Chapter 14 Hallucinogens and Club Drugs

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DOI: 10.1176/appi.books.9781585623440.347400

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Chapter 14. Hallucinogens and Club Drugs

HALLUCINOGENS AND CLUB DRUGS: INTRODUCTION

Drugs considered hallucinogens are a diverse group of compounds (Table 14–1) including lysergic

acid diethylamide (LSD), designer drugs, and many others that produce perceptual distortions

(rarely complete hallucinations). Phencyclidine (PCP) and ketamine are dissociative anesthetics

that produce perceptual distortions similar to hallucinogens, resulting in their being classified as

hallucinogens. Designer drugs are synthetic compounds that are chemically related to stimulants,

often with additions to the phenyl ring of amphetamine that cause them to have hallucinogen

properties. These ring substitutions, such as are found in methylenedioxymethamphetamine

(MDMA; “ecstasy”), can produce perceptual distortions.

TABLE 14–1. Hallucinogens

Chemical name Abbreviation Street name(s) Source

Lysergic acid diethylamide LSD Acid, blotter, microdot Synthetic

Lysergic acid hydroxyethylamide LSA Natural high, organic

high

Morning glory seeds,

Hawaiian baby woodrose

Mescaline

Mesc, peyote, cactus Peyote cactus

Psilocybin

Magic mushrooms,

‘shrooms

Mushrooms

Ibotenic acid, muscimol

Mushrooms

Bufotenine

Bufo, toad-licking Colorado river toad venom

Dimethyltryptamine DMT Dimitri, businessman’s

trip, Fantasia

Canary grass, prairie

bundleflower

Alphamethyltryptamine AMT Love pills, trip Synthetic

Bromo-dimethoxyphenethylamine 2C-B Bromo, DOB, nexus,

spectrum

Synthetic

Dimethoxy-propylthiophenethylamine 2C-T-7 7-Up, tripstacy, blue

mystic

Synthetic

Dimethoxymethyl-amphetamine DOM STP (serenity, tranquility

and peace)

Synthetic

Methylenedioxymethamphetamine MDMA Ecstasy, X, Adam Synthetic

Methylenedioxyamphetamine MDA The love drug, Eve Synthetic

Phencyclidine PCP Angel dust, PeaCe pill Synthetic

Ketamine

Special K, kit cat, cat

valium

Synthetic

Club drugs are licit and illicit drugs from different classes that are used primarily by young adults in

bars, clubs, concerts, and dance parties or “raves.” The National Institute on Drug Abuse (NIDA)

has identified six drugs as club drugs (Table 14–2), including some hallucinogens (LSD, MDMA).

However, the club drug scene changes rapidly and can include prescription and over-the-counter

drugs (Table 14–3). There is wide geographic variation in popularity of different club drugs. These

substances are used illicitly in those settings due to the perception that they enhance the sensoryPrint: Chapter 14. Hallucinogens and Club Drugs http://www.psychiatryonline.com/popup.aspx?aID=347404&print=yes…

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experience at dance parties where strobe lights, glow sticks, and techno music (wordless music

with a driving beat) are part of the overall event.

TABLE 14–2. Club drugs identified by the National Institute on Drug Abuse

Chemical name Abbreviation Street name(s) Drug class

Lysergic acid diethylamide LSD Acid, blotter, microdot Prototypical hallucinogen

Ketamine

Special K, kit cat, cat valium Arylcyclohexylamine

hallucinogen

Methamphetamine

Crank, crystal meth, ice,

speed

Stimulant

Methylenedioxymethamphetamine MDMA Ecstasy, X, Adam Designer drug stimulant

-Hydroxybutyrate GHB Georgia home boy, grievous

bodily harm, liquid ecstasy

Sedative

Flunitrazepam (Rohypnol) Roofies, rope, Mexican valium Benzodiazepine sedative

TABLE 14–3. Additional club drugs

Chemical name Brand name(s) Street name(s) Drug class

Methylphenidate Ritalin Rits, smart pills, vitamin R Stimulant

Pseudoephedrine Sudafed

Stimulant

(over-the-counter)

Alprazolam Xanax X, Blue haze Benzodiazepine

Diazepam Valium Downers, mother’s little helper,

V’s

Benzodiazepine

Hydrocodone Vicodin, Lortab, Hycodan Vike, hykes Opioid

Oxycodone Percocet, Tylox,

OxyContin

Oxy, perc, OC, hillbilly heroin Opioid

Dextromethorphan Robitussin, Coricidin Dex, DXM, robo, triple C’s Opioid (over-the-counter)

HALLUCINOGENS

There are many types of hallucinogens, including naturally occurring plant and animal derivatives,

synthetic drugs, and designer drugs. The prototypical hallucinogens are LSD, psilocybin, and

mescaline; LSD is labeled a club drug by NIDA. Designer drugs are synthetic derivatives of federally

controlled substances, created by slight alterations in the molecular structure and produced

illegally in clandestine laboratories. Designer drugs have some psychoactive properties and cause

visual disturbances but are not true hallucinogens like LSD (Beebe and Walley 1991).

Hallucinogens may be taken orally, smoked, or injected. Some hallucinogens are derived from

plants and may be consumed in this organic form (Stephens 1999). Very potent hallucinogens, such

as LSD, may exert their effects from even a single drop touched to the tongue.

Hallucinogen abuse dropped off precipitously in the mid- and late 1970s and remained at low levels

during the 1980s. A U.S. study reported in 2006 found that lifetime LSD use (13%) was second only

to ecstasy use (14%) by young adults ages 16–23 years (Wu et al. 2006). Use of LSD is associated

with frequent heavy alcohol use and high-risk sexual behavior (Rickert et al. 2003) as well as

criminal activity (Wu et al. 2006).

Acute Intoxication

Recreational users of hallucinogens describe many different experiences from their hallucinogen

use. Perceptual distortions are more common than hallucinations (Table 14–4). Some users have

described existential experiences such as feelings of oneness with the universe or greatPrint: Chapter 14. Hallucinogens and Club Drugs http://www.psychiatryonline.com/popup.aspx?aID=347404&print=yes…

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understanding.

TABLE 14–4. Hallucinogen intoxication

Physiological

effects

Psychological effects Perceptual distortions

Pupillary dilation

Tachycardia

Diaphoresis

Incoordination

Vomiting

Tremulousness

Hyperreflexia

Seizures

Anxiety

Depression

Paranoia

Hallucinations

Impaired judgment

Ideas of reference (getting personal

messages from the television or radio)

Depersonalization (“I am not real”)

Derealization (“the environment is not

real”)

Intensification of perceptions

Light trails behind moving objects

Micropsia (the sensation that the user is very

small in relation to the surroundings)

Macropsia (the sensation that the user is very

large in relation to the surroundings)

Synesthesias (cross-linking of the five

senses; e.g., “see the sounds, taste the

colors”)

Signs and symptoms

Hallucinogens produce perceptual distortions and cognitive changes with a clear sensorium and

without impairment in level of consciousness or attention (Abraham et al. 1996). The quality of the

hallucinogen-induced psychedelic state, or “trip,” is influenced by the mood and environment of the

user at the time of induction (set and setting; Zinberg 1980). A bad trip can be caused by fear,

anxiety, or anger at the time the drug is taken; most bad trips can be handled without medication

by a friend, nurse, or physician. It may be difficult to distinguish between a bad trip and an acute

psychotic reaction.

Reactions to hallucinogenic drugs are idiosyncratic, with periods of lucidity alternating with periods

of intense reaction to the drug. Individual reactions to the hallucinogen vary according to the purity

of the drug taken, the dose, and the setting. Generally, reactions are most intense and frequent in

the early part of a trip, leading to a peak and then longer periods of lucidity with gradual clearing of

the drug.

Acute physiological complications of hallucinogen intoxication rarely require medical treatment.

However, malignant hyperthermia and seizures may occur. Agitation, dry skin, and increased

muscle tension are warning signs for hallucinogen hyperthermia. Clinical features of hallucinogen

intoxication are in Table 14–4.

Treatment

It is important to make physical contact with the patient (e.g., holding hands) when treating a bad

trip; this may be the only means of contact with someone who is having very severe hallucinations.

The patient may react suddenly or violently to a touch, and the contact person should be alert for

this. The physical space in which treatment takes place should be quiet, softly lit, and away from

large groups of people; excessive stimuli may overwhelm the patient. Absence of stimuli, however,

may intensify the hallucinations. Deep, slow breathing may be helpful as a distraction. Try to make

contact with the patient during lucid intervals and maintain this contact into the intense periods of

drug reaction. Efforts to make contact with the patient during an intense period are generally not

fruitful. Severe agitation may be treated with a benzodiazepine or haloperidol.

As with any drug intoxication or overdose, if verbal contact can be made, ascertain what was taken,

how much was taken, and how long ago it was taken. It may be helpful to have parents or friends

retrieve a sample from the same batch and to talk to others who took the same dose at the same

time.

Long-Term Consequences

The long-term consequence most commonly associated with hallucinogen use is flashbacks. APrint: Chapter 14. Hallucinogens and Club Drugs http://www.psychiatryonline.com/popup.aspx?aID=347404&print=yes…

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flashback is an episode during which certain aspects of a previous hallucinogenic experience are

reexperienced unexpectedly. The content varies widely and may include emotional or somatic

components but most often involves reexperience of perceptual effects. This may consist of

afterimages, trails behind moving objects, flashes of color, or lights in the peripheral visual fields.

These episodes last several seconds to several minutes and are self-limited. Triggers include stress,

exercise, use of other drugs (especially marijuana), or entering a situation similar to the original

drug experience. Flashbacks may also occur spontaneously and their unpredictability often

provokes anxiety when they occur. Flashbacks are fairly rare and tend over time to decrease in

frequency, duration, and intensity as long as no additional hallucinogen is taken (Strassman 1984).

Flashbacks are unlikely to occur more than 1 year after the original hallucinogen experience.

Treatment of flashbacks consists of supportive care, including reassurance that the episode will be

brief. Benzodiazepines help reduce anxiety, but haloperidol can worsen flashbacks (Moskowitz

1971).

Hallucinogen use may result in long-term psychiatric consequences, such as anxiety, depression, or

psychosis. The risk of a prolonged psychiatric reaction depends on the user’s underlying

predisposition to develop psychopathology, the amount of prior hallucinogen use, the use of other

drugs, as well as the dose and purity of the hallucinogen taken (Strassman 1984). Patients may

present with apathy, hypomania, paranoia, delusions, hallucinations, formal thought disorder, or

dissociative states. Treatment of prolonged anxiety, depression, or psychosis is the same as when

these conditions are not associated with hallucinogen use.

PHENCYCLIDINE AND KETAMINE

PCP and ketamine are arylcyclohexylamines, which are dissociative anesthetics that produce

perceptual distortions similar to hallucinogens, as well as other effects. PCP at various times has

achieved popularity as a street drug and is frequently sold in mixtures with other drugs (Schnoll

1980). Its use waxes and wanes because of its unpredictable effects. Ketamine is a derivative of

PCP that is less potent and shorter-acting and is still used therapeutically in medical settings as an

anesthetic in humans (Chen et al. 1959). Ketamine use has a low prevalence among adolescents in

the general population, but use appears to be concentrated among young adults attending clubs or

parties, including raves. It is labeled a club drug by NIDA. Ketamine users are older (in their 20s as

opposed to teens), employed, and better educated compared with most other club drug users

(Dillon et al. 2003).

PCP and ketamine can be taken orally or intravenously, smoked, or inhaled. Reasons cited for

taking them are to enhance self-exploration as well as to induce relaxation and pleasure (Dalgarno

and Shewan 1996). The PCP experience is regarded as pleasant only half the time and as aversive

the other half, but some users report that this unpredictability of effects is an attractive feature

(Carroll 1985).

Acute Intoxication

Signs and symptoms

PCP produces brief dissociative psychotic reactions, similar to schizophrenic psychoses. These

reactions are characterized by changes in body image (feeling that the body is made of wood,

plastic, or rubber) and possible feelings of spiritual separation from the body. At higher doses,

users have great difficulty differentiating between themselves and their surroundings. Some users

have religious experiences while intoxicated, such as feelings of meeting God or of impending

death (Gorelick et al. 1986). Ketamine effects include profound changes in consciousness and

psychotomimetic effects similar to those of PCP, including out-of-body experiences.

In low-dose intoxication, the patient presents with nystagmus, confusion, ataxia, and sensory

impairment. This is the only drug of abuse that causes a characteristic vertical nystagmus (it can

also cause horizontal or rotatory nystagmus), which helps to identify it as the cause when a patient

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Moderate PCP intake may lead to a catatonic-like state, with the patient staring blankly and not

responding to stimuli; the eyes remain open, even when the patient is in a comatose state. In high

doses, the drug produces seizures and severe hypertension. The hypertension should be treated

vigorously because it may cause hypertensive encephalopathy or intracerebral bleeding. PCP can

also cause life-threatening hyperthermia, with temperatures above 106˚F, which may occur many

hours after use.

A dissociative phenomenon occurs occasionally, with PCP abusers exhibiting dangerous or violent

behaviors (Marrs-Simon et al. 1988). The patient also may appear psychotic. Previous psychiatric

history is associated with a higher likelihood for assaultive behavior from PCP use (McCardle and

Fishbein 1989). Levels of consciousness may fluctuate rapidly while the patient is recovering from

the intoxication. The effects of PCP can last for several days.

Ketamine can induce a state of virtual helplessness and pronounced lack of coordination. This is

known to users as “being in a K-hole” and can be problematic if the user is in a public setting

(Jansen 1993).

Treatment

The most effective treatment of PCP intoxication is to increase its urinary excretion by acidifying

the urine with ammonium chloride or ascorbic acid (Weaver and Schnoll 2007). Urine acidification

should only be performed after it is determined that the patient does not have myoglobinuria

(indicating rhabdomyolysis), to prevent the development of acute renal failure. Some practitioners

feel that the benefits of urine acidification are outweighed by the risks, especially in patients with

hepatic or renal impairment. If the patient is at low risk for hepatic or renal disease, the urine pH

should be monitored and kept around 5.5, after which a diuretic can be administered to enhance

excretion. The urine should be checked for the presence of PCP to ensure that it is being excreted.

PCP can be deposited in adipose tissue and released over time, which may result in a prolonged

state of confusion that can last for weeks; urine acidification may be helpful to deplete the reserve

drug.

In a patient who is hypertensive due to PCP, intravenous antihypertensive medications should be

administered to reduce blood pressure. Psychotic behavior can be treated with haloperidol. If the

patient is severely agitated and poses a potential threat to self or others, haloperidol or lorazepam

is effective to control agitation; barbiturates may be even more efficacious (Olney et al. 1991).

Long-Term Consequences

Phencyclidine organic mental disorder is a mental impairment that may result from chronic PCP use

(Weaver and Schnoll 2007). Characteristics include memory deficits, confusion or reduced

intellectual function, assaultiveness, visual disturbances, and speech difficulty. The most common

speech difficulty is blocking, which is the inability to retrieve the proper words. The course is

variable.

STIMULANTS

Stimulants are drugs that stimulate the central nervous system (CNS) to produce enhanced

psychomotor activity. Methamphetamine is a stimulant that is classified as a club drug by NIDA.

Ecstasy (MDMA) is a designer drug that is also a stimulant but has some hallucinogen-like effects

and is classified as a club drug by NIDA. Methylphenidate is a prescription stimulant that is used

primarily for treatment of attention-deficit disorder and is abused at parties and clubs, although it

has not been classified as a club drug by NIDA. Pseudoephedrine is an over-the-counter stimulant

found in cough and cold preparations that is abused by teenagers.

Stimulants are typically taken as tablets when used as club drugs. Methamphetamine can be

intranasally insufflated (sniffed, snorted) or smoked as well as taken orally.

Acute Intoxication

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The short-term complications of methamphetamine and other stimulants are due to increased

sympathomimetic effects (Table 14–5). Repeated use of low doses of stimulants can result in

exaggerated startle reactions, dyskinesias, and postural abnormalities (Weaver and Schnoll 1999).

Toxicity may be related to additives to the designer drugs, including ketamine and LSD.

TABLE 14–5. Stimulant intoxication

Physiological effects Psychological effects Toxic effects

Dizziness

Tremor

Hyperreflexia

Hyperpyrexia

Mydriasis

Tachypnea

Tachycardia

Hypertension

Grandiosity

Restlessness

Hypervigilance

Aggression

Impaired judgment

Stereotyped behavior

Hyperthermia

Seizures

Rhabdomyolysis

Acute renal failure

Hepatotoxicity

Increased myocardial oxygen consumption

Disseminated intravascular coagulation

Treatment

The acutely intoxicated stimulant user should be approached in a subdued manner; never speak in

a loud voice or move quickly, never approach the patient from behind, and try to avoid touching the

patient unless absolutely sure it is safe to do so (Weaver et al. 1999).

Treatment for acute toxicity includes acute stabilization of airway, breathing, and circulation;

activated charcoal; seizure control with benzodiazepines; aggressive management of hypertension

with and antagonists or vasodilators; management of hyperthermia; and consideration of urine

acidification.

Long-Term Consequences

High-dose stimulant use over long periods of time causes neurophysiological changes in brain

systems; CNS effects can take months to resolve, and occasionally do not resolve, after cessation of

stimulant use. As an example, a study in twins found that after at least 1 year of abstinence, the

abusing twin had deficits in attention and motor skills as compared with the nonabusing twin

(Toomey et al. 2003). Brain imaging of methamphetamine users has shown structural deficits,

including gray matter deficits in the cingulate, limbic, and paralimbic cortices and significant

reductions in hippocampal volume (Thompson et al. 2004).

Chronic use of MDMA can lead to a paranoid psychosis that is clinically indistinguishable from

schizophrenia; it is usually reversible after a prolonged drug-free state (Buchanan and Brown

1988). Several studies suggest that MDMA use (possibly in conjunction with marijuana) can lead to

cognitive decline in otherwise healthy young people (Gouzoulis-Mayfrank et al. 2000). This

neurotoxicity has been described to occur with typical recreational doses.

An abstinence syndrome can occur with chronic stimulant use. The severity and duration of

withdrawal depend on the intensity of the preceding months of chronic abuse and the presence of

predisposing psychiatric disorders that amplify withdrawal symptoms. Abrupt discontinuation of

stimulants does not cause gross physiological sequelae. If marked depression persists longer than

1 week after withdrawal, the patient should be evaluated carefully to determine if he or she is

“self-medicating” an underlying depression, which then should be treated with a specific

antidepressant.

The clinical features of chronic stimulant use include depression, fatigue, poor concentration, and

mild parkinsonian features such as myoclonus (inappropriate, spontaneous muscle contractions),

tremor, or bradykinesia (slowing of movements). Patients presenting with these signs should be

suspected of stimulant abuse and screened carefully (Weaver and Schnoll 1999). Long-term

methamphetamine dependence can cause neurotoxicity even in patients who are no longer users

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-HYDROXYBUTYRATE

-Hydroxybutyrate (GHB) is a sedative that is both a precursor and a metabolite of -aminobutyric

acid (GABA). It has been used as a sleep aid as well as for treatment of narcolepsy (Lammers et al.

1993). It also increases episodic secretion of growth hormone, so some bodybuilders use it to

promote muscle growth. It is relatively easy to manufacture from common household products,

although improper manufacture may result in unintended toxic by-products. NIDA has labeled GHB

a club drug.

GHB is ingested orally as a liquid, is rapidly absorbed, and reaches peak plasma concentrations in

20–60 minutes. Desired effects last for around 3 hours and repeated use may prolong its effects.

Users report that GHB induces a pleasant state of relaxation and tranquility. Its effects have been

likened to those of alcohol, another GABAlike drug (McCabe et al. 1971), with placidity, mild

euphoria, mild numbing, pleasant disinhibition, and an enhanced tendency to verbalize.

Acute Intoxication

The dose-response curve for GHB is exceedingly steep, so small increases in the amount ingested

may lead to significant intensification of effects and onset of CNS depression. GHB has an

extremely small therapeutic index, and as little as double the euphorigenic dose may cause serious

CNS depression. Furthermore, the drug has synergistic effects with alcohol and other drugs,

increasing the chance of overdose.

Signs and symptoms

Clinicians should remember to ask about GHB use, especially in younger people. Because GHB is not

detectable by routine drug screening, this history is essential. Clinical features of GHB intoxication

are in Table 14–6. Death may result from overdose, and increasing numbers of deaths have been

linked to GHB (Li et al. 1998).

TABLE 14–6. -Hydroxybutyrate intoxication

Physiological effects Psychological effects Toxic effects

Dizziness

Loss of peripheral vision

Vomiting

Weakness

Bradycardia

Ataxia

Loss of coordination

Confusion

Agitation

Hallucinations

Sleepwalking

Temporary amnesia

Clonus

Loss of bladder control

Cardiopulmonary depression

Seizures

Coma/Persistent vegetative state

Treatment

In cases of acute GHB intoxication, physicians should provide physiological support and maintain a

high index of suspicion for intoxication with other drugs. Most patients who overdose on GHB

recover completely if they receive proper medical attention. Management of GHB ingestion in a

spontaneously breathing patient includes oxygen supplementation, intravenous access, and

comprehensive physiological and cardiac monitoring (Li et al. 1998). Attempt to keep the patient

stimulated; use atropine for persistent symptomatic bradycardia. Admit the patient to the hospital

if he or she is still intoxicated after 6 hours; discharge the patient (with plans for follow-up) if he or

she is clinically well in 6 hours. Patients whose breathing is labored should be managed in the

intensive care unit.

The most dangerous effects of GHB use often occur with the use of other drugs. Concurrent use of

sedatives or alcohol may increase the risk of vomiting, aspiration, or cardiopulmonary depression;

the use of GHB and stimulants may increase the risk of seizure.

Long-Term Consequences

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times a day. The symptoms of withdrawal include anxiety, tremor, insomnia, and “feelings of

doom,” which may persist for several weeks after stopping the drug (Galloway et al. 1997). Severe

withdrawal involves agitation, delirium, and psychosis (McDaniel and Miotto 2001). GHB

withdrawal should be treated with benzodiazepines; very high doses may be required (Dyer et al.

2001). Antipsychotics or pentobarbital (Sivilotti et al. 2001) may have some utility in treatment of

severe GHB withdrawal.

PRESCRIPTION DRUGS

Flunitrazepam (Rohypnol, roofies) is a short-acting benzodiazepine that is available by prescription

in South America and Europe but not in the United States. It is labeled a club drug by NIDA. Some

prescription medications, although not officially listed as club drugs by NIDA, are used at parties

and clubs (Table 14–3). These include benzodiazepines (alprazolam, diazepam), opioids

(hydrocodone, oxycodone), and stimulants (methylphenidate, amphetamine). Over-the-counter

preparations containing dextromethorphan (Bobo et al. 2003) or pseudoephedrine may also be

used as club drugs. Teenagers may take bottles of medications from their parents’ medicine

cabinets to parties to distribute to friends for recreational use, a practice known as pharming.

Acute Intoxication

Signs and symptoms

The clinical features of acute benzodiazepine intoxication include slurred speech, incoordination,

unsteady gait, and impaired attention or memory; severe overdose may lead to stupor or coma.

Psychiatric manifestations include inappropriate behavior, labile mood, and impaired judgment and

social functioning. Physical signs include nystagmus and decreased reflexes.

Prescription opioid analgesics may be abused and can lead to intoxication or overdose. OxyContin,

an oral controlled-release formulation of oxycodone, has been abused by crushing the tablets and

then snorting the powder; when taken in this way by individuals who have no tolerance to the drug,

a single 80-mg dose (the highest strength available in a single tablet) can be fatal. Propoxyphene,

meperidine, or tramadol can cause seizures. Acute opioid intoxication is characterized by decreased

mental status, substantially decreased respiration, miotic pupils, and absent bowel sounds (Sporer

1999).

Treatment

Initial management of intoxication and overdose involves general supportive care, including

maintenance of an adequate airway, ventilation, and cardiovascular function. Following

stabilization of respiratory and cardiac function, activated charcoal should be given to prevent

further intestinal absorption of the ingested drug and to prevent active metabolites from being

absorbed through enterohepatic recirculation (Jones and Volans 1999).

A benzodiazepine antagonist, flumazenil (Romazicon), is available for the treatment of acute

benzodiazepine intoxication. However, it may not completely reverse respiratory depression; it can

provoke withdrawal seizures in patients with benzodiazepine dependence or, in a mixed overdose

with tricyclic antidepressants, may precipitate arrhythmias that were suppressed by the sedative

(Lheureux et al. 1992; Weinbroum et al. 1997).

Intravenous naloxone is the drug of choice for management of opioid overdose. It is a relatively

pure opioid antagonist that is highly lipid soluble, has a rapid onset of action, and is well absorbed

intravenously, intramuscularly, or subcutaneously.

Long-Term Consequences

Prescription and over-the-counter club drugs are used primarily by teenagers and young adults

opportunistically and intermittently in party settings. Few data are available about long-term

physiological and psychological consequences of intermittent use of these drug classes

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of long-term use of benzodiazepines are similar to acute features but may be accompanied by a

dementia consisting of recent and remote memory loss (Weaver et al. 1999). Long-term use of

benzodiazepines can worsen underlying depression and anxiety (Rickels et al. 1999).

Club drug users who abuse prescription benzodiazepines and opioids will often do so in an

intermittent or chronic pattern of high doses that are obtained illegally. Chronic use can result in a

withdrawal syndrome that often requires detoxification with cross-tolerant medication

(clonazepam or phenobarbital for benzodiazepine withdrawal and methadone or buprenorphine for

opioid withdrawal).

TREATMENT OF HALLUCINOGEN AND CLUB DRUG ADDICTION

Treatment of hallucinogen abuse and dependence is often difficult due to the young age of most

users and concurrent polysubstance abuse. Treatment involves similar components to that of other

types of substance abuse, including individual counseling, support groups, and 12-step self-help

group attendance. Patients who chronically abuse PCP display characteristics such as

impulsiveness and poor interpersonal relationships (Weaver and Schnoll 2007). This may make

successful treatment more challenging, but a treatment environment with a supportive structure

can be helpful. Due to the dissociative effects of PCP, those who abuse it may have a sense of loss

of contact with their bodies. Progressive relaxation techniques, yoga, and regular exercise may

help patients in treatment to focus and improve their concentration (Weaver and Schnoll 2007).

Treatment of club drug abuse and dependence is challenging for several reasons. The club drugs

consist of several different classes of substances that vary in their psychological and physiological

effects. The pattern of use is usually intermittent in social settings, so this may be perceived as less

of a problem. Adolescents and young adults are the primary club drug users, so family members

should be part of the treatment program. As with hallucinogens, treatment of club drug abuse and

dependence involves modalities typically utilized in other types of substance abuse, including

cognitive-behavioral therapy, motivational enhancement therapy, and 12-step self-help group

facilitation.

Mixing hallucinogen and club drug abusers together in treatment settings makes clinical sense,

since the majority of users abuse multiple drugs. There is no pharmacological treatment available

for hallucinogen abuse (Abraham et al. 1996). Most pharmacological agents have not proven

significantly better than placebo for management of stimulant-dependent men and women

(Heinzerling et al. 2006; Schuckit 1994). Treatment settings for hallucinogens and club drugs focus

on behavioral components such as individual and group counseling.

Contingency management is a strategy for promoting treatment compliance and/or drug

abstinence in substance abusers. Individualized positive reinforcement (such as a monetary

incentive or reduction in parole time) is contingent on drug abstinence. Patients receive

voucher-based incentives for achieving a specified therapeutic goal, such as drug-free urine

screenings. As the patient maintains abstinence, the abstinence becomes the primary reinforcer,

and the vouchers are no longer necessary. This modality was first developed for treatment of

cocaine abuse (Higgins et al. 1991) and has proven effective in increasing the period of continuous

abstinence from methamphetamine (Roll et al. 2006) as well as other substances of abuse (Lussier

et al. 2006). This may be an effective intervention for those who abuse hallucinogens and club

drugs, but more research is required.

KEY POINTS

There are many different types of hallucinogens, derived from different sources. Lysergic acid diethylamide

(LSD) is the prototypical hallucinogen and is the most commonly abused.

Hallucinogens cause perceptual distortions more than hallucinations, and “bad trips” do not often require

medical treatment.Print: Chapter 14. Hallucinogens and Club Drugs http://www.psychiatryonline.com/popup.aspx?aID=347404&print=yes…

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Club drugs identified by the National Institute on Drug Abuse are LSD, ketamine, methamphetamine,

methylenedioxymethamphetamine (MDMA), -hydroxybutyrate (GHB), and flunitrazepam. Other club drugs

may include prescription opioids, benzodiazepines, and over-the-counter cold preparations.

Intoxication or overdose from certain club drugs (GHB, opioids, benzodiazepines), especially in combination,

may result in serious medical consequences and death.

Treatment of hallucinogen and/or club drug abuse involves components such as individual counseling,

support groups, and 12-step self-help group attendance.

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SUGGESTED READING

Dance Safe: Available at http://www.dancesafe.org

Strassman RJ: Adverse reactions to psychedelic drugs: a review of the literature. J Nerv Ment Dis

172:577–595, 1984

Wu LT, Schlenger WE, Galvin DM: Concurrent use of methamphetamine, MDMA, LSD, ketamine, GHB, and

flunitrazepam among American youths. Drug Alcohol Depend 84:102–113, 2006

National Institute on Drug Abuse: Important information and resources on club drugs. Available at

http://www.clubdrugs.org

U.S. Office of National Drug Control Policy: Available at http://www.whitehousedrugpolicy.gov

Copyright © 2008 American Psychiatric Publishing, Inc. All Rights Reserved.