Alcohol Intoxication 497
may relate to alcohol use disorder as well. At least a part of the reported association between
depression and moderate to severe alcohol use disorder may be attributable to temporary, al-
cohol-induced comorbid depressive symptoms re sulting from the acute effects of intoxication
or withdrawal. Severe, repeated  alcohol intoxication may also suppress immune mechanisms
and predispose individuals to infections and increase the risk for cancers.
Alcohol Intoxication
Diagnostic Criteria
A. Recent ingestion of alcohol.
B. Clinically significant problematic behavioral or psychological changes (e.g., inappropri-
ate sexual or aggressive behavior, mood lability, impaired judgment) that developed
during, or shortly after, alcohol ingestion.
C. One (or more) of the following signs or symptoms developing during, or shortly after,
alcohol use:
1. Slurred speech.
2. Incoordination.
3. Unsteady gait.
4. Nystagmus.
5. Impairment in attention or memory.
6. Stupor or coma.
D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, in cluding intoxication with another substance.
Coding note:  The ICD-9-CM code is 303.00.  The ICD-10-CM code depends on whether
there is a comorbid alcohol use disorder. If a mild alcohol use disorder is comorbid, the
ICD-10-CM code is F10.129,  and if a moderate or severe alcohol use disorder is comorbid,
the ICD-10-CM code is F10.229.  If there is no comorbid alcohol use disorder, then the
ICD-10-CM code is F10.929.
Diagnostic Features


ICD-10-CM code is F10.929.
Diagnostic Features
The essential feature of alcohol intoxication is the presence of  clinically significant problematic
behavioral or psychological chan ges (e.g., inappropriate sexual  or aggressive behavior, mood
lability, impaired judgment, impaired social or occupational functioning) that develop during,
or shortly after, alcohol ingestion (Criterion B). These changes are accompanied by evidence of
impaired functioning and ju dgment and, if intoxication is inte nse, can result in a life-threaten-
ing coma. The symptoms must not be attributable  to another medical co ndition (e.g., diabetic
ketoacidosis), are not a reflection  of conditions such as delirium,  and are not related to intoxi-
cation with other depressant drugs (e.g., benzodiazepines) (Crite rion D). The levels of incoor-
dination can interfere with driving abilities and performance of usual activities to the point of
causing accidents. Evidence of alcohol use can be  obtained by smelling alcohol on the individ-
ual’s breath, eliciting a history from the indivi dual or another observer, and, when needed,
having the individual provide breath, blood , or urine samples for toxicology analyses.
Associated Features Supporting Diagnosis
Alcohol intoxication is sometimes associated with amnesia for the events that occurred
during the course of the intoxication (“bl ackouts”). This phenomenon may be related to
the presence of a high blood alcohol level an d, perhaps, to the rapidity with which this
level is reached. During even mild alcohol in toxication, different symptoms are likely to be


498 Substance-Related and Addictive Disorders
observed at different time points. Evidence of mild intoxication with alcohol can be seen in
most individuals after approximately two drin ks (each standard drink is approximately
10–12 grams of ethanol and raises the blood alcohol concentration approximately 20 mg/
dL). Early in the drinking period, when blood alcohol levels are rising, symptoms often
include talkativeness, a sensation of well-being, and a bright, expansive mood. Later, es-
pecially when blood alcohol levels are falling,  the individual is likely to become progres-
sively more depressed,  withdrawn, and cognitively impair ed. At very high blood alcohol
levels (e.g., 200–300 mg/dL), an individual who has not developed tolerance for alcohol is
likely to fall asleep and enter a first stage of anesthesia. Higher blood alcohol levels (e.g., in
excess of 300–400 mg/dL) can cause inhibition of respiration and pulse and even death in
nontolerant individuals. The duration of in toxication depends on how much alcohol was
consumed over what period of time. In general, the body is able to metabolize approxi-
mately one drink per hour, so that the blood alcohol level generally decreases at a rate of
15–20 mg/dL per hour. Signs and symptoms of in toxication are likely to be more intense
when the blood alcohol level is rising than when it is falling.
Alcohol intoxication is an important contri butor to suicidal behavior. There appears to
be an increased rate of suic idal behavior, as well as of co mpleted suicide, among persons
intoxicated by alcohol.
Prevalence
The large majority of alcohol consumers are likely to have been intoxicated to some degree at


The large majority of alcohol consumers are likely to have been intoxicated to some degree at
some point in their lives. For ex ample, in 2010, 44% of 12th-grad e students admitted to having
been “drunk in the past year,” with more than 70% of college students reporting the same.
Development and Course
Intoxication usually occurs as an episode usua lly developing over minutes to hours and typi-
cally lasting several hours. In th e United States, the average age at first intoxication is approx-
imately 15 years, with the highest prevalence at approximately 18–25 years. Frequency and
intensity usually decrease with further advancin g age. The earlier the onset of regular intoxi-
cation, the greater the likelihood the individual will go on to develop alcohol use disorder.
Risk and Prognostic Factors
Temperamental. Episodes of alcohol intoxication increase with personality characteris-
tics of sensation seeking and impulsivity.
Environmental. Episodes of alcohol intoxication increase with a heavy drinking envi-
ronment.
Culture-Related Diagnostic Issues
The major issues parallel the cultural differ ences regarding the use of alcohol overall.
Thus, college fraternities and sororities ma y encourage alcohol intoxication. This condi-
tion is also frequent on certain dates of cultur al significance (e.g., New Year’s Eve) and, for
some subgroups, during specif ic events (e.g., wakes following funerals). Other subgroups
encourage drinking at religious celebrations (e.g., Jewish and Catholic holidays), while
still others strongly discourage all drinking or intoxication (e.g., some religious groups,
such as Mormons, fundamenta list Christians, and Muslims).
Gender-Related Diagnostic Issues
Historically, in many Western societies, ac ceptance of drinking and drunkenness is more


Historically, in many Western societies, ac ceptance of drinking and drunkenness is more
tolerated for males, but such gender differences may be much less prominent in recent
years, especially during adolescence and young adulthood.


Alcohol Withdrawal 499
Diagnostic Markers
Intoxication is usually established by observing an individual’s behavior and smelling alcohol
on the breath. The degree of into xication increases with an individual’s blood or breath alcohol
level and with the ingestion of other substanc es, especially those with sedating effects.
Functional Consequences of Alcohol Intoxication
Alcohol intoxication contributes to the more than 30,000 alcohol-related drinking deaths in
the United States each year. In addition, intoxication with this drug contributes to huge
costs associated with drunk driving, lost time from school or work, as well as interpersonal
arguments and physical fights.
Differential Diagnosis
Other medical conditions. Several medical (e.g., diabetic acidosis) and neurological condi-
tions (e.g., cerebellar ataxia, multiple sclerosis) can temporarily resemble alcohol intoxication.
Sedative, hypnotic, or anxiolytic intoxication. Intoxication with se dative, hypnotic, or
anxiolytic drugs or with other sedating subs tances (e.g., antihistam ines, anticholinergic
drugs) can be mistaken for alcohol intoxicati on. The differential requires observing alco-
hol on the breath, measuring blood or breath alcohol levels , ordering a medical workup,
and gathering a good history. The signs and symptoms of sedative-hypnotic intoxication
are very similar to those observed with alco hol and include similar problematic behavioral
or psychological changes. These changes are accompanied by evidence of impaired func-
tioning and judgment—which, if intense, can result in a life-threat ening coma—and levels
of incoordination that can interfere with driving abilities and with performing usual
activities. However, there is no smell as there is with alcohol, but there is likely to be evi-


dence of misuse of the depressant drug in the blood or urine toxicology analyses.
Comorbidity
Alcohol intoxication may occu r comorbidly with other subs tance intoxication, especially
in individuals with conduct disorder or antisocial personality disorder.
Alcohol Withdrawal
Diagnostic Criteria
A. Cessation of (or reduction in) alcohol use that has been heavy and prolonged.
B. Two (or more) of the following, developing within several hours to a few days after the
cessation of (or reduction in) alcohol use described in Criterion A:
1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).
2. Increased hand tremor.
3. Insomnia.
4. Nausea or vomiting.
5. Transient visual, tactile, or auditory hallucinations or illusions.
6. Psychomotor agitation.
7. Anxiety.
8. Generalized tonic-clonic seizures.
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.


500 Substance-Related and Addictive Disorders
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawal from
another substance.
Specify if:
With perceptual disturbances:  This specifier applies in the rare instance when hal-
lucinations (usually visual or tactile) occur with intact reality testing, or auditory, visual,
or tactile illusions occur in the absence of a delirium.
Coding note:  The ICD-9-CM code is 291.81. The ICD-10-CM code for alcohol withdrawal
without perceptual disturbances is F10.239,  and the ICD-10-CM code for alcohol withdrawal
with perceptual disturbances is F10.232.  Note that the ICD-10-CM code indicates the comor-
bid presence of a moderate or severe alcohol use disorder, reflecting the fact that alcohol with-
drawal can only occur in the presence of a moderate or severe alcohol use disorder. It is not
permissible to code a comorbid mild alcohol use disorder with alcohol withdrawal.
Specifiers
When hallucinations occur in the absence of delirium (i.e., in a clea r sensorium), a diagno-
sis of substance/medication-induced ps ychotic disorder should be considered.
Diagnostic Features
The essential feature of alcoho l withdrawal is the presence of a characteristic withdrawal
syndrome that develops within several hours to a few days after the cessation of (or re-
duction in) heavy and prolon ged alcohol use (Criteria A and B). The withdrawal syn-
drome includes two or more of the sympto ms reflecting autonomic hyperactivity and
anxiety listed in Criterion B, along with gastrointestinal symptoms.
Withdrawal symptoms cause clinically signific ant distress or impairment in social, oc-


Withdrawal symptoms cause clinically signific ant distress or impairment in social, oc-
cupational, or other important areas of functi oning (Criterion C). The symptoms must not
be attributable to another me dical condition and are not be tter explained by  another men-
tal disorder (e.g., generalized anxiety diso rder), including intoxication or withdrawal
from another substance (e.g., sedative, hypnotic, or anxiolytic withdrawal) (Criterion D).
Symptoms can be relieved by administering alcohol or benzodiazepines (e.g., diazepam).
The withdrawal symptoms typically begin when blood concentrations of alcohol decline
sharply (i.e., within 4–12 hours) after alcohol us e has been stopped or re duced. Reflecting the
relatively fast metabolism of alcohol, symptoms  of alcohol withdrawal usually peak in inten-
sity during the second day of abstinence and ar e likely to improve markedly by the fourth or
fifth day. Following acute withdrawal, however, symptoms of anxiety, insomnia, and auto-
nomic dysfunction may persist for up to 3–6 months at lower levels of intensity.
Fewer than 10% of individuals who develop alcohol withdrawal will ever develop dra-
matic symptoms (e.g., severe autonomic hypera ctivity, tremors, alcohol withdrawal delir-
ium). Tonic-clonic seizures occur in fewer than 3% of individuals.
Associated Features Supporting Diagnosis
Although confusion and changes in consciousness are not core criteria for alcohol with-
drawal, alcohol withdrawal delirium (see “De lirium” in the chapte r “Neurocognitive Dis-
orders”) may occur in the context of withdrawal . As is true for any agitated, confused state,
regardless of the cause, in addition to a disturbance of cons ciousness and cognition, with-


drawal delirium can include visual, tactile, or (rarely) auditory hallucinations (delirium tre-
mens). When alcohol withdrawal delirium develo ps, it is likely that a clinically relevant
medical condition may be present (e.g., liver fa ilure, pneumonia, gastrointestinal bleeding,
sequelae of head trauma, hypoglycemia, an electrolyte imbalance, postoperative status).


Alcohol Withdrawal 501
Prevalence
It is estimated that approximately 50% of mi ddle-class, highly functional individuals with
alcohol use disorder have ev er experienced a full alcohol withdrawal syndrome. Among
individuals with alcohol use disorder who are hospitalized or homeless, the rate of al-
cohol withdrawal may be greater than 80%. Less than 10% of individuals in withdrawal
ever demonstrate alcoho l withdrawal delirium or withdrawal seizures.
Development and Course
Acute alcohol withdrawal occurs as an episode usually lasting 4–5 days and only after
extended periods of heavy drinking. Withdrawal  is relatively rare in individuals younger
than 30 years, and the risk and seve rity increase with increasing age.
Risk and Prognostic Factors
Environmental. The probability of developing alco hol withdrawal increases with the
quantity and frequency of alcohol consumptio n. Most individuals with this condition are
drinking daily, consuming large amounts (appr oximately more than eight drinks per day)
for multiple days. However, there are large inter-individual differences, with enhanced
risks for individuals with concurrent medical conditions, those with family histories of al-
cohol withdrawal (i.e., a gene tic component), those with pr ior withdrawals, and individ-
uals who consume sedative, hy pnotic, or anxiolytic drugs.
Diagnostic Markers
Autonomic hyperactivity in the context of moderately high but falling blood alcohol levels
and a history of prolonged heavy drinking in dicate a likelihood of alcohol withdrawal.
Functional Consequences  of Alcohol Withdrawal
Symptoms of withdrawal may serve to perpet uate drinking behaviors and contribute to
relapse, resulting in persistently impaired so cial and occupational functioning. Symptoms
requiring medically supervised detoxification result in hospital utilization and loss of
work productivity. Overall, the presence of withdrawal is associated with greater func-


work productivity. Overall, the presence of withdrawal is associated with greater func-
tional impairment and poor prognosis.
Differential Diagnosis
Other medical conditions. The symptoms of alcohol withdrawal can also be mimicked
by some medical conditions (e.g., hypoglycemia and diabetic ketoacidosis). Essential
tremor, a disorder that frequently runs in  families, may erroneou sly suggest the tremu-
lousness associated with alcohol withdrawal.
Sedative, hypnotic, or anxiolytic withdrawal. Sedative, hypnotic, or anxiolytic with-
drawal produces a syndrome very sim ilar to that of alcohol withdrawal.
Comorbidity
Withdrawal is more likely to occur with heavie r alcohol intake, and that might be most of-
ten observed in individuals with conduct di sorder and antisocial personality disorder.
Withdrawal states are also more severe in ol der individuals, individuals who are also de-
pendent on other depressant drugs (sedativ e-hypnotics), and individuals who have had
more alcohol withdrawal experiences in the past.


502 Substance-Related and Addictive Disorders
Other Alcohol-Induced Disorders
The following alcohol-induced disorders are desc ribed in other chapters of the manual with
disorders with which they share phenomenol ogy (see the substance/medication-induced
mental disorders in these chapters): alcohol-induced psychotic disorder (“Schizophrenia Spec-
trum and Other Psychotic Disorders”); alcoho l-induced bipolar diso rder (“Bipolar and
Related Disorders”); alcohol-induced depressive  disorder (“Depressive  Disorders”); alcohol-
induced anxiety disorder (“Anxiety Disorders”); alcohol-induced sl eep disorder (“Sleep-
Wake Disorders”); alcohol-induced sexual dysfunction (“Sexual Dysfunctions”); and alcohol-
induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For alcohol
intoxication delirium an d alcohol withdrawal delirium, see th e criteria and discussion of de-
lirium in the chapter “Neurocognitive Disorder s.” These alcohol-induced disorders are diag-
nosed instead of alcohol intoxication or alcohol withdrawal only when the symptoms are
sufficiently severe to warrant independent clinical attention.
Features
The symptom profiles for an al cohol-induced condition resemble independent mental disor-
ders as described elsewhere in  DSM-5. However, the alcohol- induced disorder is temporary
and observed after severe intoxication with an d/or withdrawal from alcohol. While the symp-
toms can be identical to those of independent mental disorders (e.g., psychoses, major depres-
sive disorder), and while they can have the same  severe consequences (e.g., suicide attempts),
alcohol-induced conditions are li kely to improve without formal treatment in a matter of days
to weeks after cessation of severe intoxication and/or withdrawal.
Each alcohol-induced mental disorder is listed  in the relevant diagnostic section and there-


Each alcohol-induced mental disorder is listed  in the relevant diagnostic section and there-
fore only a brief description is offered here. Alcohol-induced disorder s must have developed
in the context of severe intoxication and/or wi thdrawal from the substance capable of produc-
ing the mental disorder. In addition, there must  be evidence that the disorder being observed
is not likely to be better expl ained by another non-alcohol-indu ced mental disorder. The latter
is likely to occur if the mental  disorder was present before the severe intoxication or with-
drawal, or continued more than 1 month after the cessation of severe intoxication and/or with-
drawal. When symptoms are observed only during a delirium, they should be considered part
of the delirium and not diagnosed separately, as  many symptoms (including disturbances in
mood, anxiety, and reality testin g) are commonly seen during ag itated, confused states. The al-
cohol-induced disorder must be clinically relevant, causing significant levels of distress or sig-
nificant functional impairment. Finally, there are indications that the intake of substances of
abuse in the context of a preexisting mental disorder are likely to result in an intensification of
the preexisting independent syndrome.
The features associated with each relevant  major mental disorder (e.g., psychotic epi-
sodes, major depressive disorder) are similar whether observed with an independent or an
alcohol-induced condition. However, indivi duals with alcohol-induced disorders are
likely to also demonstrate the associated feat ures seen with an alcohol use disorder, as
listed in the subsections of this chapter.
Rates of alcohol-induced diso rders vary somewhat by diag nostic category. For exam-
ple, the lifetime risk for major depressive epis odes in individuals with alcohol use disorder


ple, the lifetime risk for major depressive epis odes in individuals with alcohol use disorder
is approximately 40%, but only about one-third to one-half of these represent independent
major depressive syndromes observed outside the context of intoxication. Similar rates of
alcohol-induced sleep and anxiet y conditions are likely, but alcohol-induced psychotic ep-
isodes are fairly rare.
Development and Course


alcohol-induced sleep and anxiet y conditions are likely, but alcohol-induced psychotic ep-
isodes are fairly rare.
Development and Course
Once present, the symptoms of an alcohol-in duced condition are likely to remain clinically
relevant as long as the individual continues to  experience severe intoxication and/or with-


Unspecified Alcohol-Related Disorder 503
drawal. While the symptoms are identical to those of independent mental disorders (e.g.,
psychoses, major depressive disorder), and while they can have the same severe conse-
quences (e.g., suicide attempts), all alcohol-induced syndromes other than alcohol-
induced neurocognitive disord er, amnestic confabulatory ty pe (alcohol-induced persist-
ing amnestic disorder), regardless of the se verity of the symptoms, are likely to improve
relatively quickly and unlikely to remain clin ically relevant for more than 1 month after
cessation of severe intoxication and/or withdrawal.
The alcohol-induced disorders are an important part of the differential diagnoses for
the independent mental conditions. Independ ent schizophrenia, major depressive disor-
der, bipolar disorder, and anxiety disorders, su ch as panic disorder, are likely to be asso-
ciated with much longer-lasting periods of symptoms and often require longer-term
medications to optimize the probability of improvement or recovery . The alcohol-induced
conditions, on the other hand, are likely to be much shorter in duration and disappear
within several days to 1 month after cessatio n of severe intoxication and/or withdrawal,
even without psychotropic medications.
The importance of recognizing an alcohol- induced disorder is similar to the relevance
of identifying the possible role of some endo crine conditions and medication reactions be-
fore diagnosing an independent mental disorder. In light of the high prevalence of alcohol
use disorders worldwide, it is important that these alcohol- induced diagnoses be consid-
ered before independent ment al disorders are diagnosed.
Unspecified Alcohol-Related Disorder
291.9 (F10.99)
This category applies to presentations in which symptoms characteristic of an alcohol-
related disorder that cause clinically significant distress or impairment in social, occupa-


related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific alcohol-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
Caffeine-Related Disorders
Caffeine Intoxication
Caffeine Withdrawal
Other Caffeine-Induced Disorders
Unspecified Caffeine-Related Disorder
Caffeine Intoxication
Diagnostic Criteria 305.90 (F15.929)
A. Recent consumption of caffeine (typically a high dose well in excess of 250 mg).
B. Five (or more) of the following signs or symptoms developing during, or shortly after,
caffeine use:
1. Restlessness.
2. Nervousness.


504 Substance-Related and Addictive Disorders
3. Excitement.
4. Insomnia.
5. Flushed face.
6. Diuresis.
7. Gastrointestinal disturbance.
8. Muscle twitching.
9. Rambling flow of thought and speech.
10. Tachycardia or cardiac arrhythmia.
11. Periods of inexhaustibility.
12. Psychomotor agitation.
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not bet-
ter explained by another mental disorder, including intoxication with another substance.
Diagnostic Features
Caffeine can be consumed from a number of di fferent sources, including coffee, tea, caf-
feinated soda, “energy” drinks, over-the-cou nter analgesics and cold remedies, energy
aids (e.g., drinks), weight-loss aids, and chocol ate. Caffeine is also increasingly being used
as an additive to vitamins and to food prod ucts. More than 85% of children and adults con-
sume caffeine regularly. Some caffeine user s display symptoms consistent with problem-
atic use, including tolerance and withdrawal (see “Caffeine Withdrawal” later in this
chapter); the data are not available at this time  to determine the clinical significance of a
caffeine use disorder and its pr evalence. In contrast, there is  evidence that caffeine with-
drawal and caffeine intoxication are clinically significant and sufficiently prevalent.
The essential feature of caffein e intoxication is recent cons umption of caffeine and five
or more signs or symptoms th at develop during or shortly after caffeine use (Criteria A


or more signs or symptoms th at develop during or shortly after caffeine use (Criteria A
and B). Symptoms include restlessness, nervousness, excitement, insomnia, flushed face,
diuresis, and gastrointestinal complaints, which can occur with low doses (e.g., 200 mg) in
vulnerable individuals such as children, the el derly, or individuals who have not been ex-
posed to caffeine previously. Symptoms that ge nerally appear at levels of more than 1 g/
day include muscle twitching, rambling flow of thought and speech, tachycardia or car-
diac arrhythmia, periods of inexhaustibility, and psychomotor agitation. Caffeine intoxi-
cation may not occur despite high caffeine inta ke because of the development of tolerance.
The signs or symptoms must cause clinically significant distress or impairment in social,
occupational, or other importan t areas of functioning (Criterion C). The signs or symp-
toms must not be attr ibutable to another medical condit ion and are not better explained by
another mental disorder (e.g., an anxiety disorder) or intoxi cation with another substance
(Criterion D).
Associated Features Supporting Diagnosis
Mild sensory disturbances (e.g., ringing in the ears and flashes of light) may occur with high
doses of caffeine. Although large doses of caffeine can increase heart rate, smaller doses can
slow heart rate. Whether excess caffeine intake can cause headaches is unclear. On physical
examination, agitation, restlessness, sweati ng, tachycardia, flushed face, and increased
bowel motility may be seen. Caffeine blood levels may provide important information for
diagnosis, particularly when the individual is a poor historian, although these levels are not
diagnostic by themselves in view of the individual variation in response to caffeine.


Caffeine Intoxication 505
Prevalence
The prevalence of caffeine intoxication in the gene ral population is un clear. In the United
States, approximately 7% of individuals in the population may experience five or more symp-
toms along with functional impairment consiste nt with a diagnosis of caffeine intoxication.
Development and Course
Consistent with a half-life of caffeine of approximately 4–6 hours, caffeine intoxication
symptoms usually remit within the first day or  so and do not have any known long-lasting
consequences. However, individuals who consum e very high doses of caffeine (i.e., 5–10
g) may require immediate medical attent ion, as such doses can be lethal.
With advancing age, individuals are likely to demonstrate increasingly intense reac-
tions to caffeine, with greater complaints of interference with sleep or feelings of hyper-
arousal. Caffeine intoxicati on among young individuals after consumption of highly
caffeinated products, includin g energy drinks, has been observed. Children and adoles-
cents may be at increased risk for caffeine into xication because of low body weight, lack of
tolerance, and lack of kn owledge about the pharmacolog ical effects of caffeine.
Risk and Prognostic Factors
Environmental. Caffeine intoxication is often seen among individuals who use caffeine
less frequently or in those who have recently increased their caffeine intake by a substan-
tial amount. Furthermore, oral contraceptives significantly de crease the elimination of caf-
feine and consequently may incre ase the risk of intoxication.
Genetic and physiological. Genetic factors may affect risk of caffeine intoxication.
Functional Consequences of Caffeine Intoxication
Impairment from caffeine intoxication may have serious consequences, including dys-


Impairment from caffeine intoxication may have serious consequences, including dys-
function at work or school, social indiscretions, or failure to fulfill role obligations. More-
over, extremely high doses of caffeine can be fa tal. In some cases, caffeine intoxication may
precipitate a caffeine-induced disorder.
Differential Diagnosis
Other mental disorders. Caffeine intoxication may be characterized by symptoms (e.g.,
panic attacks) that resemble primary mental diso rders. To meet criteria for caffeine intoxica-
tion, the symptoms must not be associated with another medical condition or another mental
disorder, such as an anxiety di sorder, that could better expl ain them. Manic episodes; panic
disorder; generalized anxiety disorder; amphetami ne intoxication; sedative, hypnotic, or anx-
iolytic withdrawal or tobacco withdrawal; slee p disorders; and medication-induced side ef-
fects (e.g., akathisia) can cause a clinical picture that is similar to that of caffeine intoxication.
Other caffeine-induced disorders. The temporal relationship of the symptoms to increased
caffeine use or to abstinence from caffeine help s to establish the diagno sis. Caffeine intoxica-
tion is differentiated from caffeine-induced anxiety disorder, with onset during intoxication
(see “Substance/Medicat ion-Induced Anxiety Disorder” in the chapter “Anxiety Disorders”),
and caffeine-induced sleep disorder, with onse t during intoxication (see “Substance/Medica-
tion-Induced Sleep Disorder” in the chapter “S leep-Wake Disorders”), by the fact that the
symptoms in these latter disorders are in excess  of those usually associ ated with caffeine in-
toxication and are severe enough to wa rrant independent clinical attention.


506 Substance-Related and Addictive Disorders
Comorbidity
Typical dietary doses of caffeine have not been  consistently associated with medical prob-
lems. However, heavy use (e.g., >400 mg) can cause or exacerbate anxiety and somatic
symptoms and gastrointestinal distress. With  acute, extremely high doses of caffeine,
grand mal seizures and respiratory failure may re sult in death. Excessive caffeine use is as-
sociated with depressive diso rders, bipolar disorders, eati ng disorders, psychotic disor-
ders, sleep disorders, and subs tance-related disorders, wher eas individuals with anxiety
disorders are more likely to avoid caffeine.
Caffeine Withdrawal
Diagnostic Criteria 292.0 (F15.93)
A. Prolonged daily use of caffeine.
B. Abrupt cessation of or reduction in caffeine use, followed within 24 hours by three (or
more) of the following signs or symptoms:
1. Headache.
2. Marked fatigue or drowsiness.
3. Dysphoric mood, depressed mood, or irritability.
4. Difficulty concentrating.
5. Flu-like symptoms (nausea, vomiting, or muscle pain/stiffness).
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not associated with the physiological effects of another
medical condition (e.g., migraine, viral illness) and are not better explained by another
mental disorder, including intoxication or withdrawal from another substance.
Diagnostic Features
The essential feature of caffeine withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the abrupt cessation of (or substantial reduction in) pro-
longed daily caffeine ingestion (Criterion B) . The caffeine withdrawal syndrome is indi-


longed daily caffeine ingestion (Criterion B) . The caffeine withdrawal syndrome is indi-
cated by three or more of the following (Criterion B): headache; marked fatigue or
drowsiness; dysphoric mood, depressed mood, or irritability; difficulty concentrating;
and flu-like symptoms (nausea, vomiting, or muscle pain/stiffness). The withdrawal syn-
drome causes clinical significant distress or impairment in social, occupational, or other
important areas of functioning (Criterion C) . The symptoms must not be associated with
the physiological effects of another medical co ndition and are not better explained by an-
other mental disorder (Criterion D).
Headache is the hallmark feature of caffeine withdrawal and may be diffuse, gradual
in development, throbbing, severe, and sensitive to move ment. However, other symptoms
of caffeine withdrawal can occur in the abse nce of headache. Caffeine is the most widely
used behaviorally active drug in the world and is present in many different types of bev-
erages (e.g., coffee, tea, maté, soft drinks, energy drinks), foods, energy aids, medications,
and dietary supplements. Because caffeine ingestion is often integrated into social customs
and daily rituals (e.g., coffee break, tea time ), some caffeine consumers may be unaware of
their physical dependence on caffeine. Thus, caffeine withdrawal symptoms could be un-
expected and misattributed to other causes (e.g ., the flu, migraine). Furthermore, caffeine
withdrawal symptoms may occur when indivi duals are required to abstain from foods
and beverages prior to medical procedures or  when a usual caffeine dose is missed be-
cause of a change in routine (e.g., during travel, weekends).


Caffeine Withdrawal 507
The probability and severity of caffeine with drawal generally increase as a function of
usual daily caffeine dose. However, there is large variability among individuals and
within individuals across different episodes in  the incidence, severity, and time course of
withdrawal symptoms. Caffeine withdrawal sy mptoms may occur after abrupt cessation
of relatively low chronic daily doses of caffeine (i.e., 100 mg).
Associated Features Supporting Diagnosis
Caffeine abstinence has been shown to be as sociated with impaired behavioral and cogni-
tive performance (e.g., sustai ned attention). Electroencepha lographic studies have shown
that caffeine withdrawal symptoms are significantly associated with increases in theta
power and decreases in beta-2 power. Decre ased motivation to work and decreased socia-
bility have also been reported during caffe ine withdrawal. Increased analgesic use during
caffeine withdrawal has been documented.
Prevalence
More than 85% of adults and children in th e United States regularly consume caffeine,
with adult caffeine consumers ingesting abou t 280 mg/day on average. The incidence and
prevalence of the caffeine withdrawal syndro me in the general population are unclear. In
the United States, headache may occur in a pproximately 50% of cases of caffeine absti-
nence. In attempts to permanently stop caffein e use, more than 70% of individuals may ex-
perience at least one caffeine withdrawal sy mptom (47% may experience headache), and
24% may experience headache plus one or more other symptoms as well as functional
impairment due to withdrawal. Among individu als who abstain from caffeine for at least
24 hours but are not trying to permanently stop caffeine use, 11% may experience head-
ache plus one or more other symptoms as well as functional impairment. Caffeine con-


ache plus one or more other symptoms as well as functional impairment. Caffeine con-
sumers can decrease the incidence of caffeine withdrawal by using ca ffeine daily or only
infrequently (e.g., no more than 2 consecutive days). Gradual reductio n in caffeine over a
period of days or weeks may decrease the incidence and severity of caffeine withdrawal.
Development and Course
Symptoms usually begin 12–24 hours after the last caffeine dose and peak after 1–2 days
of abstinence. Caffeine withdrawal symptoms last for 2–9 days, with the possibility of
withdrawal headaches occurring for up to  21 days. Symptoms usually remit rapidly
(within 30–60 minutes) after re-ingestion of caffeine.
Caffeine is unique in that it is a behavioral ly active drug that is consumed by individ-
uals of nearly all ages. Rates of caffeine consumption and overall level of caffeine con-
sumption increase with age until the early to mid-30s and then level off. Although caffeine
withdrawal among children and adolescents has been documented, relatively little is
known about risk factors for caffeine withdrawal among this age group. The use of highly
caffeinated energy drinks is increasing with  in young individuals, which could increase
the risk for caffeine withdrawal.
Risk and Prognostic Factors
Temperamental. Heavy caffeine use has been observ ed among individuals with mental
disorders, including eating disorders; smoker s; prisoners; and drug and alcohol abusers.
Thus, these individuals could be at higher risk for caffeine withdrawal upon acute caffeine
abstinence.
Environmental. The unavailability of caffeine is an environmental risk factor for incipi-
ent withdrawal symptoms. While caffeine is le gal and usually widely available, there are
conditions in which caffeine use may be restricted, such as during medical procedures,


conditions in which caffeine use may be restricted, such as during medical procedures,
pregnancy, hospitalizations, religious observances, wartime, travel, and research partici-


508 Substance-Related and Addictive Disorders
pation. These external enviro nmental circumstances may precipitate a withdrawal syn-
drome in vulnerable individuals.
Genetic and physiological factors. Genetic factors appear to increase vulnerability to
caffeine withdrawal, but no specific genes have been identified.
Course modifiers. Caffeine withdrawal symptoms usua lly remit within 30–60 minutes
of reexposure to caffeine. Doses of caffeine  significantly less than one’s usual daily dose
may be sufficient to prevent or attenuate caffeine withdrawal sy mptoms (e.g., consump-
tion of 25 mg by an individual who typically consumes 300 mg).
Culture-Related Diagnostic Issues
Habitual caffeine consumers who fast for religio us reasons may be at increased r isk for caf-
feine withdrawal.
Functional Consequences of
Caffeine Withdrawal Disorder
Caffeine withdrawal symptoms can vary from mild to extreme, at times causing functional
impairment in normal daily activities. Rates of functional impairment range from 10% to
55% (median 13%), with rates as high as 73% found among individuals who also show
other problematic features of caffeine use. Ex amples of functional impairment include be-
ing unable to work, exercise, or care for child ren; staying in bed all day; missing religious
services; ending a vacation early; and cancelling a social gathering. Caffeine withdrawal
headaches may be described by individuals as  “the worst headaches” ever experienced.
Decrements in cognitive and motor pe rformance have also been observed.
Differential Diagnosis
Other medical disorders an d medical side effects. Several disorders should be consid-
ered in the differential diagnosis of caffeine withdrawal. Caffeine withdrawal can mimic
migraine and other headache di sorders, viral illnesses, sinu s conditions, tension, other


drug withdrawal states (e.g., from amphetami nes, cocaine), and medication side effects.
The final determination of caffeine withdrawal should rest on a determination of the pat-
tern and amount consumed, the time interval  between caffeine ab stinence and onset of
symptoms, and the particular clinical features presented by  the individual. A challenge
dose of caffeine followed by symptom remis sion may be used to confirm the diagnosis.
Comorbidity
Caffeine withdrawal may be associated with  major depressive disorder, generalized anx-
iety disorder, panic disorder, antisocial person ality disorder in adul ts, moderate to severe
alcohol use disorder, and cannabis and cocaine use.
Other Caffeine-Induced Disorders
The following caffeine-induced disorders are described in other chapters of the manual
with disorders with which they share phenomenology (see the substance/medication-
induced mental disorders in these chapters):  caffeine-induced anxiety disorder (“Anxiety
Disorders”) and caffeine-indu ced sleep disorder (“Sleep-W ake Disorders”). These caf-
feine-induced disorders are diagnosed instead of caffeine intoxicati on or caffeine with-
drawal only when the symptoms are sufficie ntly severe to warrant independent clinical
attention.


Unspecified Caffeine-Related Disorder 509
Unspecified Caffeine-Related Disorder
292.9 (F15.99)
This category applies to presentations in which symptoms characteristic of a caffeine-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific caffeine-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.
Cannabis-Related Disorders
Cannabis Use Disorder
Cannabis Intoxication
Cannabis Withdrawal
Other Cannabis-Induced Disorders
Unspecified Cannabis-Related Disorder
Cannabis Use Disorder
Diagnostic Criteria
A. A problematic pattern of cannabis use leading to clinically significant impairment or dis-
tress, as manifested by at least two of the following, occurring within a 12-month period:
1. Cannabis is often taken in larger amounts or over a longer period than was intended.
2. There is a persistent desire or unsuccessful efforts to cut down or control cannabis use.
3. A great deal of time is spent in activities necessary to obtain cannabis, use canna-
bis, or recover from its effects.
4. Craving, or a strong desire or urge to use cannabis.
5. Recurrent cannabis use resulting in a failure to fulfill major role obligations at work,
school, or home.
6. Continued cannabis use despite having persist ent or recurrent social or interper-
sonal problems caused or exacerbated by the effects of cannabis.
7. Important social, occupational, or recreat ional activities are given up or reduced be-
cause of cannabis use.
8. Recurrent cannabis use in situations in which it is physically hazardous.
9. Cannabis use is continued despite knowledge of having a persistent or recurrent


9. Cannabis use is continued despite knowledge of having a persistent or recurrent
physical or psychological problem that is  likely to have been caused or exacerbated
by cannabis.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of cannabis to achieve intoxication or
desired effect.
b. Markedly diminished effect with continued use of the same amount of cannabis.
11. Withdrawal, as manifested by either of the following:
a. The characteristic withdrawal syndrome for cannabis (refer to Criteria A and B
of the criteria set for cannabis withdrawal, pp. 517–518).


510 Substance-Related and Addictive Disorders
b. Cannabis (or a closely related substance) is taken to relieve or avoid withdrawal
symptoms.
Specify if:
In early remission:  After full criteria for cannabis us e disorder were previously met,
none of the criteria for cannabis use disorder have been met for at least 3 months but
for less than 12 months (with the exception that Criterion A4, “Craving, or a strong de-
sire or urge to use cannabis,” may be met).
In sustained remission: After full criteria for cannabis use disorder were previously
met, none of the criteria for cannabis use disorder have been met at any time during a
period of 12 months or longer (with the exception that Criterion A4, “Craving, or a
strong desire or urge to use cannabis,” may be present).
Specify if:
In a controlled environment:  This additional specifier is used if the individual is in an
environment where access to cannabis is restricted.
Code based on current severity: Note for ICD-10-CM codes: If a cannabis intoxication,
cannabis withdrawal, or another cannabis-induced mental disorder is also present, do not
use the codes below for cannabis use disorder. Instead, the comorbid cannabis use disorder
is indicated in the 4th character of the cannabis-induced disorder code (see the coding note
for cannabis intoxication, cannabis withdrawal, or a specific cannabis-induced mental disor-
der). For example, if there is comorbid cannabis-induced anxiety disorder and cannabis use
disorder, only the cannabis-induced anxiety disorder code is given, with the 4th character
indicating whether the comorbid cannabis use disorder is mild, moderate, or severe:
F12.180 for mild cannabis use disorder with cannabis-induced anxiety disorder or F12.280


F12.180 for mild cannabis use disorder with cannabis-induced anxiety disorder or F12.280
for a moderate or severe cannabis use diso rder with cannabis-induced anxiety disorder.
Specify current severity:
305.20 (F12.10) Mild:  Presence of 2–3 symptoms.
304.30 (F12.20) Moderate: Presence of 4–5 symptoms.
304.30 (F12.20) Severe:  Presence of 6 or more symptoms.
Specifiers
“In a controlled environment” app lies as a further specifier of remission if the individual is
both in remission and in a controlled environm ent (i.e., in early remission in a controlled
environment or in sustained remission in a controlled environmen t). Examples of these
environments are closely supe rvised and substanc e-free jails, therapeutic communities,
and locked hospital units.
Changing severity across time in an individual may also be reflected by changes in the
frequency (e.g., days of use per month or ti mes used per day) and/or dose (e.g., amount
used per episode) of cannabis, as assessed by in dividual self-report, report of knowledge-
able others, clinician’s observ ations, and biological testing.
Diagnostic Features
Cannabis use disorder and the other cannabis-re lated disorders include problems that are
associated with substances derived from the cannabis plant and chemically similar syn-
thetic compounds. Over time, this plant material has accumulated many names (e.g.,
weed, pot, herb, grass, reefer, mary jane, da gga, dope, bhang, skunk, boom, gangster, kif,
and ganja). A concentrated extraction of the cannabis plant that is also commonly used is
hashish. Cannabis  is the generic and perhaps the most appropriate scientific term for the


hashish. Cannabis  is the generic and perhaps the most appropriate scientific term for the
psychoactive substance(s) derived from the pl ant, and as such it is used in this manual
to refer to all forms of cannabis-like substances, including synthetic cannabinoid com-
pounds.


Cannabis Use Disorder 511
Synthetic oral formulations (pill/capsules) of delta-9-tetrahydrocannabinol (delta-9-
THC) are available by prescripti on for a number of approved medical indications (e.g., for
nausea and vomiting caused by chemotherapy; for anorexia and weight loss in individuals
with AIDS). Other synthetic cannabinoid co mpounds have been manufactured and dis-
tributed for nonmedical use in the form of plant material that has been sprayed with a can-
nabinoid formulation (e.g., K2, Spice, JWH-018, JWH-073).
The cannabinoids have diverse effects in the brain, prominent among which are actions
on CB1 and CB2 cannabinoid receptors that ar e found throughout the central nervous sys-
tem. Endogenous ligands for these receptor s behave essentially like neurotransmitters.
The potency of cannabis (delta-9-THC concentration) that is generally available varies
greatly, ranging from 1% to approximately 15% in typical cannabis plant material and
10%–20% in hashish. During the past two de cades, a steady increase in the potency of
seized cannabis has been observed.
Cannabis is most commonly smoked via a variety of methods: pipes, water pipes
(bongs or hookahs), cigarettes (joints or reefer s), or, most recently, in the paper from hol-
lowed out cigars (blunts). Cannabis is also sometimes ingested orally, typically by mixing
it into food. More recently, devices have be en developed in which cannabis is “vapor-
ized.” Vaporization involves heating the plant material to release psychoactive cannabi-
noids for inhalation. As with other psychoactive substances, smoking (and vaporization)


noids for inhalation. As with other psychoactive substances, smoking (and vaporization)
typically produces more rapid onset and more intense experiences of the desired effects.
Individuals who regularly use cannabis can develop all the genera l diagnostic features
of a substance use disorder. Cannabis use diso rder is commonly observed as the only sub-
stance use disorder experienced by the individu al; however, it also frequently occurs con-
currently with other types of substance use di sorders (i.e., alcohol, cocaine, opioid). In
cases for which multiple types of substances are used, many times the individual may
minimize the symptoms related to cannabis, as  the symptoms may be less severe or cause
less harm than those directly related to the use of the other substances. Pharmacological
and behavioral tolerance to most of the effect s of cannabis has been reported in individuals
who use cannabis persistently. Generally, tolerance is lost when cannabis use is discontin-
ued for a significant period of time (i.e., for at least several months).
New to DSM-5 is the recognition that abrupt cessation of daily or near-daily cannabis
use often results in the onset of a cannabis withdrawal syndrome. Common symptoms of
withdrawal include irritability, anger or ag gression, anxiety, depressed mood, restless-
ness, sleep difficulty, and decreased appetite or weight loss. Although typically not as
severe as alcohol or opiate withdrawal, the cannabis withdrawal syndrome can cause sig-
nificant distress and contribute to difficulty quitting or relapse among those trying to
abstain.
Individuals with cannabis use disorder may use cannabis throughout the day over a
period of months or years, and thus may spend many hours a da y under the influence.
Others may use less frequently, but their use causes recurrent problems related to family,


Others may use less frequently, but their use causes recurrent problems related to family,
school, work, or other important activities (e.g ., repeated absences at work; neglect of fam-
ily obligations). Periodic cannabis use and intoxication can negatively affect behavioral
and cognitive functioning and thus interfere with optimal performance at work or school,
or place the individual at increased physical risk when performing activities that could be
physically hazardous (e.g., driving a car; playing certain sports; performing manual work
activities, including operating machinery). Ar guments with spouses or parents over the


physically hazardous (e.g., driving a car; playing certain sports; performing manual work
activities, including operating machinery). Ar guments with spouses or parents over the
use of cannabis in the home, or its use in th e presence of children, can adversely impact
family functioning and are common features of  those with cannabis use disorder. Last, in-
dividuals with cannabis use disorder may continue using despite knowledge of physical
problems (e.g., chronic cough related to smoking) or psychological problems (e.g., exces-
sive sedation or exacerbation of other ment al health problems) associated with its use.
Whether or not cannabis is being used for legitimate medical reasons may also affect
diagnosis. When a substance is taken as indicated for a medical condition, symptoms of


512 Substance-Related and Addictive Disorders
tolerance and withdrawal will naturally occur and should not be used as the primary cri-
teria for determining a diagnosis of a substance use disorder. Although medical uses of
cannabis remain controversial and equivocal,  use for medical circumstances should be
considered when a diagnosis is being made.
Associated Features Supporting Diagnosis
Individuals who regularly use cannabis often report that it is being used to cope with
mood, sleep, pain, or other physiological or psychological problems, and those diagnosed
with cannabis use disorder frequently do have  concurrent other mental disorders. Careful
assessment typically reveals reports of cannabis use contributing to exacerbation of these
same symptoms, as well as other reasons for freq uent use (e.g., to experience euphoria, to
forget about problems, in respon se to anger, as an enjoyable social activity). Related to this
issue, some individuals who use cannabis mult iple times per day for the aforementioned
reasons do not perceive themselves as (and thus do not report) spending an excessive
amount of time under the influence or recovering from the effects of cannabis, despite be-
ing intoxicated on cannabis or coming down from  it effects for the majority of most days.
An important marker of a substance use disorder  diagnosis, particularly in milder cases, is
continued use despite a clear risk of negative co nsequences to other valued activities or re-
lationships (e.g., school, work, sport activity, partner or parent relationship).
Because some cannabis users are motivated to  minimize their amount or frequency of
use, it is important to be aware of common signs and symptoms of cannabis use and intox-
ication so as to better assess the extent of us e. As with other substances, experienced users
of cannabis develop behavioral and pharmacolo gical tolerance such that it can be difficult


of cannabis develop behavioral and pharmacolo gical tolerance such that it can be difficult
to detect when they are under the influence. Signs of acute and chro nic use include red eyes
(conjunctival injection), cannabis odor on clot hing, yellowing of finger tips (from smoking
joints), chronic cough, burning of incense (to hide the odor), and exaggerated craving and
impulse for specific foods, sometimes at unusual times of the day or night.
Prevalence
Cannabinoids, especially cann abis, are the most widely us ed illicit psychoactive sub-
stances in the United States. The 12-month prevalence of ca nnabis use disorder (DSM-IV
abuse and dependence rates combined) is appr oximately 3.4% among 12- to 17-year-olds
and 1.5% among adults age 18 years and older.  Rates of cannabis use disorder are greater
among adult males (2.2%) than among adult females (0.8%) and among 12- to 17-year-old
males (3.8%) than among 12- to 17-year-old  females (3.0%). Twelve-month prevalence
rates of cannabis use disorder among adults decrease with age, with rates highest among
18- to 29-year-olds (4.4%) and lowest amon g individuals age 65 years and older (0.01%).
The high prevalence of cannabis use disord er likely reflects the much more widespread
use of cannabis relative to other illicit drug s rather than greater addictive potential.
Ethnic and racial differences in prevalence are moderate. Twelve-month prevalences
of cannabis use disorder vary markedly across racial-ethnic subgroups in the United
States. For 12- to 17-year-olds, rates are hi ghest among Native American and Alaska Na-


tives (7.1%) compared with Hispanics (4.1%) , whites (3.4%), African Americans (2.7%),
and Asian Americans and Pacific Islanders (0.9%). Among adults, the prevalence of can-
nabis use disorder is also highest among Nati ve Americans and Alaska Natives (3.4%) rel-
ative to rates among African Americans (1.8%) , whites (1.4%), Hispanics (1.2%), and Asian
and Pacific Islanders (1.2%). During the past decade the prevalence of cannabis use disor-
der has increased among adults and adolescent s. Gender differences in cannabis use dis-


and Pacific Islanders (1.2%). During the past decade the prevalence of cannabis use disor-
der has increased among adults and adolescent s. Gender differences in cannabis use dis-
order generally are concordant with those in  other substance use disorders. Cannabis use
disorder is more commonly observed in males,  although the magnitude of this difference
is less among adolescents.


Cannabis Use Disorder 513
Development and Course
The onset of cannabis use disorder can occur at  any time during or following adolescence,
but onset is most commonly during adolescenc e or young adulthood. Although much less
frequent, onset of cannabis use disorder in the preteen years or in the late 20s or older can
occur. Recent acceptance by some of the us e and availability of “medical marijuana” may
increase the rate of onset of cannabis use disorder among older adults.
Generally, cannabis use disorder develops over an extended period of time, although
the progression appears to be more rapid in ad olescents, particularly those with pervasive
conduct problems. Most people who develop a cannabis use disorder typically establish a
pattern of cannabis use that gradually increases in both frequency and amount. Cannabis,
along with tobacco and alcohol, is traditiona lly the first substance that adolescents try.
Many perceive cannabis use as less harmful than alcohol or tobacco use, and this percep-
tion likely contributes to increased use. Moreover, cannabis intoxication does not typically
result in as severe behavioral and cognitive dysfunction as does sig nificant alcohol intox-
ication, which may increase the probability of  more frequent use in more diverse situa-
tions than with alcohol. These factors likely contribute to the potential rapid transition
from cannabis use to a cannabis use disord er among some adolescents and the common
pattern of using throughout the day that is commonly ob served among those with more
severe cannabis use disorder.
Cannabis use disorder among preteens, adoles cents, and young adults is typically ex-
pressed as excessive use with peers that is a component of a pattern of other delinquent
behaviors usually associated with conduct pr oblems. Milder cases primarily reflect con-
tinued use despite clear problems related to di sapproval of use by other peers, school ad-


ministration, or family, which also places the youth at risk for physical or behavioral
consequences. In more severe cases, there is a progression to using alone or using through-
out the day such that use interferes with da ily functioning and takes the place of previ-
ously established, prosocial activities.
With adolescent users, changes in mood stab ility, energy level, and eating patterns are
commonly observed. These signs and symptoms ar e likely due to the direct effects of can-
nabis use (intoxication) and the subsequent effects following acute intoxication (coming
down), as well as attempts to conceal use from others. Sc hool-related problems are com-
monly associated with cannabis use disorder in  adolescents, particularly a dramatic drop
in grades, truancy, and reduced interest in general school activities and outcomes.
Cannabis use disorder among adults typically involves well-establish ed patterns of daily
cannabis use that continue despite clear psycho social or medical problems. Many adults have
experienced repeated desire to st op or have failed at repeated cessation attempts. Milder adult
cases may resemble the more common adolescent cases in that cannabis use is not as frequent
or heavy but continues despite po tential significant consequences of sustained use. The rate of
use among middle-age and older adults appears to be increasing, likely because of a cohort ef-
fect resulting from high prevalence of use in the late 1960s and the 1970s.
Early onset of cannabis use (e.g., prior to ag e 15 years) is a robust predictor of the de-
velopment of cannabis use disorder and other types of substance use disorders and mental
disorders during young adulthood. Such early onset is likely related to concurrent other
externalizing problems, most notably conduc t disorder symptoms. However, early onset


externalizing problems, most notably conduc t disorder symptoms. However, early onset
is also a predictor of internalizing problems and as such probably reflects a general risk
factor for the development of  mental health disorders.
Risk and Prognostic Factors


is also a predictor of internalizing problems and as such probably reflects a general risk
factor for the development of  mental health disorders.
Risk and Prognostic Factors
Temperamental. A history of conduct disorder in ch ildhood or adolescence and antiso-
cial personality disorder are risk factors for the developmen t of many substance-related
disorders, including cannabis-related disorders. Other risk factors include externalizing


514 Substance-Related and Addictive Disorders
or internalizing disorders during childhood or  adolescence. Youths with high behavioral
disinhibition scores show early-onset substance use disorders, including cannabis use dis-
order, multiple substance involvem ent, and early conduct problems.
Environmental. Risk factors include academic failure , tobacco smoking, unstable or abu-
sive family situation, use of cannabis among immediate family members, a family history
of a substance use disorder, and low socioecono mic status. As with all substances of abuse,
the ease of availability of the substance is a ri sk factor; cannabis is relatively easy to obtain
in most cultures, which increases the risk  of developing a cannabis use disorder.
Genetic and physiological. Genetic influences contribute to the development of canna-
bis use disorders. Heritable factors contribute between 30% and 80% of the total variance
in risk of cannabis use disorders. It should be noted that common genetic and shared en-
vironmental influences between cannabis and other types of substance use disorders sug-
gest a common genetic basis for adolesce nt substance use and conduct problems.
Culture-Related Diagnostic Issues
Cannabis is probably the world’s most commo nly used illicit substance. Occurrence of
cannabis use disorder across countries is unkn own, but the prevalence rates are likely sim-
ilar among developed countries. It is frequently among the fi rst drugs of experimentation
(often in the teens) of all cultur al groups in the United States.
Acceptance of cannabis for medical purposes varies widely across and within cultures.
Cultural factors (acceptability and legal status ) that might impact diagnosis relate to dif-
ferential consequences across cultures for dete ction of use (i.e., arrest, school suspensions,
or employment suspension). The general change in substance use disorder diagnostic cri-


or employment suspension). The general change in substance use disorder diagnostic cri-
teria from DSM-IV to DSM-5 (i.e., removal of  the recurrent substance-related legal prob-
lems criterion) mitigates this concern to some degree.
Diagnostic Markers
Biological tests for cannabinoid metabolites are useful for determining if an individual has
recently used cannabis. Such testing is help ful in making a diagnosis, particularly in
milder cases if an individual denies using while others (family, work, school) purport con-
cern about a substance use problem. Because cannabinoids are fat soluble, they persist in
bodily fluids for extended periods of time an d are excreted slowly. Expertise in urine test-
ing methods is needed to reliably interpret results.
Functional Consequences of Cannabis Use Disorder
Functional consequences of cannabis use disord er are part of the di agnostic criteria. Many
areas of psychosocial, cognitive, and health  functioning may be co mpromised in relation
to cannabis use disorder. Cognitive function, particularly higher executive function, ap-
pears to be compromised in cannabis users, an d this relationship appears to be dose de-
pendent (both acutely and chronically). This  may contribute to increased difficulty at
school or work. Cannabis use has been related to a reduction in prosocial goal-directed ac-
tivity, which some have labeled an amotivational syndrome,  that manifests itself in poor
school performance and employ ment problems. These problems may be related to perva-
sive intoxication or recovery from the effects of intoxication . Similarly, cannabis-associated
problems with social relationships are common ly reported in those with cannabis use dis-
order. Accidents due to engagement in pote ntially dangerous behaviors while under the


order. Accidents due to engagement in pote ntially dangerous behaviors while under the
influence (e.g., driving, sport, recreational or employment ac tivities) are also of concern.
Cannabis smoke contains high levels of carc inogenic compounds that place chronic users
at risk for respiratory illnesses similar to those experienced by to bacco smokers. Chronic
cannabis use may contribute to the onset or exacerbation of many ot her mental disorders.


at risk for respiratory illnesses similar to those experienced by to bacco smokers. Chronic
cannabis use may contribute to the onset or exacerbation of many ot her mental disorders.
In particular, concern has been raised about cannabis use as a causal factor in schizophrenia
and other psychotic disorders. Cannabis use ca n contribute to the onset of an acute psy-


Cannabis Use Disorder 515
chotic episode, can exacerbate some sympto ms, and can adversely affect treatment of a
major psychotic illness.
Differential Diagnosis
Nonproblematic use of cannabis. The distinction between nonproblematic use of can-
nabis and cannabis use disorder can be difficult  to make because social, behavioral, or psy-
chological problems may be difficult to attribut e to the substance, especially in the context
of use of other substances. Also, denial of heavy cannabis use and the attribution that can-
nabis is related to or causing substantial problems are common among individuals who
are referred to treatment by others (i.e., sch ool, family, employer, criminal justice system).
Other mental disorders. Cannabis-induced disorder may be characterized by symp-
toms (e.g., anxiety) that resemble primary mental disorders (e.g., gene ralized anxiety dis-
order vs. cannabis-induced anxiety disorder, with generalized anxiety, with onset during
intoxication). Chronic intake of cannabis can produce a lack of motivation that resembles
persistent depressive disorder (dysthymia). Acute adverse reactions to cannabis should be
differentiated from the symptoms of panic di sorder, major depressive disorder, delusional
disorder, bipolar disorder, or schizophrenia , paranoid type. Physical examination will
usually show an increased pulse and conjunctiv al injection. Urine toxicological testing can
be helpful in making a diagnosis.
Comorbidity
Cannabis has been commonly thought of as a “gateway” drug because individuals who
frequently use cannabis have a much greater lifetime probabili ty than nonusers of using
what are commonly considered more dangerou s substances, like opioids or cocaine. Can-
nabis use and cannabis use disorder are highly comorbid with other substance use disor-


nabis use and cannabis use disorder are highly comorbid with other substance use disor-
ders. Co-occurring mental co nditions are common in canna bis use disorder. Cannabis use
has been associated with poor er life satisfaction; increased mental health treatment and
hospitalization; and higher rates of depressi on, anxiety disorders, suicide attempts, and
conduct disorder. Individuals with past-year or lifetime cannabis use disorder have high
rates of alcohol use disorder (greater than 50%) and tobacco use disorder (53%). Rates of
other substance use disorders are also likely to be high among individuals with cannabis
use disorder. Among those seeking treatmen t for a cannabis use disorder, 74% report
problematic use of a secondary or tertiary su bstance: alcohol (40%), cocaine (12%), meth-
amphetamine (6%), and heroin or other opia tes (2%). Among those younger than 18 years,
61% reported problematic use of a secondary su bstance: alcohol (48%), cocaine (4%), meth-
amphetamine (2%), and heroin or other opiates (2%). Cannabis use disorder is also often
observed as a secondary problem among those with a primary diagnosis of other substance
use disorders, with approximately 25%–80% of those in treatment for another substance
use disorder reporting use of cannabis.
Individuals with past-year or lifetime diag noses of cannabis use disorder also have
high rates of concurrent ment al disorders other than substa nce use disorders. Major de-
pressive disorder (11%), any anxiety disorder (24%), and bipolar I disorder (13%) are quite
common among individuals with a past-year di agnosis of a cannabis use disorder, as are
antisocial (30%), obsessive-co mpulsive, (19%), and paranoid (18%) personality disorders.
Approximately 33% of adolescents with canna bis use disorder have internalizing disor-


Approximately 33% of adolescents with canna bis use disorder have internalizing disor-
ders (e.g., anxiety, depressio n, posttraumatic stre ss disorder), and 60% have externalizing
disorders (e.g., conduct disorder, atte ntion-deficit/hyperactivity disorder).
Although cannabis use can impact multiple asp ects of normal human functioning, in-
cluding the cardiovascular, immune, neuromuscular, ocular, reproductive, and respira-
tory systems, as well as appetite and cognit ion/perception, there are few clear medical


cluding the cardiovascular, immune, neuromuscular, ocular, reproductive, and respira-
tory systems, as well as appetite and cognit ion/perception, there are few clear medical
conditions that commonly co-occur with cannab is use disorder. The most significant health


516 Substance-Related and Addictive Disorders
effects of cannabis involve the respiratory system, and chronic cannabis smokers exhibit
high rates of respiratory symptoms of bronch itis, sputum production, shortness of breath,
and wheezing.
Cannabis Intoxication
Diagnostic Criteria
A. Recent use of cannabis.
B. Clinically significant problematic behavio ral or psychological changes (e.g., impaired
motor coordination, euphoria, anxiety, sensat ion of slowed time, impaired judgment,
social withdrawal) that developed during, or shortly after, cannabis use.
C. Two (or more) of the following signs or symptoms developing within 2 hours of canna-
bis use:
1. Conjunctival injection.
2. Increased appetite.
3. Dry mouth.
4. Tachycardia.
D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication with another substance.
Specify if:
With perceptual disturbances:  Hallucinations with intact reality testing or auditory, vi-
sual, or tactile illusions occur in the absence of a delirium.
Coding note:  The ICD-9-CM code is 292.89.  The ICD-10-CM code depends on whether
or not there is a comorbid cannabis use diso rder and whether or not there are perceptual
disturbances.
For cannabis intoxication, with out perceptual disturbances: If a mild cannabis use
disorder is comorbid, the ICD-10-CM code is F12.129,  and if a moderate or severe
cannabis use disorder is comorbid, the ICD-10-CM code is F12.229.  If there is no co-


morbid cannabis use disorder, then the ICD-10-CM code is F12.929.
For cannabis intoxication, wit h perceptual disturbances:  If a mild cannabis use
disorder is comorbid, the ICD-10-CM code is F12.122,  and if a moderate or severe
cannabis use disorder is comorbid, the ICD-10-CM code is F12.222.  If there is no co-
morbid cannabis use disorder, then the ICD-10-CM code is F12.922.
Specifiers
When hallucinations occur in the absence of inta ct reality testing, a diagnosis of substance/
medication-induced psychotic di sorder should be considered.
Diagnostic Features
The essential feature of cannabis intoxication is the presence of clinically significant prob-
lematic behavioral or psychological changes th at develop during, or shortly after, canna-
bis use (Criterion B). Intoxication typically  begins with a “high” feeling followed by
symptoms that include euphoria with inapprop riate laughter and grandiosity, sedation,
lethargy, impairment in short- term memory, difficulty carrying out complex mental pro-
cesses, impaired judgment, distorted sensory perceptions, impaired motor performance,
and the sensation that time is passing slowly. Occasionally, anxiety (which can be severe),


Cannabis Withdrawal 517
dysphoria, or social withdrawal occurs. These psychoactive effects are accompanied by
two or more of the following signs, developi ng within 2 hours of cannabis use: conjuncti-
val injection, increased appetite, dry mouth, and tachycardia (Criterion C).
Intoxication develops within minutes if the cannabis is smoked but may take a few
hours to develop if the cannabis is ingested orally. The effects usually last 3–4 hours, with
the duration being somewhat lo nger when the substance is in gested orally. The magnitude
of the behavioral and physiological changes depends on the dose, the method of adminis-
tration, and the characteristics of the individual using the substance, such as rate of absorp-
tion, tolerance, and sensitivity to the effects of the substance. Because most cannabinoids,
including delta-9-tetrahydrocannabinol (delta-9-T HC), are fat soluble, the effects of canna-
bis or hashish may occasionally persist or re occur for 12–24 hours because of the slow re-
lease of psychoactive substances from fa tty tissue or to ente rohepatic circulation.
Prevalence
The prevalence of actual episodes of cannabis intoxication in the general population is un-
known. However, it is probable that most ca nnabis users would at some time meet criteria
for cannabis intoxication. Given this, the prev alence of cannabis users and the prevalence
of individuals experiencing canna bis intoxication are likely similar.
Functional Consequences of Cannabis Intoxication
Impairment from cannabis intoxication ma y have serious consequences, including dys-
function at work or school, social indiscretion s, failure to fulfill role  obligations, traffic ac-
cidents, and having unprotected sex. In rare cases, cannabis intoxication may precipitate a


cidents, and having unprotected sex. In rare cases, cannabis intoxication may precipitate a
psychosis that may vary in duration.
Differential Diagnosis
Note that if the clinical presentation includes  hallucinations in the absence of intact reality
testing, a diagnosis of subs tance/medication-induced psyc hotic disorder should be con-
sidered.
Other substance intoxication. Cannabis intoxicati on may resemble intoxication with
other types of substances. However, in contrast to cannabis intoxication, alcohol intoxica-
tion and sedative, hypnotic, or anxiolytic in toxication frequently decrease appetite, in-
crease aggressive behavior, and produce nyst agmus or ataxia. Hallucinogens in low doses
may cause a clinical picture that resembles cannabis intoxication. Phencyclidine, like can-
nabis, can be smoked and also causes perceptual changes, but phencyclidine intoxication
is much more likely to cause ataxia and aggressive behavior.
Other cannabis-induced disorders. Cannabis intoxication is distinguished from the other
cannabis-induced disorders (e.g., cannabis-in duced anxiety disorder, with onset during
intoxication) because the symptoms in these latter disorders predomin ate the clinical pre-
sentation and are severe enough to wa rrant independent clinical attention.
Cannabis Withdrawal
Diagnostic Criteria 292.0 (F12.288)
A. Cessation of cannabis use that has been heavy and prolonged (i.e., usually daily or
almost daily use over a period of at least a few months).
B. Three (or more) of the following signs and symptoms develop within approximately 1 week
after Criterion A:


518 Substance-Related and Addictive Disorders
1. Irritability, anger, or aggression.
2. Nervousness or anxiety.
3. Sleep difficulty (e.g., insomnia, disturbing dreams).
4. Decreased appetite or weight loss.
5. Restlessness.
6. Depressed mood.
7. At least one of the following physical symptoms causing significant discomfort: ab-
dominal pain, shakiness/tremors, sweating, fever, chills, or headache.
C. The signs or symptoms in Criterion B cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The signs or symptoms are not attributable to another medical condition and are not
better explained by another mental disorder, including intoxication or withdrawal from
another substance.
Coding note:  The ICD-9-CM code is 292.0. The ICD-10-CM code for cannabis withdrawal
is F12.288. Note that the ICD-10-CM code indicates the comorbid presence of a moderate
or severe cannabis use disorder, reflecting the fact that cannabis withdrawal can only oc-
cur in the presence of a moderate or severe cannabis use disorder. It is not permissible to
code a comorbid mild cannabis use disorder with cannabis withdrawal.
Diagnostic Features
The essential feature of cannabis withdrawal is the presence of a characteristic withdrawal
syndrome that develops after the cessation of  or substantial reduction in heavy and pro-
longed cannabis use. In addition to the sympto ms in Criterion B, the following may also be
observed postabstinence: fatigu e, yawning, difficulty concentrating, and rebound periods
of increased appetite and hypersomnia that follo w initial periods of loss of appetite and in-
somnia. For the diagnosis, withdrawal symptoms  must cause clinically significant distress


somnia. For the diagnosis, withdrawal symptoms  must cause clinically significant distress
or impairment in social, occu pational, or other important ar eas of functioning (Criterion
C). Many cannabis users report smoking cannabi s or taking other substances to help re-
lieve withdrawal symptoms, and many report  that withdrawal symptoms make quitting
difficult or have contributed to relapse. Th e symptoms typically ar e not of sufficient se-
verity to require medical attention, but medica tion or behavioral strategies may help alle-
viate symptoms and improve prognosis in those trying to quit using cannabis.
Cannabis withdrawal is commonly observed in individuals seeking treatment for can-
nabis use as well as in heavy cannabis users who are not seeking treatment. Among indi-
viduals who have used cannabis regularly during  some period of their lifetime, up to one-
third report having experienced cannabis wi thdrawal. Among adults and adolescents en-
rolled in treatment or  heavy cannabis users, 50%–95% report cannabis withdrawal. These
findings indicate that cannabis withdrawal occurs am ong a substantial subset of regular
cannabis users who try to quit.
Development and Course
The amount, duration, and frequency of canna bis smoking that is required to produce an
associated withdrawal disorder during a quit attempt are unknown. Most symptoms have
their onset within the first 24–72 hours of ce ssation, peak within the first week, and last
approximately 1–2 weeks. Sleep difficulties may last more than 30 days. Cannabis with-
drawal has been documented among adolescents and adults. Withdrawal tends to be more
common and severe among adults, most likely related to the more persistent and greater
frequency and quantity of use among adults.


Unspecified Cannabis-Related Disorder 519
Risk and Prognostic Factors
Environmental. Most likely, the prevalence and severity of cannabis withdrawal are
greater among heavier cannabis users, and part icularly among those seeking treatment for
cannabis use disorders. Withdrawal severity also appears to be positiv ely related to the se-
verity of comorbid sympto ms of mental disorders.
Functional Consequences of Cannabis Withdrawal
Cannabis users report using cannabis to re lieve withdrawal symp toms, suggesting that
withdrawal might contribute to ongoing expr ession of cannabis use disorder. Worse out-
comes may be associated with greater withdraw al. A substantial proportion of adults and
adolescents in treatment for moderate to se vere cannabis use disorder acknowledge mod-
erate to severe withdrawal symptoms, and ma ny complain that these symptoms make ces-
sation more difficult. Cannabis users report having relapsed to cannabis use or initiating
use of other drugs (e.g., tranquilizers) to pr ovide relief from cannabis withdrawal symp-
toms. Last, individuals living with cannabis us ers observe significant withdrawal effects,
suggesting that such symptoms ar e disruptive to daily living.
Differential Diagnosis
Because many of the symptoms of cannabis wi thdrawal are also symptoms of other sub-
stance withdrawal syndromes or of depressi ve or bipolar disorder s, careful evaluation
should focus on ensuring that the symptoms ar e not better explained by cessation from an-
other substance (e.g., tobacco or alcohol with drawal), another mental  disorder (general-
ized anxiety disorder, major depressive disorder), or another medical condition.
Other Cannabis-Induced Disorders
The following cannabis-induced disorders are desc ribed in other chapters of the manual with
disorders with which they share phenomenology (see the substance/medication-induced


disorders with which they share phenomenology (see the substance/medication-induced
mental disorders in these chapters): cannab is-induced psychotic disorder (“Schizophrenia
Spectrum and Other Psychotic Disorders”); cannabis-induced anxiet y disorder (“Anxiety
Disorders”); and cannabis-induced sleep diso rder (“Sleep-Wake Disorders”). For cannabis
intoxication delirium, see the criteria and disc ussion of delirium in  the chapter “Neurocog-
nitive Disorders.” These cannabis-induced diso rders are diagnosed instead of cannabis in-
toxication or cannabis withdrawal when the symptoms are sufficiently severe to warrant
independent clinical attention.
Unspecified Cannabis-Related Disorder
292.9 (F12.99)
This category applies to presentations in which symptoms characteristic of a cannabis-
related disorder that cause clinically significant distress or impairment in social, occupa-
tional, or other important areas of functioning predominate but do not meet the full criteria
for any specific cannabis-related disorder or any of the disorders in the substance-related
and addictive disorders diagnostic class.


520 Substance-Related and Addictive Disorders
Hallucinogen-Related Disorders
Phencyclidine Use Disorder
Other Hallucinogen Use Disorder
Phencyclidine Intoxication
Other Hallucinogen Intoxication
Hallucinogen Persisting Perception Disorder
Other Phencyclidine-Induced Disorders
Other Hallucinogen-Induced Disorders
Unspecified Phencyclidine-Related Disorder
Unspecified Hallucino gen-Related Disorder
Phencyclidine Use Disorder
Diagnostic Criteria
A. A pattern of phencyclidine (or a pharmacologically similar substance) use leading to
clinically significant impairment or distress, as manifested by at least two of the follow-
ing, occurring within a 12-month period:
1. Phencyclidine is often taken in larger amounts or over a longer period than was in-
tended.
2. There is a persistent desire or unsuccessful efforts to cut down or control phency-
clidine use.
3. A great deal of time is spent in activities necessary to obtain phencyclidine, use the
phencyclidine, or recover from its effects.
4. Craving, or a strong desire or urge to use phencyclidine.
5. Recurrent phencyclidine use resulting in a failure to fulfill major role obligations at
work, school, or home (e.g., repeated absences from work or poor work performance
related to phencyclidine use; phencyclidine-related absences, suspensions, or ex-
pulsions from school; neglec t of children or household).
6. Continued phencyclidine use despite having persistent or recurrent social or inter-
personal problems caused or exacerbated by the effects of the phencyclidine (e.g.,
arguments with a spouse about consequences of intoxication; physical fights).


arguments with a spouse about consequences of intoxication; physical fights).
7. Important social, occupational, or recreat ional activities are given up or reduced be-
cause of phencyclidine use.
8. Recurrent phencyclidine use in situations in which it is physically hazardous (e.g.,
driving an automobile or operating a machine when impaired by a phencyclidine).
9. Phencyclidine use is continued despite knowledge of having a persistent or recur-
rent physical or psychological problem that is likely to have been caused or exac-
erbated by the phencyclidine.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the phencyclidine to achieve intoxi-
cation or desired effect.
b. A markedly diminished effect with continued use of the same amount of the
phencyclidine.


Phencyclidine Use Disorder 521
Note: Withdrawal symptoms and signs are not established for phencyclidines, and so this
criterion does not apply. (Withdrawal from phencyclidines has been reported in animals
but not documented in human users.)
Specify if:
In early remission:  After full criteria for phencyclidine use disorder were previously
met, none of the criteria for phencyclidine use disorder have been met for at least
3 months but for less than 12 months (with the exception that Criterion A4, “Craving,
or a strong desire or urge to use the phencyclidine,” may be met).
In sustained remission:  After full criteria for phencyclidine use disorder were previ-
ously met, none of the criteria for phencyclidine use disorder have been met at any time
during a period of 12 months or longer (wit h the exception that Criterion A4, “Craving,
or a strong desire or urge to use the phencyclidine,” may be met).
Specify if:
In a controlle d environment:  This additional specifier is used if the individual is in an
environment where access to phencyclidines is restricted.
Coding based on current severity:  Note for ICD-10-CM codes: If a phencyclidine intoxica-
tion or another phencyclidine-induced mental disorder is also present, do not use the codes
below for phencyclidine use disorder. Instead, the comorbid phencyclidine use disorder is in-
dicated in the 4th character of the phencyclidine-induced disorder code (see the coding note
for phencyclidine intoxication or a specific phencyclidine-induced mental disorder). For ex-


ample, if there is comorbid phencyclidine-induced psychotic disorder, only the phencyclidine-
induced psychotic disorder code is given, with the 4th character indicating whether the co-
morbid phencyclidine use disorder is mild, moderate, or severe: F16.159 for mild phencycli-
dine use disorder with phencyclidine-induced psyc hotic disorder or F16.259 for a moderate
or severe phencyclidine use disorder with phencyclidine-induced psychotic disorder.
Specify current severity:
305.90 (F16.10) Mild:  Presence of 2–3 symptoms.
304.60 (F16.20) Moderate: Presence of 4–5 symptoms.
304.60 (F16.20) Severe:  Presence of 6 or more symptoms.
Specifiers
“In a controlled environment” app lies as a further specifier of remission if the individual is
both in remission and in a controlled environm ent (i.e., in early remission in a controlled
environment or in sustained remission in a controlled environment). Examples of these
environments are closely supe rvised and substanc e-free jails, therapeutic communities,
and locked hospital units.
Diagnostic Features
The phencyclidines (or phencyclidine-like substances) include phencyclidine (e.g., PCP,
“angel dust”) and less potent but similarly ac ting compounds such as ketamine, cyclohex-
amine, and dizocilpine. These substances were  first developed as dissociative anesthetics
in the 1950s and became street drugs in the 1960s. They produce feelings of separation
from mind and body (hence “d issociative”) in low doses, an d at high doses, stupor and


coma can result. These substances are most commonly smoked or taken orally, but they
may also be snorted or injected. Although the primary psychoactive ef fects of PCP last for
a few hours, the total elimination rate of this  drug from the body typically extends 8 days
or longer. The hallucinogenic effects in vulne rable individuals may last for weeks and may
precipitate a persistent psychotic episode resembling schizophrenia. Ketamine has been
observed to have utility in the treatment of  major depressive disorder. Withdrawal symp-


522 Substance-Related and Addictive Disorders
toms have not been clearly established in hu mans, and therefore the withdrawal criterion
is not included in the diagnosis of phencyclidine use disorder.
Associated Features Supporting Diagnosis
Phencyclidine may be detected in urine for up to 8 days or even longer at very high doses. In
addition to laboratory tests to detect its presence, characteristic symptoms resulting from
intoxication with phencyclidine or related su bstances may aid in its diagnosis. Phencycli-
dine is likely to produce dissociative sympto ms, analgesia, nystagmus, and hypertension,
with risk of hypotension and shock. Violen t behavior can also occur with phencyclidine
use, as intoxicated persons may believe that  they are being attacked. Residual symptoms
following use may resemble schizophrenia.
Prevalence
The prevalence of phen cyclidine use disorder is unknown.  Approximately 2.5% of the pop-
ulation reports having ever used phencyclidine. The proportion of users increases with
age, from 0.3% of 12- to 17-year-olds, to 1.3% of 18- to 25-year -olds, to 2.9% of those age 26
years and older reporting ever using phencyclid ine. There appears to have been an in-
crease among 12th graders in both ever used (to 2.3% from 1.8%) and past-year use (to 1.3%
from 1.0%) of phencyclidine. Past-year use of  ketamine appears relatively stable among
12th graders (1.6%–1.7% over the past 3 years).
Risk and Prognostic Factors


Risk and Prognostic Factors
There is little information about risk factor s for phencyclidine use disorder. Among indi-
viduals admitted to substanc e abuse treatment, those for whom phencyclidine was the
primary substance were younger than those admitted for other substance use, had lower
educational levels, and were more likely to be  located in the West and Northeast regions of
the United States, compared with other admissions.
Culture-Related Diagnostic Issues
Ketamine use in youths ages 16–23 years ha s been reported to be more common among
whites (0.5%) than among other ethnic gr oups (range 0%–0.3%). Among individuals ad-
mitted to substance abuse treatment, those for whom phencyclidine was the primary sub-
stance were predominantly black (49%) or Hispanic (29%).
Gender-Related Diagnostic Issues
Males make up about three-quarters of those with phencyclidine-related emergency room
visits.
Diagnostic Markers
Laboratory testing may be useful, as phencyclidin e is present in the urine in intoxicated in-
dividuals up to 8 days after ingestion. The in dividual’s history, along with certain physical
signs, such as nystagmus, analgesia and pr ominent hypertension, may aid in distinguish-
ing the phencyclidine clinical picture from that of other hallucinogens.
Functional Consequences of Phencyclidine Use Disorder
In individuals with phencyclidine use disorder, there may be physical evidence of injuries
from accidents, fights, and falls. Chronic use of phencyclidine may lead to deficits in mem-
ory, speech, and cognition that may last for months. Cardiovascular and neurological tox-


ory, speech, and cognition that may last for months. Cardiovascular and neurological tox-
icities (e.g., seizures, dystonias, dyskinesia s, catalepsy, hypothermia or hyperthermia)
may result from intoxication with phencyclid ine. Other consequences include intracranial
hemorrhage, rhabdomyolysis, respiratory problems, and (occasionally) cardiac arrest.


Other Hallucinogen Use Disorder 523
Differential Diagnosis
Other substance use disorders. Distinguishing the effects of phencyclidine from those
of other substances is import ant, since it may be a common additive to other substances
(e.g., cannabis, cocaine).
Schizophrenia and other mental disorders. Some of the effects of phencyclidine and
related substance use may resemble symptoms of  other psychiatric disorders, such as psy-
chosis (schizophrenia), low mood (major de pressive disorder), vi olent aggressive be-
haviors (conduct disorder, antisocial person ality disorder). Discerning whether these
behaviors occurred before the intake of the dr ug is important in the differentiation of acute
drug effects from preexisting mental disord er. Phencyclidine-induced psychotic disorder
should be considered when there is impaired  reality testing in individuals experiencing
disturbances in perception result ing from ingestion of phencyclidine.
Other Hallucinogen Use Disorder
Diagnostic Criteria
A. A problematic pattern of hallucinogen (other than phencyclidine) use leading to clini-
cally significant impairment or distress, as manifested by at least two of the following,
occurring within a 12-month period:
1. The hallucinogen is often taken in larger amounts or over a longer period than was
intended.
2. There is a persistent desire or unsuccessfu l efforts to cut down or control halluci-
nogen use.
3. A great deal of time is spent in activities necessary to obtain the hallucinogen, use
the hallucinogen, or recover from its effects.
4. Craving, or a strong desire or urge to use the hallucinogen.
5. Recurrent hallucinogen use resulting in a failure to fulfill major role obligations at


5. Recurrent hallucinogen use resulting in a failure to fulfill major role obligations at
work, school, or home (e.g., repeated absences from work or poor work perfor-
mance related to hallucinogen use; hallucinogen-related absences, suspensions,
or expulsions from school; neglect of children or household).
6. Continued hallucinogen use despite having persistent or recurrent social or inter-
personal problems caused or exacerbated by the effects of the hallucinogen (e.g.,
arguments with a spouse about consequences of intoxication; physical fights).
7. Important social, occupational, or recreat ional activities are given up or reduced be-
cause of hallucinogen use.
8. Recurrent hallucinogen use in situations in which it is physically hazardous (e.g.,
driving an automobile or operating a mach ine when impaired by the hallucinogen).
9. Hallucinogen use is continued despite knowledge of having a persistent or recur-
rent physical or psychological problem t hat is likely to have been caused or exac-
erbated by the hallucinogen.
10. Tolerance, as defined by either of the following:
a. A need for markedly increased amounts of the hallucinogen to achieve intoxi-
cation or desired effect.
b. A markedly diminished effect with continued use of the same amount of the hal-
lucinogen.
Note: Withdrawal symptoms and signs are not established for hallucinogens, and so this
criterion does not apply.


524 Substance-Related and Addictive Disorders
Specify the particular hallucinogen.
Specify if:
In early remission:  After full criteria for other hallucinogen use disorder were previ-
ously met, none of the criteria for other hallucinogen use disorder have been met for
at least 3 months but for less than 12 months (with the exception that Criterion A4,
“Craving, or a strong desire or urge to use the hallucinogen,” may be met).
In sustained remission:  After full criteria for other hallucinogen use disorder were
previously met, none of the criteria for other hallucinogen use disorder have been met
at any time during a period of 12 months or longer (with the exception that Criterion A4,
“Craving, or a strong desire or urge to use the hallucinogen,” may be met).
Specify if:
In a controlled environment:  This additional specifier is used if the individual is in an
environment where access to hallucinogens is restricted.
Coding based on current severity:  Note for ICD-10-CM codes: If a hallucinogen intoxication
or another hallucinogen-induced mental disorder is also present, do not use the codes below
for hallucinogen use disorder. Instead, the comorb id hallucinogen use disorder is indicated in
the 4th character of the hallucinogen-induced disorder code (see the coding note for halluci-
nogen intoxication or specific hallucinogen-induced mental disorder). For example, if there is
comorbid hallucinogen-induced psychotic disorder and hallucinogen use disorder, only the
hallucinogen-induced psychotic disorder code is given, with the 4th character indicating wheth-
er the comorbid hallucinogen use disorder is mild, moderate, or severe: F16.159 for mild hal-


lucinogen use disorder with hallucinogen-induced  psychotic disorder or F16.259 for a
moderate or severe hallucinogen use disorder  with hallucinogen-induced psychotic disorder.
Specify current severity:
305.30 (F16.10) Mild:  Presence of 2–3 symptoms.
304.50 (F16.20) Moderate: Presence of 4–5 symptoms.
304.50 (F16.20) Severe:  Presence of 6 or more symptoms.
Specifiers
“In a controlled environment” app lies as a further specifier of remission if the individual is
both in remission and in a controlled environm ent (i.e., in early remission in a controlled
environment or in sustained remission in a controlled environmen t). Examples of these
environments are closely supe rvised and substanc e-free jails, therapeutic communities,
and locked hospital units.
Diagnostic Features
Hallucinogens comprise a diverse group of subs tances that, despite ha ving different chem-
ical structures and possibly involving diffe rent molecular mechan isms, produce similar
alterations of percepti on, mood, and cognition in users. Hallucinogens included are phenyl-
alkylamines (e.g., mescaline, DOM [2,5-d imethoxy-4-methylam phetamine], and MDMA
[3,4-methylenedioxymethamphetamine; also called “ecstasy ”]); the indoleamines, includ-
ing psilocybin (i.e., psilocin) and dimethyltryptamine (DMT); an d the ergolines, such as LSD
(lysergic acid diethylamide) and morning glory seeds. In addition, miscellaneous other


ethnobotanical compounds are classifi ed as “hallucinogens,” of which Salvia divinorum  and
jimsonweed are two examples. Excluded from the hallucinogen group are cannabis and its
active compound, delta-9-tetrahydrocannabino l (THC) (see the section “Cannabis-Related
Disorders”). These substances can have hallucinogenic effects but are diagnosed separately
because of significant differences in their psychological and behavioral effects.
Hallucinogens are usually taken orally, al though some forms are smoked (e.g., DMT,
salvia) or (rarely) taken intranasally or by in jection (e.g., ecstasy). Duration of effects varies