53 reported that a single tablet of MDMA resulted in fatal hyperthermia. The use of dantrolene (Dantrium) is questionable and no longer recommended.54 Alkalinization of the urine, which usually is recommended for rhabdomyolysis, should be used cautiously because it reduces the renal clearance of amphetamine. The serotonin antagonists chlorpromazine (Thorazine) and cyproheptadine (Periactin) appear to be effective in mild to moderate cases of serotonin syndrome.55
There are no specific antidotes for ingestion of club drugs, except for Rohypnol, which has the antidote flumazenil. With supportive care, patients usually will recover completely within seven hours.
GHB has a rapid elimination, and the drug is cleared within four to six hours after ingestion, regardless of the dose. Intubation should be avoided unless it is absolutely necessary, because patients may become unexpectedly combative or have protracted periods of emesis.56 The presence of trismus suggests ingestion of stimulants and makes intubation more difficult. A benzodiazepine may be given for withdrawal symptoms.
Urine or blood tests for amphetamine or methamphetamine may detect MDMA; these tests also will detect MDMA-related compounds such as 2-CB, but with decreased sensitivity.57 A 50-mg dose of MDMA can be detected as unchanged drug in the urine up to 72 hours after ingestion. Standard toxicologic tests cannot detect GHB, but the National Forensic Laboratory (National Medical Services, 800–522–6671) will perform urinalysis for detection of GHB for a fee.
Rohypnol and its active metabolite 7-amino-flunitrazepam may be detected by gas chromatography/mass spectrometry testing up to 72 hours after ingestion. For assistance with assay in cases of suspected rape, contact Roche Laboratories (800–608–6540) for a free screening for Rohypnol. Tests for ingestion of ketamine are seldom available, but ketamine may be suspected if a toxicologic test is positive for PCP.58
Providing the patient and family with educational materials about specific substances may be helpful. These materials are available on many Web sites.
1. Gahlinger PM. Illegal drugs: a complete guide to their history, chemistry, use and abuse. New York: Plume, 2004.
2. Cami J, Farre M, Mas M, Roset PN, Poudevida S, Mas A, et al. Human pharmacology of 3,4-methylenedioxymetham-phetamine (“ecstasy”): psychomotor performance and subjective effects. J Clin Psychopharmacol. 2000;20:455–66.
3. Drug Abuse Warning Network. Club drugs. Rockville, Md: Office of Applied Studies, Substance Abuse and Mental Health Services Administration (SAMHSA), 2000.
4. Partnership Attitude Tracking Study Spring 2000. Teens in grades 7 through 12. Accessed March 17 2004 at: http://www.drugfreeamerica.org/acrobat/pats2000full.pdf.
5. Koesters SC, Rogers PD, Rajasingham CR. MDMA (‘ecstasy’) and other ‘club drugs.’ The new epidemic. Pediatr Clin North Am. 2002;49:415–33.
6. Fendrich M, Wislar JS, Johnson TP, Hubbell A. A contextual profile of club drug use among adults in Chicago. Addiction. 2003;98:1693–1703.
7. Lenton S, Boys A, Norcross K. Raves, drugs and experience: drug use by a sample of people who attend raves in Western Australia. Addiction. 1997;92:1327–37.
8. National Institute on Drug Abuse. The Monitoring the Future national results on adolescent drug use: overview of key findings, 2001. Ann Arbor, Mich: University of Michigan Institute for Social Research, 2002.
9. Graeme KA. New drugs of abuse. Emerg Med Clin North Am. 2000;18:625–36.
10. Baggott M, Heifets B, Jones RT, Mendelson J, Sferios E, Zehnder J. Chemical analysis of ecstasy pills. JAMA. 2000;284:2190
11. National Institute on Drug Abuse. Epidemiologic trends in drug abuse: proceedings. Rockville, Md.: National Institute on Drug Abuse, Division of Epidemiology and Prevention Research, 2000.
12. Schwartz RH, Miller NS. MDMA (ecstasy) and the rave: a review. Pediatrics. 1997;100:705–8.
13. Morland J. Toxicity of drug abuse—amphetamine designer drugs (ecstasy): mental effects and consequences of single dose use. Toxicol Lett. 2000;112–3:147–52.
14. Smith KM, Larive LL, Romanelli F. Club drugs: methylene-dioxymethamphetamine, flunitrazepam, ketamine hydrochloride, and gamma-hydroxybutyrate. Am J Health Syst Pharm. 2002;59:1067–76.
15. Olson KR, ed. Poisoning & drug overdose. 4th ed. New York: Lange Medical Books/McGraw-Hill, 2004:209.
16. Lester SJ, Baggott M, Welm S, Schiller NB, Jones RT, Foster E, et al. Cardiovascular effects of 3,4-methylene-dioxymethamphetamine. A double-blind, placebo-controlled trial. Ann Intern Med. 2000;133:969–73.
17. Mueller PD, Korey WS. Death by “ecstasy”: the serotonin syndrome?. Ann Emerg Med. 1998;32:377–80.
18. Inman DS, Greene D. The agony and the ecstasy: acute urinary retention after MDMA abuse. BJU Int. 2003;91:123
19. Teter CJ, Guthrie SK. A comprehensive review of MDMA and GHB: two common club drugs. Pharmacotherapy. 2001;21:1486–513.
20. Mason PJ, Morris VA, Balcezak TJ. Serotonin syndrome. Presentation of 2 cases and review of the literature. Medicine. 2000;79:201–9.
21. Steele TD, McCann UD, Ricaurte GA. 3,4-Methylene-dioxymethamphetamine (MDMA, “Ecstasy”): pharmacology and toxicology in animals and humans. Addiction. 1994;89:539–51.
22. Henry JA, Fallon JK, Kicman AT, Hutt AJ, Cowan DA, Forsling M. Low-dose MDMA (“ecstasy”) induces vasopressin secretion. Lancet. 1998;351:1784
23. Holmes SB, Banerjee AK, Alexander WD. Hyponatremia and seizures after ecstasy use. Postgrad Med J. 1999;75:32–3.
24. Vollenweider FX, Gamma A, Liechti M, Huber T. Psychological and cardiovascular effects and short-term sequelae of MDMA (“ecstasy”) in MDMA-naive healthy volunteers. Neuropsychopharmacology. 1998;19:241–51.
25. Curran HV, Travill RA. Mood and cognitive effects of 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’): week-end ‘high’ followed by mid-week low. Addiction. 1997;92:821–31.
26. Parrott AC, Lasky J. Ecstasy (MDMA) effects upon mood and cognition: before, during and after a Saturday night dance. Psychopharmacology. 1998;139:261–8.
27. Ricaurte GA, McCann UD, Szabo Z, Scheffel U. Toxicodynamics and long-term toxicity of the recreational drug, 3,4-methylenedioxymethamphetamine (MDMA, ‘Ecstasy’). Toxicol Lett. 2000;112–113:143–6.
28. Broening HW, Morford LL, Inman-Wood SL, Fukumura M, Vorhees CV. 3,4-methylenedioxymethamphetamine (ecstasy)-induced learning and memory impairments depend on the age of exposure during early development. J Neurosci. 2001;21:3228–35.
29. Doyon S. The many faces of ecstasy. Curr Opin Pediatr. 2001;13:170–6.
30. Yates KM, O'Connor A, Horsley CA. “Herbal Ecstasy”: a case series of adverse reactions”. N Z Med J. 2000;113:315–7.
31. Li J, Stokes SA, Woeckener A. A tale of novel intoxication: a review of the effects of gamma-hydroxybutyric acid with recommendations for management. Ann Emerg Med. 1998;31:729–36.
32. Freese TE, Miotto K, Reback CJ. The effects and consequences of selected club drugs. J Subst Abuse Treat. 2002;23:151–6.
33. Smith KM. Drugs used in acquaintance rape. J Am Pharm Assoc. 1999;39:519–25.
34. Multistate outbreak of poisonings associated with illicit use of gamma hydroxy butyrate. MMWR Morb Mortal Wkly Rep. 1990;39:861–3.
35. U.S. Drug Enforcement Administration. Gamma Hydroxybutyric Acid (GHB, liquid X, Goop, Georgia Home Boy). DEA News. March 13, 2000. Accessed March 17, 2004 at: http://www.usdoj.gov/dea/pubs/pressrel/pr031300_01.htm.
36. Nimmerrichter AA, Walter H, Gutierrez-Lobos KE, Lesch OM. Double-blind controlled trial of gamma-hydroxybutyrate and clomethiazole in the treatment of alcohol withdrawal. Alcohol Alcohol. 2002;37:67–73.
37. Addolorato G, Balducci G, Capristo E, Attilia ML, Taggi F, Gasbarrini G, et al. Gamma-hydroxybutyric acid (GHB) in the treatment of alcohol withdrawal syndrome: a randomized comparative study versus benzodiazepine. Alcohol Clin Exp Res. 1999;23:1596–604.
38. Ingels M, Rangan C, Bellezzo J, Clark RF. Coma and respiratory depression following the ingestion of GHB and its precursors: three cases. J Emerg Med. 2000;19:47–50.
39. Eckstein M, Henderson SO, DelaCruz P, Newton E. Gamma hydroxybutyrate (GHB): report of a mass intoxication and review of the literature. Prehosp Emerg Care. 1999;3:357–61.
40. Chin MY, Kreutzer RA, Dyer JE. Acute poisoning from gamma-hydroxybutyrate in California. West J Med. 1992;156:380–4.
41. Garrison G, Mueller P. Clinical features and outcomes after unintentional gamma hydroxybutyrate (GHB) overdose [Abstract]. J Toxicol Clin Toxicol. 1998;36:503–4.
42. Dyer JE. Gamma-hydroxybutyrate: a health-food product producing coma and seizurelike activity. Am J Emerg Med. 1991;9:321–4.
43. Chin RL, Sporer KA, Cullison B, Dyer JE, Wu TD. Clinical course of gamma-hydroxybutyrate overdose. Ann Emerg Med. 1998;31:716–22.
44. Dyer JE, Roth B, Hyma BA. Gamma-hydroxybutyrate withdrawal syndrome. Ann Emerg Med. 2001;37:147–53.
45. Anglin D, Spears KL, Hutson HR. Flunitrazepam and its involvement in date or acquaintance rape. Acad Emerg Med. 1997;4:323–6.
46. Schwartz RH, Weaver AB. Rohypnol, the date rape drug. Clin Pediatr. 1998;37:321
47. Miotto K, Darakjian J, Basch J, Murray S, Zogg J, Rawson R. Gamma-hydroxybutyric acid: patterns of use, effects and withdrawal. Am J Addict. 2001;10:232–41.
48. Kohrs R, Durieux ME. Ketamine: teaching an old drug new tricks. Anesth Analg. 1998;87:1186–93.
49. Krystal JH, Karper LP, Seibyl JP, Freeman GK, Delaney R, Bremner JD, et al. Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses. Arch Gen Psychiatry. 1994;51:199–214.
50. Tellier PP. Club drugs: is it all ecstasy?. Pediatric Ann. 2002;31:550–6.
51. Jansen KL. Non-medical use of ketamine. BMJ. 1993;306:601–2.
52. Ellenhorn MJ, Barceloux DG, Ellenhorn MJ. Ellenhorn's Medical toxicology: diagnosis and treatment of human poisoning. 2d ed. Baltimore: Williams & Wilkins, 1997.
53. Dar KJ, McBrien ME. MDMA induced hyperthermia: report of a fatality and review of current therapy. Intensive Care Med. 1996;22:995–6.
54. Watson JD, Ferguson C, Hinds CJ, Skinner R, Coakley JH. Exertional heat stroke induced by amphetamine analogues. Does dantrolene have a place?. Anaesthesia. 1993;48:1057–60.
55. Martin TG. Serotonin syndrome. Ann Emerg Med. 1996;28:520–6.
56. O'Connell T, Kaye L, Plosay JJ . 3d Gamma-hydroxybutyrate (GHB): a newer drug of abuse. Am Fam Physician. 2000;62:2478–83.
57. Christophersen AS. Amphetamine designer drugs— an overview and epidemiology. Toxicol Lett. 2000;112–113:127–31.
58. Weiner AL, Vieira L, McKay CA, Bayer MJ. Ketamine abusers presenting to the emergency department: a case series. J Emerg Med. 2000;18:447–51.
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