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Other Specified Disruptive, Impulse-Control, and Conduct Disorder 479 Risk and Prognostic Factors Genetic and physiological. There are no controlled family history studies of kleptoma- nia. However, first-degree relatives of in dividuals with klepto mania may have higher rates of obsessive-compulsive disorder than the general population. There also appears to be a higher rate of substance use disorders, including alcohol use disorder, in relatives of individuals with kleptomania than in the general population. Functional Consequenc es of Kleptomania The disorder may cause legal, family , career, and personal difficulties. Differential Diagnosis Ordinary theft. Kleptomania should be distinguishe d from ordinary acts of theft or shoplifting. Ordinary theft (whether planned or impulsive) is deliberate and is motivated by the usefulness of the object or its monetary worth. Some individuals, especially adoles- cents, may also steal on a dare, as an act of re bellion, or as a rite of passage. The diagnosis is not made unless other characteristic featur es of kleptomania are also present. Klepto- mania is exceedingly rare, whereas sh oplifting is relatively common. Malingering. In malingering, individuals may simulate the symptoms of kleptomania to avoid criminal prosecution. Antisocial personality disorder and conduct disorder. Antisocial personality disorder and conduct disorder are distinguished from kleptomania by a general pattern of antiso- cial behavior. Manic episodes, psychotic episodes, and major neurocognitive disorder. Kleptomania should be distinguished from intentional or inadvertent stealing that may occur during a manic episode, in response to delusions or ha llucinations (as in, e.g. , schizophrenia), or as
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a result of a major neurocognitive disorder. Comorbidity Kleptomania may be associated with compulsive buying as well as with depressive and bipolar disorders (especially major depressive disorder), anxiety disorders, eating disor- ders (particularly bulimia ner vosa), personality disorders, substance use disorders (espe- cially alcohol use disorder), and other disruptive, impulse-control, and conduct disorders. Other Specified Disruptive, Impulse-Control, and Conduct Disorder 312.89 (F91.8) This category applies to presentations in which symptoms characteristic of a disruptive, impulse-control, and conduct disorder that cause clinically significant distress or impair- ment in social, occupational, or other impor tant areas of functioning predominate but do not meet the full criteria for any of the disor ders in the disruptive, impulse-control, and con- duct disorders diagnostic class. The other specified disruptive, impulse-control, and con- duct disorder category is used in situations in which the clinician chooses to communicate the specific reason that the presentation does not meet the criteria for any specific disrup- tive, impulse-control, and conduct disorder. This is done by recording “other specified dis- ruptive, impulse-control, and conduct disorder” followed by the specific reason (e.g., “recurrent behavioral outbursts of insufficient frequency”).
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480 Disruptive, Impulse-Control, and Conduct Disorders Unspecified Disruptive, Impulse-Control, and Conduct Disorder 312.9 (F91.9) This category applies to presentations in which symptoms characteristic of a disruptive, impulse-control, and conduct disorder that cause clinically significant distress or impair- ment in social, occupational, or other impor tant areas of functioning predominate but do not meet the full criteria for any of the disorders in the disruptive, impulse-control, and con- duct disorders diagnostic class. The unspecif ied disruptive, impulse-control, and conduct disorder category is used in situations in which the clinician chooses not to specify the rea- son that the criteria are not met for a specific disruptive, impulse-control, and conduct dis- order, and includes presentations in which there is insufficient information to make a more specific diagnosis (e.g., in emergency room settings).
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481Substance-Related and Addictive Disorders The substance-related disorders encompass 10 separate classes of drugs: alco- hol; caffeine; cannabis; hallucinogens (with separate categories for phencyclidine [or sim- ilarly acting arylcyclohexylamines] and ot her hallucinogens); inhalants; opioids; sedatives, hypnotics, and anxiolytics; stimul ants (amphetamine-type substances, cocaine, and other stimulants); tobacco ; and other (or unknown) subs tances. These 10 classes are not fully distinct. All drugs that are taken in excess have in common direct activation of the brain reward system, which is involved in the reinforcement of behaviors and the pro- duction of memories. They produce such an in tense activation of the reward system that normal activities may be neglected. Inst ead of achieving reward system activation through adaptive behaviors, drugs of abuse directly activate the reward pathways. The pharmacological mechanisms by which each class of drugs produces reward are different, but the drugs typically activate the system and produce feelings of pleasure, often re- ferred to as a “high.” Furthe rmore, individuals with lower levels of self-control, which may reflect impairments of brain inhibitory mechanisms, may be particularly predisposed to develop substance use disord ers, suggesting that the root s of substance use disorders for some persons can be seen in behaviors long before the onset of actual substance use itself. In addition to the substance-related disorders, this chapter also includes gambling dis- order, reflecting evidence that gambling be haviors activate reward systems similar to those activated by drugs of abuse and produce some behavi oral symptoms that appear comparable to those produced by the substa nce use disorders. Other excessive behavioral
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comparable to those produced by the substa nce use disorders. Other excessive behavioral patterns, such as Internet gaming, have also been described, but the research on these and other behavioral syndromes is less clear. Thus, groups of repetitive behaviors, which some term behavioral addictions, with such subcategories as “sex addiction,” “exercise addiction,” or “shopping addiction,” are not included becaus e at this time there is insufficient peer-re- viewed evidence to establish the diagnostic criteria and co urse descriptions needed to identify these behaviors as mental disorders. The substance-related disorder s are divided into two groups: substance use disorders and substance-induced disorders. The followi ng conditions may be classified as sub- stance-induced: intoxication, withdrawal, an d other substance/medication-induced men- tal disorders (psychotic disord ers, bipolar and related disorders, depressive disorders, anxiety disorders, obsessive-compulsive and re lated disorders, sleep disorders, sexual dys- functions, delirium, and neurocognitive disorders). The current section begins with a general di scussion of criteria sets for a substance use disorder, substance intoxication and withdrawal, and other substance/medication- induced mental disorders, at least some of which are a pplicable across classes of sub- stances. Reflecting some unique aspects of the 10 substance classes relevant to this chapter, the remainder of the chapter is organized by the class of substance and describes their unique aspects. To facilitate differential diagnosis, the text and criteria for the remaining substance/medication-induced mental disorder s are included with disorders with which they share phenomenology (e.g ., substance/medication-induced depressive disorder is in the chapter “Depressive Disorder s”). The broad diagnostic cate gories associated with each specific group of substances are shown in Table 1.
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482 Substance-Related and Addictive DisordersTABLE 1 Diagnoses associated with substance class  Psychotic disordersBipolar disordersDepres- sive disordersAnxiety disordersObsessive- compulsive and related disordersSleep disordersSexual dysfunc- tions DeliriumNeuro- cognitive disordersSubstance use disordersSub- stance intoxi- cationSub- stance with- drawal Alcohol I/W I/W I/W I/W I/W I/W I/W I/W/P X X X Caffeine     I   I/W       X X Cannabis I   I   I/W   I X X X Hallucinogens Phencyclidine I I I I     I X X   Other hallucino- gensI* I I I     I X X   Inhalants I I  I        I I/P X X   Opioids I/W W   I/W I/W I/W X X X Sedatives, hypnotics, or anxiolyticsI/W I/W I/W W I/W I/W I/W I/W/P X X X Stimulants** I I/W I/W I/W I/W I/W I I X X X Tobacco         W     X   X Other (or unknown)I/W I/W I/W I/W I/W I/W I/W I/W I/W/P X X X Note. X = The category is recognized in DSM-5. I = The specifier “with onset during intoxication” may be noted for the category. W = The specifier “with onset during with drawal” may be noted for the category.
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W = The specifier “with onset during with drawal” may be noted for the category. I/W = Either “with onset during intoxication” or “with onset during withdrawal” may be noted for the category. P = The disorder is persisting. *Also hallucinogen persisting perception disorder (flashbacks). **Includes amphetamine-type substances, coca ine, and other or unspecified stimulants.
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Substance Use Disorders 483 Substance-Related Disorders Substance Use Disorders Features The essential feature of a substance use disorder is a cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues using the substance de- spite significant substance-related problems. As seen in Table 1, the diagnosis of a sub- stance use disorder can be applied to all 10 cl asses included in this chapter except caffeine. For certain classes some symptoms are less sa lient, and in a few instances not all symptoms apply (e.g., withdrawal symptoms are not sp ecified for phencyclidin e use disorder, other hallucinogen use disorder, or inhalant use disorder). An important characteristic of substance use disorders is an underlying change in brain cir- cuits that may persist beyond detoxification, part icularly in individuals with severe disorders. The behavioral effect s of these brain changes may be exhibited in the repeated relapses and in- tense drug craving when the individuals are exposed to drug-related stimuli. These persistent drug effects may benefit from long-term approaches to treatment. Overall, the diagnosis of a su bstance use disorder is based on a pathological pattern of behaviors related to use of the substance. To as sist with organization, Criterion A criteria can be considered to fit within overall groupings of impaired control, social impairment, risky use, and pharmacological criteria. Impaired control over substance use is the first criteria grouping (Criteria 1–4). The individual may take the substance in larger amounts or over a longer pe- riod than was originally intended (Criterion 1). The individual may express a persistent de- sire to cut down or regulate substance use and may report multiple unsuccessful efforts to
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sire to cut down or regulate substance use and may report multiple unsuccessful efforts to decrease or discontinue use (Cri terion 2). The individual may sp end a great deal of time ob- taining the substance, using the substance, or recovering from its effects (Criterion 3). In some instances of more severe substance use disorders, virtually all of the individual’s daily activities revolve around the substance. Craving (Criterion 4) is manifested by an intense de- sire or urge for the drug that may occur at an y time but is more likely when in an environ- ment where the drug previous ly was obtained or used. Cr aving has also been shown to involve classical conditioning and is associated with activation of specific reward structures in the brain. Craving is queried by asking if there has ever been a time when they had such strong urges to take the drug th at they could not think of anythi ng else. Current craving is of- ten used as a treatment outcome measure becaus e it may be a signal of impending relapse. Social impairment is the second grouping of criteria (Criteria 5–7) . Recurrent substance use may result in a failure to fulfill major role obligations at work, sc hool, or home (Crite- rion 5). The individual may continue substanc e use despite having persistent or recurrent social or interpersonal problems caused or ex acerbated by the effects of the substance (Cri- terion 6). Important social, occupational, or re creational activities ma y be given up or re- duced because of substance us e (Criterion 7). The individual may withdraw from family activities and hobbies in order to use the substance. Risky use of the substance is the third grouping of criteria (Criteria 8–9). This may take
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the form of recurrent substanc e use in situations in which it is physically hazardous (Cri- terion 8). The individual may continue substance use despite knowledge of having a per- sistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance (Criterion 9). The key issue in evaluating this criterion is not the existence of the problem, but rather the in dividual’s failure to abstain from using the substance despite the difficulty it is causing.
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484 Substance-Related and Addictive Disorders Pharmacological criteria are the final grouping (Criteria 10 and 11). Tolerance (Crite- rion 10) is signaled by requiring a markedly in creased dose of the substance to achieve the desired effect or a markedly reduced effect when the usual dose is consumed. The degree to which tolerance develops varies greatly across different individuals as well as across substances and may involve a va riety of central nervous system effects. For example, tol- erance to respiratory depression and tolerance to sedating and motor coordination may develop at different rates, depending on the substance. Tolerance ma y be difficult to de- termine by history alone, and la boratory tests may be helpful (e .g., high blood levels of the substance coupled with little evidence of into xication suggest that tolerance is likely). Tol- erance must also be distinguished from indi vidual variability in the initial sensitivity to the effects of particular substances. For exam ple, some first-time alcohol drinkers show very little evidence of intoxication with thre e or four drinks, whereas others of similar weight and drinking histories have slurred speech and incoordination. Withdrawal (Criterion 11) is a syndrome th at occurs when blood or tissue concentra- tions of a substance decline in an individual who had maintained prolonged heavy use of the substance. After developi ng withdrawal symptoms, the individual is likely to con- sume the substance to relieve the symptoms . Withdrawal symptoms vary greatly across the classes of substances, and separate criter ia sets for withdrawal are provided for the drug classes. Marked and generally easily me asured physiological signs of withdrawal are common with alcohol, opioids, and sedatives, hypnotics, and anxiolytics. Withdrawal
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signs and symptoms with stimulants (amphetamines and cocaine), as well as tobacco and cannabis, are often present but may be le ss apparent. Significant withdrawal has not been documented in humans after repeated use of phencyclidine, other hallucinogens, and in- halants; therefore, this criterion is not incl uded for these substances. Neither tolerance nor withdrawal is necessary for a diagnosis of a substance use disorder. However, for most classes of substances, a past history of withdraw al is associated with a more severe clinical course (i.e., an earlier onset of a substance us e disorder, higher levels of substance intake, and a greater number of substance-related problems). Symptoms of tolerance and withdrawal occurring during appropriate medical treat- ment with prescribed medications (e.g., opio id analgesics, sedatives, stimulants) are spe- cifically not counted when diagnosing a substance use disorder. The appearance of normal, expected pharmacological tolerance and withdrawal during the course of medical treat- ment has been known to lead to an erroneou s diagnosis of “addiction” even when these were the only symptoms pr esent. Indivi duals whose only symptoms are those that occur as a result of medical treatment (i.e., tolera nce and withdrawal as part of medical care when the medications are taken as prescribed) sh ould not receive a diagnosis solely on the basis of these symptoms. However, prescripti on medications can be used inappropriately, and a substance use disorder can be correc tly diagnosed when there are other symptoms of compulsive, drug-seeking behavior. Severity and Specifiers Substance use disorders occur in a broad range of severity, from mild to severe, with se- verity based on the number of symptom criteria endorsed. As a general estimate of sever-
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verity based on the number of symptom criteria endorsed. As a general estimate of sever- ity, a mild substance use disorder is suggested by the presence of two to three symptoms, moderate by four to five symptoms, and severe by six or more symptoms. Changing severity across time is also reflected by reductions or increases in the fr equency and/or dose of substance use, as assessed by the individual’s own report, report of knowledgeable others,
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across time is also reflected by reductions or increases in the fr equency and/or dose of substance use, as assessed by the individual’s own report, report of knowledgeable others, clinician’s observations, and biological testing. The following course specifiers and descrip- tive features specifiers are a lso available for substance use di sorders: “in early remission,” “in sustained remission,” “on maintenance th erapy,” and “in a cont rolled environment.” Definitions of each are provided within respective criteria sets.
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Substance Use Disorders 485 Recording Procedures for Substance Use Disorders The clinician should use the code that applies to the class of substances but record the name of the specific substance. For example, the clinician should record 304.10 (F13.20) moderate alprazolam use disorder (rather than moderate seda tive, hypnotic, or anxiolytic use disorder) or 305.70 (F15.10) mild methamphetamine use disorder (rather than mild stimulant use disorder). For substances that do not fit into any of the classes (e.g., anabolic steroids), the appropriate code for “other su bstance use disorder” should be used and the specific substance indicated (e.g., 305.90 [F19.10] mild anabolic steroid use disorder). If the substance taken by the individual is unknown, the code for the class “other (or unknown)” should be used (e.g., 304.90 [F 19.20] severe unknown substance use disorder). If criteria are met for more than one substance use diso rder, all should be diagnosed (e.g., 304.00 [F11.20] severe heroin use disorder; 304.20 [F14.20] moderate cocaine use disorder). The appropriate ICD-10-CM code for a subs tance use disorder depends on whether there is a comorbid substance-induced disorder (including intoxication and withdrawal). In the above example, the diagnostic code for moderate alprazolam use disorder, F13.20, re- flects the absence of a comorbid alprazolam -induced mental disorder. Because ICD-10-CM codes for substance-induced disorders indicate both the presence (or absence) and severity
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codes for substance-induced disorders indicate both the presence (or absence) and severity of the substance use disorder, ICD-10-CM co des for substance use disorders can be used only in the absence of a substance-induced di sorder. See the individu al substance-specific sections for additional coding information. Note that the word addiction is not applied as a diagnostic term in this classification, although it is in common usage in many countr ies to describe severe problems related to compulsive and habitual use of substances. The more neutral term substance use disorder is used to describe the wide range of the disorder , from a mild form to a severe state of chron- ically relapsing, compulsive drug taking. So me clinicians will choose to use the word ad- diction to describe more extreme presentations, but the word is omitted from the official DSM-5 substance use disorder diagnostic term inology because of its uncertain definition and its potentially negative connotation. Substance-Induced Disorders The overall category of subs tance-induced disorders includ es intoxication, withdrawal, and other substance/medication-induced ment al disorders (e.g., substance-induced psy- chotic disorder, substance-in duced depressive disorder). Substance Intoxication and Withdrawal Criteria for substance intoxica tion are included within the substance-specific sections of this chapter. The essential fe ature is the development of a reversible substance-specific syndrome due to the recent ingestion of a subs tance (Criterion A). The clinically significant problematic behavioral or psychological changes associated with intoxication (e.g., bellig- erence, mood lability, impaired judgment) are attributable to the phy siological effects of the substance on the central nervous system and develop during or shortly after use of the substance (Criterion B). The symptoms are not attributable to another medical condition
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substance (Criterion B). The symptoms are not attributable to another medical condition and are not better explained by another mental disorder (Criterion D). Substance intoxi- cation is common among those with a substance use disorder but also occurs frequently in individuals without a substance use disorder. This category does not apply to tobacco. The most common changes in intoxication involve disturba nces of perception, wake- fulness, attention, thinking, judgment, psychomotor behavi or, and interpersonal behav- ior. Short-term, or “acute,” intoxications may have different signs and symptoms than
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486 Substance-Related and Addictive Disorders sustained, or “chronic,” intoxications. For example, moderate cocaine doses may initially produce gregariousness, but social withdrawal may develop if such doses are frequently repeated over days or weeks. When used in the physiological sense, the term intoxication is broader than substance intoxication as defined here. Many substances may produce physiological or psychologi- cal changes that are not necessarily problematic. For example, an individual with tachy- cardia from substance use has a physiological effe ct, but if this is the only symptom in the absence of problematic behavior, the diagnosis of intoxication would not apply. Intoxica- tion may sometimes persist beyond the time when the substance is detectable in the body. This may be due to enduring central nervous system effects, the recovery of which takes longer than the time for elimination of the su bstance. These longer-term effects of intoxi- cation must be distinguished from withdraw al (i.e., symptoms initiated by a decline in blood or tissue concentrat ions of a substance). Criteria for substance withdrawal are included within the su bstance-specific sections of this chapter. The essential feat ure is the development of a subs tance-specific problematic be- havioral change, with physiologic al and cognitive concomitants, that is due to the cessation of, or reduction in, heavy and prolonged substance use (Criterion A). The substance-specific syn- drome causes clinically significant distress or impairment in social, oc cupational, or other im- portant areas of functioning (Criterion C). The symptoms are not due to another medical condition and are not better explained by anot her mental disorder (Criterion D). Withdrawal is usually, but not always, as sociated with a substance use disorder. Most individuals with
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is usually, but not always, as sociated with a substance use disorder. Most individuals with withdrawal have an urge to re-administe r the substance to reduce the symptoms. Route of Administration and Speed of Substance Effects Routes of administration that produce more rapid and efficient absorption into the blood- stream (e.g., intravenous, smoking, intranasal “snorting”) te nd to result in a more intense intoxication and an increased likelihood of an escalating pattern of substance use leading to withdrawal. Similarly, rapi dly acting substances are more likely than slower-acting substances to produce immediate intoxication. Duration of Effects Within the same drug category, relatively sh ort-acting substances tend to have a higher potential for the development of withdrawal th an do those with a longer duration of ac- tion. However, longer-acting substances tend to have longer withdrawal duration. The half-life of the substance parallels aspects of wi thdrawal: the longer the duration of action, the longer the time between cessation and th e onset of withdrawal symptoms and the lon- ger the withdrawal duration. In general, the longer the acute withdrawal period, the less intense the syndrome tends to be. Use of Multiple Substances Substance intoxication and withdrawal often involve several substances used simultane- ously or sequentially. In these cases, each diagnosis should be recorded separately. Associated Laboratory Findings Laboratory analyses of blood and urine samples can help determine recent use and the specific substances involved. However, a positive laboratory test result do es not by itself indicate that the individual has a pattern of substance use that meets criteria for a substance-induced or sub- stance use disorder, and a negative test result does not by itself rule out a diagnosis. Laboratory tests can be useful in identify ing withdrawal. If the individual presents
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Laboratory tests can be useful in identify ing withdrawal. If the individual presents with withdrawal from an unknown substance, laboratory tests may help identify the sub- stance and may also be helpful in differentiating withdrawal from other mental disorders.
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Substance-Induced Disorders 487 In addition, normal functionin g in the presence of high bl ood levels of a substance sug- gests considerable tolerance. Development and Course Individuals ages 18–24 years have relatively hi gh prevalence rates for the use of virtually every substance. Intoxication is usually the initial substance-related disorder and often be- gins in the teens. Withdrawal can occur at any age as long as the relevant drug has been taken in sufficient doses over an extended period of time. Recording Procedures for Intoxication and Withdrawal The clinician should use the code that applies to the class of substances but record the name of the specific substance. For example, the clinician sh ould record 292. 0 (F13.239) seco- barbital withdrawal (rather than sedative, hypnotic, or anxiolytic withdrawal) or 292.89 (F15.129) methamphetamine intoxication (rathe r than stimulant intoxication). Note that the appropriate ICD-10-CM diagnostic code fo r intoxication depends on whether there is a comorbid substance use diso rder. In this case, the F15.129 code for methamphetamine in- dicates the presence of a comorbid mild methamphetamine use disorder. If there had been no comorbid methamphetamine use disorder , the diagnostic code would have been F15.929. ICD-10-CM coding rules require th at all withdrawal codes imply a comorbid moderate to severe substance use disorder fo r that substance. In the above case, the code for secobarbital withdrawal (F13.239) indicates the comorbid presence of a moderate to se- vere secobarbital use disorder . See the coding note for the substance-specific intoxication
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vere secobarbital use disorder . See the coding note for the substance-specific intoxication and withdrawal syndromes for the actual coding options. For substances that do not fit into any of the cl asses (e.g., anabolic steroids), the appropriate code for “other substance intoxication” should be used and the specific substance indicated (e.g., 292.89 [F19.929] anabolic steroid intoxication). If the substance taken by the individual is unknown, the code for the class “other (or unknown)” should be used (e.g., 292.89 [F19.929] unknown substance intoxication). If there are sy mptoms or problems associated with a partic- ular substance but criteria are not met for any of the substance-specific disorders, the unspec- ified category can be used (e.g., 292.9 [F12.99] unspecified cannabis-related disorder). As noted above, the substance-related codes in ICD-10-CM combine the substance use dis- order aspect of the clinical picture and the su bstance-induced aspect into a single combined code. Thus, if both heroin withdrawal and modera te heroin use disorder are present, the single code F11.23 is given to cover both presentati ons. In ICD-9-CM, separate diagnostic codes (292.0 and 304.00) are given to indicate withdr awal and a moderate heroin use disorder, re- spectively. See the individual substance-specific sections for additional coding information. Substance/Medication-Induced Mental Disorders The substance/medication-induced mental di sorders are potentially severe, usually tem- porary, but sometimes persisti ng central nervous system (C NS) syndromes that develop in the context of the effects of substances of abuse, medications, or several toxins. They are
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in the context of the effects of substances of abuse, medications, or several toxins. They are distinguished from the substance use disorder s, in which a cluster of cognitive, behav- ioral, and physiological symptoms contribute to the continued use of a substance despite significant substance-related problems. The substance/medication-induced mental disor- ders may be induced by the 10 classes of subs tances that produce su bstance use disorders, or by a great variety of other medications used in medical treatment. Each substance- induced mental disorder is desc ribed in the relevant chapter (e.g., “Depressive Disorders,” “Neurocognitive Disorders”), an d therefore, only a brief description is offered here. All substance/medication-induced disorders share common characte ristics. It is important to
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“Neurocognitive Disorders”), an d therefore, only a brief description is offered here. All substance/medication-induced disorders share common characte ristics. It is important to recognize these common features to aid in th e detection of these disorders. These features are described as follows:
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488 Substance-Related and Addictive Disorders A. The disorder represents a clinically signif icant symptomatic presentation of a relevant mental disorder. B. There is evidence from the history, physical examination, or laboratory findings of both of the following: 1. The disorder developed during or within 1 month of a substance intoxication or withdrawal or taking a medication; and 2. The involved substance/medication is ca pable of producing th e mental disorder. C. The disorder is not better explained by an in dependent mental disorder (i.e., one that is not substance- or medication-induced). Such evidence of an independent mental dis- order could include the following: 1. The disorder preceded the onset of severe intoxication or withdrawal or exposure to the medication; or 2. The full mental disorder persisted for a substa ntial period of time (e.g., at least 1 month) after the cessation of acute withdrawal or severe intoxication or taking the medica- tion. This criterion does not apply to su bstance-induced neurocognitive disorders or hallucinogen persisting perception disorder, which persist beyond the cessation of acute intoxication or withdrawal. D. The disorder does not occur exclusiv ely during the course of a delirium. E. The disorder causes clinically significant distress or impairment in social, occupa- tional, or other important areas of functioning. Features Some generalizations can be made regarding the categories of substances capable of produc- ing clinically relevant substance-induced mental disorders. In general, the more sedating drugs (sedative, hypnotics, or anxiolytics, and alcohol) can produce prominent and clini- cally significant depressive disorders during in toxication, while anxiet y conditions are likely
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cally significant depressive disorders during in toxication, while anxiet y conditions are likely to be observed during withdrawal syndromes from these substances. Also, during intoxica- tion, the more stimulating substances (e.g., am phetamines and cocaine) are likely to be as- sociated with substance-induced psychoti c disorders and substance-induced anxiety disorders, with substance-indu ced major depressive episodes observed during withdrawal. Both the more sedating and mo re stimulating drugs are likely to produce significant but temporary sleep and sexual dist urbances. An overview of the relationship between specific categories of substanc es and specific psychiatric syndromes is presented in Table 1. The medication-induced conditions includ e what are often idiosyncratic CNS reac- tions or relatively extreme examples of side effects for a wide range of medications taken for a variety of medical concerns. These includ e neurocognitive complications of anesthet- ics, antihistamines, antihypertensives, and a variety of other medications and toxins (e.g., organophosphates, insecticides, carbon monoxi de), as described in the chapter on neuro- cognitive disorders. Psychotic syndromes may be temporarily experienced in the context of anticholinergic, cardiovascul ar, and steroid drugs, as well as during use of stimulant- like and depressant-like prescription or over-the-counter drugs. Temporary but severe mood disturbances can be observed with a wi de range of medications, including steroids, antihypertensives, disulfiram, and any prescription or over-the- counter depressant or stimulant-like substances. A similar range of medications can be associated with tempo- rary anxiety syndromes, sexual dysfunct ions, and conditions of disturbed sleep.
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rary anxiety syndromes, sexual dysfunct ions, and conditions of disturbed sleep. In general, to be considered a substance/ medication-induced mental disorder, there must be evidence that the diso rder being observed is not likely to be better explained by an independent mental condition. The latter are most likely to be seen if the mental disorder was present before the severe intoxication or withdrawal or medication administration, or, with the exception of several substance-induced persisting disorders listed in Table 1, con- tinued more than 1 month after cessation of acute withdrawal, severe intoxication, or use
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Substance-Induced Disorders 489 of the medications. When symptoms are only observed during a delirium (e.g., alcohol withdrawal delirium), the mental disorder sh ould be diagnosed as a delirium, and the psychiatric syndrome occurring during the delirium should not also be diagnosed sepa- rately, as many symptoms (including disturba nces in mood, anxiety, and reality testing) are commonly seen during agitated, confused states. The features associated with each rel- evant major mental disorder are similar whether observed with independent or sub- stance/medication-induced mental disorders. However, individuals with substance/ medication-induced mental disorders are lik ely to also demonstrate the associated fea- tures seen with the specific category of subs tance or medication, as listed in other subsec- tions of this chapter. Development and Course Substance-induced mental disord ers develop in the context of intoxication or withdrawal from substances of abuse, and medication-i nduced mental disorders are seen with pre- scribed or over-the-counter medications that are taken at the suggest ed doses. Both condi- tions are usually temporary and li kely to disappear with in 1 month or so of cessation of acute withdrawal, severe intoxication, or use of th e medication. Exceptions to these generaliza- tions occur for certain long-d uration substance-in duced disorders: substance-associated neurocognitive disorders that relate to conditions such as alcohol- induced neurocognitive disorder, inhalant-induced neurocognitive disord er, and sedative-, hypnotic-, or anxiolytic- induced neurocognitive disorder; and hallucinogen persisting perception disorder (“flash- backs”; see the section “Hallucinogen-Related Disorders” later in this chapter). However,
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most other substance/medication -induced mental disorders, re gardless of the severity of the symptoms, are likely to impr ove relatively quickly with ab stinence and unlikely to re- main clinically relevant for more than 1 month after complete cessation of use. As is true of many consequences of heavy substance use, some individuals are more and others less prone toward specific substance-induced disorders. Similar types of pre- dispositions may make some individuals more likely to develop psychiatric side effects of some types of medications, but not others. However, it is unclear whether individuals with family histories or personal prior hist ories with independent psychiatric syndromes are more likely to develop the induced synd rome once the consideration is made as to whether the quantity and frequency of the substance was sufficient to lead to the devel- opment of a substanc e-induced syndrome. There are indications that the intake of su bstances of abuse or some medications with psychiatric side effects in the context of a pree xisting mental disorder is likely to result in an intensification of the preexisting indepe ndent syndrome. The risk for substance/med- ication-induced mental disorders is likely to increase with both the quantity and the fre- quency of consumption of the relevant substance. The symptom profiles for the substance/medication-induced mental disorders resem- ble independent mental disorders. While the symptoms of substance/medication-in- duced mental disorders can be identical to those of independent mental disorders (e.g., delusions, hallucinations, psychoses, major de pressive episodes, anxiety syndromes), and although they can have the same severe conseq uences (e.g., suicide) , most induced mental disorders are likely to improve in a matt er of days to weeks of abstinence.
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disorders are likely to improve in a matt er of days to weeks of abstinence. The substance/medication-induced mental di sorders are an important part of the dif- ferential diagnoses for the independent psychiatric conditions. The importance of recog- nizing an induced mental disorder is similar to the relevance of identifying the possible role of some medical conditions and medication reaction s before diagnosing an indepen-
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nizing an induced mental disorder is similar to the relevance of identifying the possible role of some medical conditions and medication reaction s before diagnosing an indepen- dent mental disorder. Symptoms of substanc e- and medication-induced mental disorders may be identical cross-sectionally to those of independent mental disorders but have dif- ferent treatments and prognoses from the independent condition.
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490 Substance-Related and Addictive Disorders Functional Consequences of Substance/Medication- Induced Mental Disorders The same consequences related to the relevant independent mental disorder (e.g., suicide attempts) are likely to apply to the substance/medi cation-induced mental disorders, but these are likely to disappear within 1 month after abstinence. Similarly, the same func- tional consequences associated with the relevant substance use disorder are likely to be seen for the substance-indu ced mental disorders. Recording Procedures fo r Substance/Medication- Induced Mental Disorders Coding notes and separate recording procedures for ICD-9-CM and ICD-10-CM codes for other specific substance/medi cation-induced mental diso rders are provided in other chapters of the manual with disorders with which they share phenomenology (see the sub- stance/medication-indu ced mental disorders in these chapters: “Schizophrenia Spectrum and Other Psychotic Disorders,” “Bipolar and Related Disorders,” “Depressive Disor- ders,” “Anxiety Disorders,” “Obsessive-Compulsive and Related Disorders,” “Sleep- Wake Disorders,” “Sexual Dysfunctions,” and “Neurocognitive Disorders”). Generally, for ICD-9-CM, if a mental disorder is induced by a substance use disorder, a separate di- agnostic code is given for the specific substance use disorder, in addition to the code for the substance/medication-induced mental disord er. For ICD-10-CM, a single code combines the substance-induced mental disorder with the substance use disorder. A separate diag- nosis of the comorbid substance use disorder is not given, although the name and severity of the specific substance use disorder (whe n present) are used when recording the sub-
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of the specific substance use disorder (whe n present) are used when recording the sub- stance/medication-induced mental disorder. ICD-10-CM codes are also provided for sit- uations in which the substance/ medication-induced mental di sorder is not induced by a substance use disorder (e.g., when a disorder is induced by one-time use of a substance or medication). Additional information needed to record the diagnostic name of the sub- stance/medication-induce d mental disorder is provided in the sect ion “Recording Proce- dures” for each substance/medication-induced mental disorder in its respective chapter. Alcohol-Related Disorders Alcohol Use Disorder Alcohol Intoxication Alcohol Withdrawal Other Alcohol-Induced Disorders Unspecified Alcohol-Related Disorder Alcohol Use Disorder Diagnostic Criteria A. A problematic pattern of alcohol 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. Alcohol 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 alcohol use.
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Alcohol Use Disorder 491 3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects. 4. Craving, or a strong desire or urge to use alcohol. 5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home. 6. Continued alcohol use despite having persist ent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol. 7. Important social, occupational, or recreat ional activities are given up or reduced be- cause of alcohol use. 8. Recurrent alcohol use in situations in which it is physically hazardous. 9. Alcohol 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 alcohol. 10. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of alcohol to achieve intoxication or de- sired effect. b. A markedly diminished effect with continued use of the same amount of alcohol. 11. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome fo r alcohol (refer to Criteria A and B of the criteria set for alcohol withdrawal, pp. 499–500). b. Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms. Specify if: In early remission: After full criteria for alcohol us e disorder were previously met, none of the criteria for alcohol 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 alcohol,” may be met).
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or urge to use alcohol,” may be met). In sustained remission: After full criteria for alcohol use disorder were previously met, none of the criteria for alcohol 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 alcohol,” 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 alcohol is restricted. Code based on current severity: Note for ICD-10-CM codes: If an alcohol intoxication, alcohol withdrawal, or another alcohol-induced m ental disorder is also present, do not use the codes below for alcohol use disorder. Instead, the comorbid alcohol use disorder is indicated in the 4th character of the alco hol-induced disorder code (see the coding note for alcohol intoxication, alcohol withdrawal, or a specific alcohol-induced mental disorder). For example, if there is comorbid alcohol intoxication and alcohol use disorder, only the alcohol intoxication code is given, with the 4th character indicating whether the comorbid alcohol use disorder is mild, moderate, or severe: F10.129 for mild alcohol use disorder with alcohol intoxication or F10.229 for a moderat e or severe alcohol use disorder with al- cohol intoxication. Specify current severity: 305.00 (F10.10) Mild: Presence of 2–3 symptoms. 303.90 (F10.20) Moderate: Presence of 4–5 symptoms. 303.90 (F10.20) Severe: Presence of 6 or more symptoms.
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492 Substance-Related and Addictive Disorders 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. Severity of the disorder is based on the number of diagno stic criteria endorsed. For a given individual, changes in severity of alcoho l use disorder across ti me are also reflected by reductions in the frequency (e.g., days of use per month) and/or dose (e.g., number of standard drinks consumed per day) of alcohol used, as assessed by the individual’s self- report, report of knowledgeabl e others, clinician observations, and, when practical, bio- logical testing (e.g., elevations in blood test s as described in the section “Diagnostic Mark- ers” for this disorder). Diagnostic Features Alcohol use disorder is defined by a cluste r of behavioral and physical symptoms, which can include withdrawal, tolerance, and cravin g. Alcohol withdrawal is characterized by withdrawal symptoms that de velop approximately 4–12 hours after the reduction of in- take following prolonged, heavy alcohol inge stion. Because withdrawal from alcohol can be unpleasant and intense, individuals may continue to consume alcohol despite adverse consequences, often to avoid or to relieve withdrawal symptoms. Some withdrawal symp- toms (e.g., sleep problems) can persist at lower intensities for months and can contribute to relapse. Once a pattern of re petitive and intense use develo ps, individuals with alcohol use disorder may devote substantial periods of time to obtaining and consuming alcoholic
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use disorder may devote substantial periods of time to obtaining and consuming alcoholic beverages. Craving for alcohol is indicated by a strong desire to drink that makes it difficult to think of anything else and that often results in the onset of drinking. School and job per- formance may also suffer either from the aftereffects of drinking or from actual intoxica- tion at school or on the job; child care or household responsibilities may be neglected; and alcohol-related absences may o ccur from school or work. The individual may use alcohol in physically hazardous circumstances (e.g., driving an automobile, swimming, operating machinery while intoxicated). Finally, individu als with an alcohol use disorder may con- tinue to consume alco hol despite the knowledge that continued consumption poses sig- nificant physical (e.g., blackouts, liver disease ), psychological (e.g., depression), social, or interpersonal problems (e.g., violent argume nts with spouse while intoxicated, child abuse). Associated Features Supporting Diagnosis Alcohol use disorder is often associated wi th problems similar to those associated with other substances (e.g., cannabis ; cocaine; heroin; amphetamin es; sedatives, hypnotics, or anxiolytics). Alcohol may be used to alleviate the unwanted effects of these other substances or to substitute for them when they are not av ailable. Symptoms of conduct problems, depression, anxiety, and insomnia frequently accompany heavy drinking and sometimes precede it. Repeated intake of high doses of alcohol can affect nearly every organ system, espe- cially the gastrointestinal tract, cardiovasc ular system, and the central and peripheral ner- vous systems. Gastrointestinal effects includ e gastritis, stomach or duodenal ulcers, and,
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in about 15% of individuals who use alcohol he avily, liver cirrhosis and/or pancreatitis. There is also an increased rate of cancer of the esophagus, stomach, and other parts of the gastrointestinal tract. One of the most comm only associated conditions is low-grade hy- pertension. Cardiomyopathy and other myopat hies are less common but occur at an in-
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Alcohol Use Disorder 493 creased rate among those who drink very he avily. These factors, along with marked increases in levels of triglycerides and low- density lipoprotein cholesterol, contribute to an elevated risk of heart disease. Periphe ral neuropathy may be evidenced by muscular weakness, paresthesias, and decreased peripher al sensation. More persistent central ner- vous system effects include cognitive deficits, severe memory impairment, and degener- ative changes in the cerebellum. These effects are related to the direct effects of alcohol or of trauma and to vitamin deficiencies (parti cularly of the B vitamins, including thiamine). One devastating central nervous system e ffect is the relatively rare alcohol-induced per- sisting amnestic disorder, or Wernicke-Korsakoff syndrome, in which the ability to encode new memory is severely impaired. This condition would now be described within the chap- ter “Neurocognitive Disorder s” and would be termed a substance/medicati on-induced neuro- cognitive disorder. Alcohol use disorder is an important contribu tor to suicide risk du ring severe intoxi- cation and in the context of a temporary alco hol-induced depressive and bipolar disorder. There is an increased rate of suicidal behavior as well as of completed suicide among in- dividuals with the disorder. Prevalence Alcohol use disorder is a common disorder. In the United States, the 12-month prevalence of alcohol use disorder is estimated to be 4.6% among 12- to 17-year-olds and 8.5% among adults age 18 years and older in the United St ates. Rates of the disorder are greater among adult men (12.4%) than among adult women (4 .9%). Twelve-month prevalence of alcohol
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use disorder among adults decreases in midd le age, being greatest among individuals 18- to 29-years-old (16.2%) and lowest among individuals age 65 years and older (1.5%). Twelve-month prevalence varies markedly across race/ethnic subgroups of the U.S. population. For 12- to 17-year-olds, rates ar e greatest among Hispanics (6.0%) and Native Americans and Alaska Natives (5.7%) relative to whites (5.0%), Afri can Americans (1.8%), and Asian Americans and Pacific Islanders (1.6 %). In contrast, amon g adults, the 12-month prevalence of alcohol use di sorder is clearly greater among Native Americans and Alaska Natives (12.1%) than among whites (8.9%), Hispanics (7.9%), African Americans (6.9%), and Asian Americans and Pacific Islanders (4.5%). Development and Course The first episode of alcohol into xication is likely to occur during the mid-teens. Alcohol- related problems that do not m eet full criteria for a use disord er or isolated problems may occur prior to age 20 years, but the age at onse t of an alcohol use disorder with two or more of the criteria clustered together peaks in th e late teens or early to mid 20s. The large ma- jority of individuals who develop alcohol-relate d disorders do so by their late 30s. The first evidence of withdrawal is not likely to appear until after many other aspects of an alcohol use disorder have developed. An earlier onset of alcohol use disorder is observed in ado- lescents with preexisting conduct problems and those with an earlier onset of intoxication. Alcohol use disorder has a variable course th at is characterized by periods of remission
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Alcohol use disorder has a variable course th at is characterized by periods of remission and relapse. A decision to stop drinking, often in response to a crisis, is likely to be followed by a period of weeks or more of abstinence , which is often followed by limited periods of controlled or nonproblematic drinking. However, once alcohol intake resumes, it is highly likely that consumption will rapidly escalate and that severe problems will once again develop. Alcohol use disorder is often erroneously pe rceived as an intractable condition, per- haps based on the fact that individuals who present for treatment typically have a history of many years of severe alco hol-related problems. However, these most severe cases rep-
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haps based on the fact that individuals who present for treatment typically have a history of many years of severe alco hol-related problems. However, these most severe cases rep- resent only a small proportion of individuals with this disorder, and the typical individual with the disorder has a much more promising prognosis.
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494 Substance-Related and Addictive Disorders Among adolescents, conduct disorder and repeated antisocial behavior often co-occur with alcohol- and with other substance-relate d disorders. While most individuals with al- cohol use disorder develop the condition be fore age 40 years, perhaps 10% have later onset. Age-related physical changes in older individuals result in increased brain suscep- tibility to the depressant effect s of alcohol; decreased rates of liver metabolism of a variety of substances, including alcohol; and decrease d percentages of body water. These changes can cause older people to develop more seve re intoxication and su bsequent problems at lower levels of consumption. Al cohol-related problems in older people are also especially likely to be associated with other medical complications. Risk and Prognostic Factors Environmental. Environmental risk and prognostic factors may include cultural atti- tudes toward drinking and intoxication, the availability of alcohol (including price), acquired personal experiences with alcohol, and stress levels. Additional potential medi- ators of how alcohol problems develop in predisposed individuals include heavier peer substance use, exaggerated positive expectations of the effects of alcohol, and suboptimal ways of coping with stress. Genetic and physiological. Alcohol use disorder runs in families, with 40%–60% of the variance of risk explained by genetic influenc es. The rate of this condition is three to four times higher in close relatives of individuals with alcohol use disorder, with values highest for individuals with a greater nu mber of affected relatives, closer genetic relationships to the affected person, and higher severity of the alcohol-related problems in those relatives. A significantly higher rate of alcohol use disorders exists in the monozygotic twin than in the dizygotic twin of an individual with the condition. A three- to fourfold increase in risk
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has been observed in children of individuals with alcohol use disorder, even when these children were given up for adoption at birth and raised by adoptive parents who did not have the disorder. Recent advances in our understanding of genes that operate through intermediate characteristics (or phe notypes) to affect the risk of alco hol use disorder can help to identify individuals who might be at pa rticularly low or high risk for alcohol use disorder. Among the low-risk phenotypes are the acute alcohol-related skin flush (seen most prominently in Asians). High vulnerability is associated with preexisting schizophrenia or bipolar disor- der, as well as impulsivity (producing enha nced rates of all substance use disorders and gambling disorder), and a high risk specifically for alcohol use disorder is associated with a low level of response (low sensitivity) to alcohol. A number of gene variations may ac- count for low response to alcohol or modulate the dopamine reward systems; it is impor- tant to note, however, that any one gene variat ion is likely to explain only 1%–2% of the risk for these disorders. Course modifiers. In general, high levels of impulsivity are associated with an earlier onset and more severe alcohol use disorder. Culture-Related Diagnostic Issues In most cultures, alcohol is the most frequently used intoxicating substance and contrib- utes to considerable morbidity and mortality. An estimate d 3.8% of all global deaths and 4.6% of global disability-adjusted life-years are attribut able to alcohol. In the United States, 80% of adults (age 18 years and older) have co nsumed alcohol at some time in their lives, and 65% are current drinkers (last 12 months). An estimated 3.6% of the world population
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(15–64 years old) has a current (12-month) alcohol use disorder, with a lower prevalence (1.1%) found in the Afri can region, a higher rate (5.2%) found in the Am erican region (North, South, and Central America and the Caribbean) , and the highest rate (10.9%) found in the
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(1.1%) found in the Afri can region, a higher rate (5.2%) found in the Am erican region (North, South, and Central America and the Caribbean) , and the highest rate (10.9%) found in the Eastern Europe region.
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Alcohol Use Disorder 495 Polymorphisms of genes for the alcohol- metabolizing enzymes alcohol dehydroge- nase and aldehyde dehydrogenase are most ofte n seen in Asians and affect the response to alcohol. When consuming alcoho l, individuals with these gene variations can experience a flushed face and palpitations, reactions that ca n be so severe as to lim it or preclude future alcohol consumption and diminish the risk fo r alcohol use disorder. These gene variations are seen in as many as 40% of Japanese, Chinese, Korean, and related groups worldwide and are related to lower risks for the disorder. Despite small variations regarding individual criterion items, the diagnostic criteria perform equally well across mo st race/ethnicity groups. Gender-Related Diagnostic Issues Males have higher rates of drinking and rela ted disorders than fema les. However, because females generally weigh less than males, have more fat and less water in their bodies, and metabolize less alcohol in their esophagus and stomach, they are likely to develop higher blood alcohol levels per drink than males. Females who drink heavily may also be more vulnerable than males to some of the physical consequences associated with alcohol, in- cluding liver disease. Diagnostic Markers Individuals whose heavier drinking places them at elevated risk for alcohol use disorder can be identified both through standardized qu estionnaires and by elevations in blood test results likely to be seen with regular heavie r drinking. These measures do not establish a diagnosis of an alcohol-related disorder but can be useful in highlighting individuals for whom more information should be gathered. Th e most direct test available to measure al- cohol consumption cross-sectionally is blood alcohol concentration, which can also be used to
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cohol consumption cross-sectionally is blood alcohol concentration, which can also be used to judge tolerance to alcohol. For example, an individual with a conc entration of 150 mg of ethanol per deciliter (dL) of blood who does not show signs of intoxication can be pre- sumed to have acquired at le ast some degree of tolerance to alcohol. At 200 mg/dL, most nontolerant individuals demons trate severe intoxication. Regarding laboratory tests, one sensitive la boratory indicator of heavy drinking is a modest elevation or high-normal levels (>35 units) of gamma-glutamyltransferase (GGT). This may be the only laboratory finding. At least 70% of indi viduals with a high GGT level are persistent heavy drinkers (i.e., consuming ei ght or more drinks daily on a regular basis). A second test with comparable or even higher levels of sensitivity and specificity is carbo- hydrate-deficient transferrin (CDT), with levels of 20 units or higher us eful in identifying in- dividuals who regularly consum e eight or more drinks daily. Since both GGT and CDT levels return toward normal within days to weeks of stopping drinking, both state markers may be useful in monitoring abstinence, espe cially when the clinician observes increases, rather than decreases, in thes e values over time—a finding indicating that the person is likely to have returned to heavy drinking. The combination of tests for CDT and GGT may have even higher levels of sens itivity and specificity than eith er test used alone. Additional useful tests include the mean corpuscular volume (MCV), whic h may be elevated to high- normal values in individuals who drink heavily— a change that is due to the direct toxic ef-
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normal values in individuals who drink heavily— a change that is due to the direct toxic ef- fects of alcohol on erythropoiesis. Although the MCV can be used to help identify those who drink heavily, it is a poor method of monitori ng abstinence because of the long half-life of red blood cells. Liver function tests (e.g., alanine aminotransfe rase [ALT] and alkaline phos- phatase) can reveal liver injury that is a co nsequence of heavy drinking. Other potential markers of heavy drinking that are more nons pecific for alcohol but can help the clinician think of the possible effects of alcohol include elevations in blood levels or lipids (e.g., tri-
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markers of heavy drinking that are more nons pecific for alcohol but can help the clinician think of the possible effects of alcohol include elevations in blood levels or lipids (e.g., tri- glycerides and high-density li poprotein cholesterol) and high -normal levels of uric acid. Additional diagnostic markers relate to sign s and symptoms that reflect the consequences often associated with persistent heavy drinki ng. For example, dyspepsia, nausea, and bloat-
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496 Substance-Related and Addictive Disorders ing can accompany gastritis, and hepatomegaly, esophageal varices, and hemorrhoids may reflect alcohol-induced changes in the liver. Other physical signs of heavy drinking include tremor, unsteady gait, insomnia, and erectile dy sfunction. Males with chronic alcohol use dis- order may exhibit decreased testicular size and feminizing effects associated with reduced testosterone levels. Repeated he avy drinking in females is associated with menstrual irregu- larities and, during pregnancy, spontaneous abortion and fetal alcohol syndrome. Individu- als with preexisting histories of epilepsy or se vere head trauma are more likely to develop alcohol-related seizures. Alcohol withdrawal ma y be associated with nausea, vomiting, gas- tritis, hematemesis, dry mouth, puffy blot chy complexion, and mild peripheral edema. Functional Consequences of Alcohol Use Disorder The diagnostic features of alcohol use disord er highlight major area s of life functioning likely to be impaired. These include driving and operating machinery, school and work, interpersonal relationships and communication, and health. Alcoho l-related disorders contribute to absenteeism from work, job-re lated accidents, and low employee productiv- ity. Rates are elevated in homeless individual s, perhaps reflecting a downward spiral in social and occupational functioning, although most individuals with alcohol use disorder continue to live with their families and function within their jobs. Alcohol use disorder is associated with a significant increase in the risk of accidents, vi- olence, and suicide. It is estimated that one in five intensive care un it admissions in some urban hospitals is related to al cohol and that 40% of individu als in the United States ex- perience an alcohol-related adverse event at so me time in their lives, with alcohol account-
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perience an alcohol-related adverse event at so me time in their lives, with alcohol account- ing for up to 55% of fatal driving events. Severe alcohol use disorder, especially in individuals with antisocial personality disorder, is associated with the commission of criminal acts, including homicide. Severe problematic alcohol use also contributes to dis- inhibition and feelings of sadness and irritab ility, which contribute to suicide attempts and completed suicides. Unanticipated alcohol withdrawal in hospitalized individuals for whom a diagnosis of alcohol use disorder has been overlooked can a dd to the risks and costs of hospitalization and to time spent in the hospital. Differential Diagnosis Nonpathological use of alcohol. The key element of alcohol use disorder is the use of heavy doses of alcohol with resulting repeated and significant distress or impaired func- tioning. While most drinkers sometimes consume enough alcohol to feel intoxicated, only a minority (less than 20%) ever develop al cohol use disorder. Therefore, drinking, even daily, in low doses and occasional intoxication do not by themselves make this diagnosis. Sedative, hypnotic, or anxiolytic use disorder. The signs and symptoms of alcohol use disorder are similar to those seen in sedative, hypnotic, or anxiolytic use disorder. The two must be distinguished, however, because the c ourse may be different, especially in rela- tion to medical problems. Conduct disorder in childhood and adult antisocial personality disorder. Alcohol use disorder, along with other substa nce use disorders, is seen in the majority of individuals with antisocial personality and preexisting conduct disorder. Because these diagnoses are associated with an early onset of alcohol use disorder as well as a worse prognosis, it is im- portant to establish both conditions. Comorbidity
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portant to establish both conditions. Comorbidity Bipolar disorders, schizophrenia, and antisocial personality disorder are associated with a markedly increased rate of alcohol use disorder , and several anxiety and depressive disorders
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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
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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
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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
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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
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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.
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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-
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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.
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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-
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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-
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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).
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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-
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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.
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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-
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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
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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
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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-
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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-
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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.
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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
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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.
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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-
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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.
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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-
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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).
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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-
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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,
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conditions in which caffeine use may be restricted, such as during medical procedures, pregnancy, hospitalizations, religious observances, wartime, travel, and research partici-
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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
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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.
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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
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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).
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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
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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
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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.
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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)
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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,
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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
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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
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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
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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-
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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-
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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.
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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-
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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
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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
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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
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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-
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