Misrepresented sometimes as a natural and safe hypnotic, the low therapeutic
index and the unknown purity of illicit supplies, particularly when sold in solution,
make GHB a potentially dangerous drug. Physical dependency is a possibility as
well. GHB, along with the benzodiazepine flunitrazepam, are considered “date rape”
drugs because they cause profound hypnosis and amnesia. This is intensified when
mixed with alcohol which is often how the sexual predator gives it to his victim.
CENTRAL NERVOUS SYSTEM STIMULANTS
Cocaine is a naturally occurring alkaloid derived from the Erythroxylon coca plant,
found mainly in the Andes Mountains of South America. Cocaine was first isolated in
the 1800s and was a common ingredient in tonics and elixirs of the 1900s. The
Harrison Narcotic Act of 1914 prohibited nonmedical use, and in 1970 it became a
schedule II controlled substance. According to the 2014 National Survey on Drug
Use and Health, nearly 1 million people in the continental United States have a
diagnosed cocaine use disorder within the last year which is similar to the rate in
4 Cocaine is a CNS stimulant and has vasoconstrictive and local anesthetic
properties. Cocaine’s stimulant effects are primarily caused by blockade of the
reuptake of dopamine, norepinephrine, with a small effect on serotonin. It also
facilitates the release of dopamine and norepinephrine. This results in an overall
increase in availability of neurotransmitters. Cocaine also has other indirect effects
on neurophysiology, including effects on the endogenous opioid systems.
is associated with compulsive use. The powerful reinforcing effects of cocaine have
been identified as occurring in brain regions rich in dopaminergic nerve terminals.
DOSAGE FORMS AND ROUTES OF ADMINISTRATION
In the manufacture of cocaine, organic solvents are used to solubilize the alkaloidal
bases from the leaves, which are then precipitated to form a sticky material, called
“pasta” or “cocaine paste.” The benzoylmethylecgonine (cocaine) in this “pasta” is
separated from most of the other plant alkaloids, converted to the hydrochloride or
other salts, precipitated, and dried. This product is the white cocaine hydrochloride
powder usually seen in the illicit market. The final product is usually “stepped on” or
“cut” (diluted) with various adulterants to increase profits for the dealers. According
to the DEA, in 2009 the average purity of cocaine was down from 68.1% in 2006 to
56 Powdered cocaine is generally snorted. Usually 10 to 25 mg of powdered
cocaine is placed on a mirror or flat surface, formed into a line, and then insufflated
through a straw or rolled dollar bill. A typical low to moderate user may consume 1
simultaneously with heroin, this is known as a “speedball.”
Cocaine hydrochloride melts at a high temperature, destroying much of its
psychoactivity in the process. Therefore, it is inefficient to smoke cocaine
hydrochloride in this form. The use of “freebase” cocaine became popular during the
late 1970s, because this form of cocaine has a lower melting point and can therefore
be smoked, producing an intense rush. For freebase, the cocaine hydrochloride is
dissolved into ethyl ether. The synthesis of freebase is dangerous, and the resultant
product may contain residual organic solvents, thus making it highly volatile and
putting the user at risk of burns.
In the mid-1980s a safer, easier method for extracting the cocaine base supplanted
the traditional freebase process. In the manufacture of “crack,” cocaine
hydrochloride is dissolved in water. When alkali (bleach or sodium bicarbonate) is
added to this aqueous solution, the free alkaloidal base (“crack”) precipitates out
whereas the salts and some adulterants stay in aqueous solution. The precipitate is
commonly referred to as a “rock.” The size of the rock varies but generally ranges
from one-tenth of a gram to a half a gram.
Cocaine generally produces a euphoriant action with a rapid onset and short duration.
Snorting cocaine generally produces euphoria and stimulation within 2 minutes;
smoking produces these effects within 6 to 8 seconds. Cocaine has a short
elimination half-life of approximately 30 minutes owing to its rapid metabolism by
esterases in the plasma, liver, brain, and other tissues.
are consumed together, a metabolite, cocaethylene, is formed. Cocaethylene
intensifies the euphoric as well as the toxic effects of cocaine. The risk of death from
cocaethylene is 18 to 25 times greater than with cocaine alone.
An initial relaxed, euphoric, gregarious, talkative, hyperactive state characterizes
the “high” of cocaine. Additionally, the person may report increased interest in
sexual matters, diminished short-term memory, periods of intense concentration on
usually resolve into a state of mild depression, fatigue, hunger, and sleepiness by 1 to
3 hours. Physiologic manifestations include mydriasis, sinus tachycardia,
vasoconstriction with hypertension, bruxism, repetitive behavior, hyperthermia, and
talkativeness. After a few hours, continuous self-administration of cocaine will begin
to progress from euphoria to dysphoria and hallucinosis and then to psychosis. Some
users engage in nonstop binges of self-administration until psychological toxicity
In 2007, 553,530 cocaine-related visits to an emergency department were reported in
58 The potential adverse effects associated with both acute and
chronic use of cocaine are numerous and involve most organ systems in the body.
The cardiac complications associated with cocaine use include hypertension,
arrhythmias, myocardial ischemia and infarction, dilated and hypertrophic
cardiomyopathy, myocarditis, aortic dissection, and acceleration of atherosclerosis.
These cardiac effects have occurred in individuals with and without underlying heart
disease who have taken large or small doses by all routes of administration and may
be associated with acute or chronic use. The cardiac events can occur before, during,
or after other toxicities, such as seizures, and can be fatal. The mechanism of
cocaine-induced myocardial infarction is most likely multifactorial, involving one or
more of the following processes: coronary artery vasoconstriction, increased
myocardial oxygen demand related to increased blood pressure and increased heart
rate, increased platelet aggregation and thrombus formation, coronary vasospasm,
and arrhythmia. The risk is greatest within the first hour after use.
shown 6% of patients presenting to emergency departments with chest pain after
cocaine use have myocardial infarctions.
The medical management of acute coronary syndromes differs when cocaine is the
cause. Specifically, nonselective β-blocker therapy (i.e., propranolol) is
contraindicated due to unopposed alpha affects, thrombolysis should be used with
caution, and nitroglycerine and benzodiazepines are part of first-line therapy.
patients with cocaine-associated chest pain, a 12-hour observation period to rule out
myocardial infarction or ischemia is probably sufficient before discharge from a
Cocaine has also been associated with cerebrovascular catastrophes. Stroke can
occur as a result of increased blood pressure, vasoconstriction, or thrombosis.
Seizures are another CNS complication. Seizures can occur with first use and are
most often single, generalized tonic–clonic seizures. Most occur within 90 minutes of
drug use, when drug plasma concentrations are highest.
The route of cocaine administration also affects the nature of the adverse effects.
For example, pulmonary complications, including pneumomediastinum,
pneumothorax, pneumopericardium, acute exacerbation of asthma, diffuse alveolar
hemorrhage, pulmonary edema, and “crack lung,” are associated with smoking crack
cocaine. Crack lung is a syndrome of acute pulmonary infiltrates associated with a
spectrum of clinical and histologic findings.
56 Snorting cocaine can lead to
perforation of the nasal septum because of the drug’s local anesthetic and
vasoconstrictive effects. IV use of cocaine has been associated with renal infarction,
wound botulism, viral hepatitis, HIV infection, bacterial endocarditis, sepsis, and
other infectious complications.
A person who uses cocaine despite adverse consequences (emergency department
visit), uses it compulsively, suffers withdrawal symptoms, and alleviates symptoms
with further use is diagnosed with cocaine use disorder per the DSM-5. Prolonged or
heavy use of cocaine has been associated with the development of tolerance to some
of its central effects. Tolerance is caused by adaptive changes in the brain.
withdrawal syndrome may follow long-term or binge use. The initial, acute
symptoms, referred to as the “crash,” consist of depression, fatigue, craving,
hypersomnolence, and anxiety. Anhedonia and hyperphagia soon follow. Although
most symptoms are mild and resolve within 1 to 2 weeks, the dysphoria and
anhedonia can persist for weeks. These symptoms do not produce profound
physiologic changes and are generally not life-threatening.
TREATMENT OF COCAINE USE DISORDER
Most cases of simple cocaine withdrawal do not require medical treatment.
However, multiple pharmacologic therapies to facilitate abstinence from cocaine
have been, and continue to be, under investigation. Most studies have yielded
variable results, and to date no drug exists that is proven effective in treating cocaine
15 Studies of dopamine agonists (amantadine, selegiline,
levodopa/carbidopa, pergolide), antidepressants (desipramine, fluoxetine,
bupropion), and carbamazepine have yielded inconsistent findings. Methylphenidate
has been investigated as “maintenance treatment” to satisfy the cocaine addict’s
desire for further enhancement of mood; however, methylphenidate also can stimulate
a powerful craving for the more intense euphoria of cocaine and has significant abuse
potential. Recent research shows promise for topiramate, baclofen, tiagabine, and
modafinil, but these findings require replication.
15 A cocaine vaccine is currently
under investigation. Psychosocial treatments focusing on abstinence have been
effective in the treatment of cocaine dependence.
15 Cognitive-behavioral therapies
and behavioral therapies, such as contingency management, along with 12-step–
oriented individual counseling can be useful, although the efficacy of these therapies
varies. Participation in a 12-step self-help group (AA, NA), as an adjunct to
treatment, seems to predict less cocaine use.
Central nervous system stimulants have been used both with and without social
acceptance for thousands of years. The Chinese prepared ephedrine-containing
products from a plant called Ma-Huang (Ephedra vulgaris).
and the Arabian Peninsula chew the leaves of the khat bush (Catha edulis) for the
stimulating effects of the alkaloid cathinone.
54 Caffeine is consumed worldwide in a
usually socially acceptable manner in the form of coffee and energy drinks.
Amphetamine was synthesized in 1887, and methamphetamine in 1919. The legal
sanctions against widespread prescribing of amphetamines in the 1970s restricted
their supply and fostered a black market thriving on the illicit production of
methamphetamine powder (“speed,” “meth,” “crank,” “crystal meth”). During the
1990s, California and the West Coast experienced a dramatic resurgence of
methamphetamine-related hospital admissions, poison center calls, and law
enforcement actions. Methamphetamine misuse has since become a nationwide
problem, prompting government restrictions on retail sales of ephedrine and
pseudoephedrine (precursor chemicals used in the manufacture of methamphetamine).
A new marketing tool developed by savvy drug dealers aimed at younger, new users
involves bright coloring and flavoring (strawberry, cola, cherry, orange) added to
crystal methamphetamine to help mask the bitter taste. According to the National
Survey on Drug Use and Health for 2014, there were 569,000 current users of
PHYSICAL AND PSYCHOLOGICAL EFFECTS
symptoms of a stimulant use disorder?
Methamphetamine produces CNS stimulation by enhancing the effects of
norepinephrine, serotonin, and dopamine. This is accomplished by both blocking the
reuptake and stimulating release of these neurotransmitters. These effects are greater
for dopamine and norepinephrine than for serotonin.
The powerful stimulating effects of amphetamine and methamphetamine have made
their use popular among a wide variety of groups, including students, athletes, the
military, dieters, and long-distance truck drivers. Initially, the user may experience
alertness, euphoria, increased energy, the illusion of increased productivity,
sociability, and decreased appetite. Continuous dosing, however, produces
stereotypical grooming and other repetitive motions. Physiologic effects include
bruxism, tremor, muscle twitching, mydriasis, hypertension, diaphoresis, elevated
body temperature, nausea, dry mouth, weight loss, and malnutrition. Continued use
for several days decreases productivity and is associated with disordered thoughts,
paranoia, and psychosis. Tolerance develops very rapidly after continued use.
Illicit methamphetamine is commonly insufflated or injected and, less commonly,
taken orally. In a pattern similar to that seen with smoking cocaine, users freebase
methamphetamine and smoke it. Heating the crystals and smoking the vapor of
“crystal meth,” as with crack, is a common route of administration; however, snorting
and IV administration are also used. Absorption is rapid after smoking, and the
effects can last as long as 24 hours. Methamphetamine-induced psychosis may occur
D.C. will probably be able to stay awake to study if he uses more
methamphetamine; however, if he is up for too many days without sleep, his
performance on the examination will suffer.
ADVERSE EFFECTS AND TOXICITIES
D.C. is exhibiting classic signs of chronic methamphetamine abuse, which will likely
progress if he continues using. A “speed freak” or “tweaker” (chronic
methamphetamine user) is generally regarded even by other drug users as mentally
unstable, aggressive, and emotionally labile, with unpredictable periods of violent,
even homicidal, behavior. Chronic users characteristically develop complex
paranoid delusional systems with hallucinations during extended periods of
intoxication that may involve several sleepless days and nights of continuous
methamphetamine administration. This “speed psychosis” may include tactile
hallucinations, such as formication (the sensation of something crawling under the
skin). The initial treatment approach for stimulant-induced adverse psychologic
effects is nonpharmacologic. The distressed patient may be calmed by reducing
c a lm Reassurance that the condition is caused by the drug and will resolve
eventually; and Talk-down, which involves reassuring, reality-oriented
57 An extremely agitated, anxious, psychotic user, however, will often
require administration of a benzodiazepine, such as diazepam (10 to 30 mg orally or
2 to 10 mg intramuscularly or intravenously) or lorazepam (2 to 4 mg orally,
intramuscularly, or intravenously). If psychosis persists, a high-potency neuroleptic,
such as haloperidol (5 to 10 mg orally, intramuscularly, or intravenously) or
risperidone (2 to 4 mg orally), is preferred owing to its minimal anticholinergic
activity. Low-potency neuroleptics, such as chlorpromazine, with higher
anticholinergic activity, may worsen symptoms of delirium and hyperthermia.
The physiologic toxicity of stimulant drugs includes hypertension, stroke, seizures,
hyperthermia, sexual dysfunction, dental caries, rhabdomyolysis, renal failure,
cardiac arrhythmias and cardiomyopathies, myocardial infarction, and malnutrition.
The development of neurotoxicities involving dopaminergic and serotonergic
neurons (possibly through interference with monoamine transport and increased
production of reactive oxygen species) has been demonstrated in animals. It also
appears to cause permanent neuronal toxicity with prolonged use.
unable to post bail. What withdrawalsymptoms might he experience during incarceration?
D.C. will probably suffer intense cravings for methamphetamine and initial
agitation, followed by fatigue and hypersomnolence. A withdrawal state after acute
cessation of chronic stimulant use is generally the same as that previously described
for cocaine. As with cocaine, the crash is notable for marked fatigue, depression, and
anhedonia. Most symptoms are mild and will resolve within 1 to 2 weeks, although
anhedonia and depression may persist.
Clinical studies investigating treatments for methamphetamine dependence is
similar to cocaine treatments. Currently, no pharmacologic treatments have been
proved effective for methamphetamine dependence. The most effective treatment so
far appears to be psychosocial therapies, such as cognitive-behavioral therapy and
DISSOCIATIVE DRUGS: PHENCYCLIDINE,
KETAMINE, AND DEXTROMETHORPHAN
Phencyclidine (phenylcyclohexylpiperidine) and ketamine are arylcycloalkylamine,
dissociative, anesthetic agents. Phencyclidine (PCP) at one time was marketed as an
IV anesthetic agent under the trade name of Sernyl.
postanesthetic dysphoric reactions caused the drug to be withdrawn in 1965. It was
reintroduced in 1967 as Sernylan and marketed as a veterinary anesthetic until 1978,
when the manufacture and sale of the drug became illegal. Ketamine is currently used
clinically as an anesthetic in both animals and humans. There is some data supporting
its use in treatment refractory depression but common side effect of dissociation has
confounded the blinding of studies and is a significant side effect. More research is
necessary but it is possible that it could be used for very short-term treatment during
the efficacy lag of established antidepressants.
62 Ketamine is shorter acting and
somewhat less potent than PCP.
Abuse of arylcycloalkylamines occurs primarily in large metropolitan areas. PCP
is relatively easy to synthesize and is inexpensive; therefore, it is often
misrepresented as other street drugs, such as lysergic acid diethylamide (LSD),
amphetamine, mescaline, or Δ-9-tetrahydrocannabinol (THC). Ketamine (“K,”
“Special K,” “Super K,” “cat valium”) is commonly used as a “club drug” and is
sometimes misrepresented as 3,4-methylenedioxymethamphetamine (MDMA;
ecstasy). Ketamine is often diverted from veterinarian supplies. PCP (“angel dust,”
“dust”) in powdered form is often applied to parsley, marijuana (“dusted joint,”
“superweed”), or tobacco cigarettes and smoked. Oral, intranasal and parenteral
routes of administration are used by some. The combination of cocaine and PCP in a
freebase smoking mixture is called “SpaceBase.” Although ketamine is manufactured
as an injectable liquid, it is frequently evaporated to a powder. The powder can be
snorted or compressed into tablets.
Dextromethorphan is an antitussive agent found in some over-the-counter cough
remedies. Its appeal as a drug of abuse may be because it is inexpensive, licit, lacks
social disapproval associated with other drugs, and available over-the-counter, and
abusers believe it to be safe because it is produced by a pharmaceutical company.
Street names include “Skittles,” “DXM,” “Dex,” “Robo,” “C-C-C,” and “Red
Devils.” Use is referred to as “dexing,” “robotripping,” and “robodosing.”
Dextromethorphan is the D-isomer of the codeine analog of levorphanol. The
61 When dextromethorphan is ingested in
large doses, it produces effects similar to PCP or ketamine. When abused, doses
range from 300 to 1,800 mg. The most commonly abused form is Coricidin HBP
Cough and Cold (called “C-C-C” on the street) because it contains the highest
concentration of dextromethorphan per dosage unit on the market (30 mg).
Dextromethorphan is also available for sale on the internet in powdered form, which
can be ingested orally or snorted. The dextromethorphan “high” can last 3 to 6 hours
and can consist of euphoria, dissociation, hallucinosis, increased perceptual
awareness, altered time perception, hyperexcitability, pressure of thought, and
disorientation; increased blood pressure, heart rate, and body temperature; and blurry
61 Other ingredients found in the over-the-counter preparations, such as
acetaminophen, chlorpheniramine, guaifenesin, and alcohol, may be problematic
when ingested in large doses. PCP is considered the typical dissociative drug, and
review of its effects largely applies to ketamine and dextromethorphan as well.
Persons who use PCP may appear agitated, diaphoretic, and disoriented. There is an
increase in blood pressure, pulse, and temperature, and the person may experience
vertical and horizontal nystagmus. These symptoms are consistent with PCP
intoxication. PCP and ketamine are noncompetitive antagonists of the NMDA
receptor subtype of the major excitatory neurotransmitter, glutamate. The dose, route
of administration, and serum concentration of phencyclidine all influence the
pharmacologic effects of this drug and, thus, the symptoms of intoxication.
low doses causes inebriation, ataxia, changes in body image, numbness, and a mind–
body dissociative feeling. Horizontal or vertical nystagmus or both are often present,
and the anesthetic effect of the drug raises the pain threshold. Amnesia can occur
As the dose of PCP increases, the patient may manifest agitation, combativeness,
catatonia (ketamine users refer to this as a “k-hole”), and psychosis. The action of
PCP on the autonomic nervous system becomes more prominent and is characterized
by a confusing combination of adrenergic, cholinergic, and dopaminergic effects. A
hypertensive response is typically encountered. Tachycardia, tachypnea, and
hyperthermia may also be noted in the moderately intoxicated patient. The agitated,
combative patient often has feelings of great strength. This, combined with the
anesthetic effect of PCP, can result in serious injury because there is no pain
sensation to stop the physical activity.
With large doses of PCP, marked CNS depression occurs, and nystagmus may no
longer be present. In addition to the physiologic effects noted earlier, respiratory
depression, seizures, acidosis, and rhabdomyolysis may further compromise the
patient’s condition. Rhabdomyolysis, particularly in the presence of acidemia, can
result in acute renal failure.
57 Opisthotonic posturing and muscular rigidity occur
frequently in the severely intoxicated patient.
MEDICAL MANAGEMENT OF INTOXICATION
Diagnosis of PCP intoxication should be confirmed through a blood or urine
specimen. Currently, no clinically useful antidote to PCP exists, and treatment should
be supportive. Environmental stimuli should be minimized. Even attempts to talk
down the patient may trigger a combative response, and chemical restraints may be
indicated. Physical restraints may increase risk of rhabdomyolysis and should be
reserved for patients who pose threat of great danger to themselves or others.
Benzodiazepines are useful in the management of the anxious, agitated patient with
mild to moderate PCP intoxication. If benzodiazepines are insufficient, haloperidol
57 Low-potency neuroleptics should be avoided because a
greater possibility of precipitating a hypotensive response or a seizure exists.
Hypertension may be managed with β-blockers or calcium-channel blockers.
Diazepam (5 to 10 mg intravenously to 30 mg total) is a useful anticonvulsant for the
management of PCP-induced seizures.
57 Because extreme agitation, seizures, and
hyperthermia can initiate rhabdomyolysis and secondarily cause myocardial, renal,
or hepatic dysfunction, anxiolytics, neuroleptics, anticonvulsants, and cooling
measures should be used as needed.
The urinary excretion of PCP (a basic compound) is enhanced when the urine is
acidic; however, this approach is not recommended because it may exacerbate
51 Activated charcoal in a dose of 50 to 150 g initially,
then 30 to 40 g every 6 to 8 hours, can prevent the intestinal reabsorption of this drug
PSYCHOLOGICAL AND PROLONGED EFFECTS
Chronic PCP use can result in prolonged residual psychological symptoms, including
anxiety, depression, and psychosis.
Pharmacotherapy for these symptoms may be necessary. Prolonged psychiatric
sequelae are almost always associated with premorbid psychopathology. Perceptual
disorders, including auditory and visual hallucinations, such as after images seen
following moving objects (“trails”), may also occur. Flashbacks (discussed in detail
in the subsequent section on LSD) have been reported after PCP use.
The DSM-5 does not recognize PCP withdrawal; however, about one-fourth of
heavy PCP users report symptoms after discontinuation of use.
include depression, anxiety, irritability, hypersomnolence, diaphoresis, and tremor.
Animal studies have described a withdrawal syndrome, but it is unclear whether a
true withdrawal syndrome occurs in humans.
57 Currently, no pharmacologic
treatments for PCP use disorder exist. Some animal data indicate neurotoxicity;
however, the long-term consequences and significance for humans are unknown and
require further study. Chronic users often complain of feeling “spaced”; they may be
irritable and antisocial and feel depersonalized and isolated from people. Memory
lapses, speech and visual disturbances, and confusion have been described in longterm users as well.
Hallucinogens can be categorized as indole alkylamines (e.g., LSD, psilocybin, and
dimethyltryptamine) or phenethylamines (e.g., mescaline; MDMA). LSD is
considered the prototype hallucinogen. Although MDMA is classified as a
phenethylamine, it has structural similarities to amphetamine and mescaline. It has
been labeled an entactogen or empathogen because of its strong empathy-producing
effects and mild hallucinogenic effects. The term entactogen can be translated as “a
touching within.” Hallucinogens are commonly referred to as psychedelics.
In 2014, 1.2 million Americans were current hallucinogen users. The popularity of
MDMA (ecstasy, X) has risen dramatically in recent years, partly because of its use
as a “club drug.” In 2014, 609,000 Americans reported using MDMA sometime in
“mind expansion.” Certain individuals may develop psychological dependence and
use hallucinogens in a more chronic and compulsive manner.
Perhaps the most famous of all hallucinogens, LSD-25 was first synthesized by
Albert Hofmann of Sandoz Laboratories in 1938. It was developed as an analeptic
agent but produced significant uterine stimulation and caused experimental animals to
become excited or cataleptic. Five years later, while resynthesizing LSD-25 for
further pharmacologic testing, Dr. Hofmann experienced a restlessness that forced
him to go home. This was followed by 2 hours of intense visual hallucinations of
kaleidoscopic images and colors. Later, he identified LSD-25 as a potent
hallucinogen. Clinical experimentation produced hundreds of papers describing LSD
as a drug that could facilitate psychotherapy, particularly in the management of
addictive behavior. Widespread public self-experimentation with LSD for recreation
and self-exploration, coupled with growing attention to adverse psychological
consequences, led Sandoz to discontinue production of LSD-25 (as well as
psilocybin, psilocin, and related congeners) in August 1965. The United States made
LSD a schedule I controlled substance in 1970 after the proliferation of illicit
suppliers to meet the huge public demand for this drug.
Although the mechanism of action of classic hallucinogens is not fully understood,
they appear to predominately act as agonists or partial agonists at serotonin (5-HT)
receptors, specifically the 5-HT2
63 LSD, one of the most potent
hallucinogens known, is active at doses of 25 to 250 mcg. Most users take about 100
to 150 mcg of LSD for a significant effect. This dose produces mild to moderate
sympathomimetic effects, profound visual hallucinosis, and the sensation of
disordered integration of sensory input. For example, sounds and music are
perceived as visual imagery, odors are felt, and inanimate objects assume lifelike
qualities. In addition to these sensory-perceptual effects, psychic effects occur, such
as depersonalization, dreamlike feelings, and rapid alterations of affect. These are
accompanied by somatic effects, including dizziness, nausea, weakness, tremor, and
63 These combined effects begin within an hour of ingestion of LSD and
usually peak in intensity during the first 2 to 4 hours. After taking LSD, most people
feel they have returned to a normal psychological state by 10 to 12 hours.
hour after ingestion, a person will begin to experience altered sensations of his/her
surroundings, in addition to some psychic and somatic effects.
The most frequently encountered adverse reaction associated with the hallucinogenic
drugs is a mental state of acute anxiety and fear, typically referred to as a “bad trip.”
The hallucinogen experience is influenced by set (the user’s mental state and
expectations of drug effects) and setting (the environment in which drug use takes
place, including the social conditions). Users may be able to calm themselves
without outside intervention. The initial therapy of people undergoing a bad trip is
frequently called “reality therapy” and consists of talking down the fear and panic.
This consists of getting the person to a quiet, relaxed setting and helping him or her
focus on explanations for the uncertainties that are causing the panic. This process
also tends to reassure the person that he or she is in a safe physical environment and
that the drug effects will diminish in a few hours. Most of these bad trips are
resolved during the state of intoxication (generally, 6–12 hours), but some last as
If the talk-down approach is not successful in resolving the panic, drug therapy can
be considered. Sedation with an oral benzodiazepine (i.e., diazepam 10–30 mg) or a
parenteral benzodiazepine (i.e., lorazepam 2 mg IM) will frequently alleviate the
57 Supportive talking down should be continued because the benzodiazepine
will not stop the trip; it will simply sedate the patient. Haloperidol 2 mg IM may also
be used if benzodiazepines are insufficient. Phenothiazines should not be used for
initial management of bad trips because they have been associated with poor
Regarding adverse physical effects, classic hallucinogens have a high margin of
safety, although patients should be monitored for seizures or elevations in body
temperature, which may indicate a potential hyperthermic crisis. Anticonvulsant
therapy may not be effective until body temperature has been lowered.
FLASHBACKS AND LONG-TERM EFFECTS
Use of hallucinogens can trigger a transient psychosis or unmask an underlying
psychiatric disorder; however, a true psychotic episode is rare. Psychiatric
conditions after hallucinogen use that persist more than a month are likely caused by
57 Hallucinogen use does not seem to be associated with
Hallucinogen persisting perceptual disorder (HPPD), commonly referred to as
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