Substance-Related and Addictive Disorders

Substance-Related and Addictive Disorders

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The substance-related disorders encompass 10 separate classes of drugs: alcohol; caffeine; cannabis; hallucinogens (with separate categories for phencyclidine [or similarly acting arylcyclohexylamines] and other hallucinogens); inhalants; opioids; sedatives, hypnotics, and anxiolytics; stimulants (amphetamine-type substances, cocaine, and other stimulants); tobacco; and other (or unknown) substances. 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 production of memories. They produce such an intense activation of the reward system that normal activities may be neglected. Instead of achieving reward system activation through adaptive behaviors, drugs of abuse directly activate the reward pathways(Koob 2006). 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 referred to as a “high.” Furthermore, individuals with lower levels of self-control, which may reflect impairments of brain inhibitory mechanisms, may be particularly predisposed to develop substance use disorders, suggesting that the roots of substance use disorders for some persons can be seen in behaviors long before the onset of actual substance use itself(Moffitt et al. 2011).

In addition to the substance-related disorders, this chapter also includes gambling disorder, reflecting evidence that gambling behaviors activate reward systems similar to those activated by drugs of abuse and produce some behavioral symptoms that appear comparable to those produced by the substance 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 because at this time there is insufficient peer-reviewed evidence to establish the diagnostic criteria and course descriptions needed to identify these behaviors as mental disorders.

The substance-related disorders are divided into two groups: substance use disorders and substance-induced disorders. The following conditions may be classified as substance-induced: intoxication, withdrawal, and other substance/medication-induced mental disorders (psychotic disorders, bipolar and related disorders, depressive disorders, anxiety disorders, obsessive-compulsive and related disorders, sleep disorders, sexual dysfunctions, delirium, and neurocognitive disorders).

The current section begins with a general discussion 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 applicable across classes of substances. 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 disorders are included with disorders with which they share phenomenology (e.g., substance/medication-induced depressive disorder is in the chapter “Depressive Disorders”). The broad diagnostic categories associated with each specific group of substances are shown in Table.

Diagnoses associated with substance class

Enlarge table

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 despite significant substance-related problems. As seen in Table, the diagnosis of a substance use disorder can be applied to all 10 classes included in this chapter except caffeine. For certain classes some symptoms are less salient, and in a few instances not all symptoms apply (e.g., withdrawal symptoms are not specified for phencyclidine use disorder, other hallucinogen use disorder, or inhalant use disorder).

An important characteristic of substance use disorders is an underlying change in brain circuits that may persist beyond detoxification, particularly in individuals with severe disorders. The behavioral effects of these brain changes may be exhibited in the repeated relapses and intense drug craving when the individuals are exposed to drug-related stimuli. These persistent drug effects may benefit from long-term approaches to treatment(McLellan et al. 2000).

Overall, the diagnosis of a substance use disorder is based on a pathological pattern of behaviors related to use of the substance. To assist 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 period than was originally intended (Criterion 1). The individual may express a persistent desire to cut down or regulate substance use and may report multiple unsuccessful efforts to decrease or discontinue use (Criterion 2). The individual may spend a great deal of time obtaining 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 desire or urge for the drug that may occur at any time but is more likely when in an environment where the drug previously was obtained or used. Craving 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 that they could not think of anything else. Current craving is often used as a treatment outcome measure because it may be a signal of impending relapse(Miller et al. 1996).

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, school, or home (Criterion 5). The individual may continue substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance (Criterion 6). Important social, occupational, or recreational activities may be given up or reduced because of substance use (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 the form of recurrent substance use in situations in which it is physically hazardous (Criterion 8). The individual may continue substance use despite knowledge of having a persistent 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 individual’s failure to abstain from using the substance despite the difficulty it is causing.

Pharmacological criteria are the final grouping (Criteria 10 and 11). Tolerance (Criterion 10) is signaled by requiring a markedly increased 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 variety of central nervous system effects. For example, tolerance to respiratory depression and tolerance to sedating and motor coordination may develop at different rates, depending on the substance. Tolerance may be difficult to determine by history alone, and laboratory tests may be helpful (e.g., high blood levels of the substance coupled with little evidence of intoxication suggest that tolerance is likely). Tolerance must also be distinguished from individual variability in the initial sensitivity to the effects of particular substances. For example, some first-time alcohol drinkers show very little evidence of intoxication with three or four drinks, whereas others of similar weight and drinking histories have slurred speech and incoordination(Schuckit et al. 2011).

Withdrawal (Criterion 11) is a syndrome that occurs when blood or tissue concentrations of a substance decline in an individual who had maintained prolonged heavy use of the substance. After developing withdrawal symptoms, the individual is likely to consume the substance to relieve the symptoms. Withdrawal symptoms vary greatly across the classes of substances, and separate criteria sets for withdrawal are provided for the drug classes. Marked and generally easily measured physiological signs of withdrawal are common with alcohol, opioids, and sedatives, hypnotics, and anxiolytics. Withdrawal signs and symptoms with stimulants (amphetamines and cocaine), as well as tobacco and cannabis, are often present but may be less apparent. Significant withdrawal has not been documented in humans after repeated use of phencyclidine, other hallucinogens, and inhalants; therefore, this criterion is not included 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 withdrawal is associated with a more severe clinical course (i.e., an earlier onset of a substance use disorder, higher levels of substance intake, and a greater number of substance-related problems)(Chen et al. 2009).

Symptoms of tolerance and withdrawal occurring during appropriate medical treatment with prescribed medications (e.g., opioid analgesics, sedatives, stimulants) are specifically not counted when diagnosing a substance use disorder. The appearance of normal, expected pharmacological tolerance and withdrawal during the course of medical treatment has been known to lead to an erroneous diagnosis of “addiction” even when these were the only symptoms present. Individuals whoseonly symptoms are those that occur as a result of medical treatment (i.e., tolerance and withdrawal as part of medical care when the medications are taken as prescribed) should not receive a diagnosis solely on the basis of these symptoms. However, prescription medications can be used inappropriately, and a substance use disorder can be correctly 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 severity based on the number of symptom criteria endorsed. As a general estimate of severity, 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 frequency 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 descriptive features specifiers are also available for substance use disorders: “in early remission,” “in sustained remission,” “on maintenance therapy,” and “in a controlled environment.” Definitions of each are provided within respective criteria sets.

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 sedative, 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 substance 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 [F19.20] severe unknown substance use disorder). If criteria are met for more than one substance use disorder, 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 substance 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, reflects 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 of the substance use disorder, ICD-10-CM codes for substance use disorders can be used only in the absence of a substance-induced disorder. See the individual 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 countries 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 chronically relapsing, compulsive drug taking. Some clinicians will choose to use the word addiction to describe more extreme presentations, but the word is omitted from the official DSM-5 substance use disorder diagnostic terminology because of its uncertain definition and its potentially negative connotation.

References: Recording Procedures for Substance Use Disorders

· Chen CY , Storr CL , Anthony JC : Early-onset drug use and risk for drug dependence problems. Addict Behav 34(3):319–322, 2009 10.1016/j.addbeh.2008.10.021

· Koob GF : The neurobiology of addiction: a neuroadaptational view relevant for diagnosis. Addiction 101(suppl 1):23–30,2006

· McLellan AT , Lewis DC , O’Brien CP , Kleber HD : Drug dependence, a chronic medical illness: implications for treatment, insurance, and outcomes evaluation. JAMA 284(13):1689–1695, 2000

· Miller WR , Westerberg VS , Harris RJ , Tonigan JS : What predicts relapse? Prospective testing of antecedent models.Addiction 91(suppl):155–172, 1996

· Moffitt TE , Arseneault L , Belsky D , et al: A gradient of childhood self-control predicts health, wealth, and public safety. Proc Natl Acad Sci U S A 108(7):2693–2698, 2011 10.1073/pnas.1010076108

· Schuckit MA , Smith TL , Heron J , et al: Testing a level of response to alcohol-based model of heavy drinking and alcohol problems in 1,905 17-year-olds. Alcohol Clin Exp Res 35(10):1897–1904, 2011 10.1111/j.1530-0277.2011.01536.x

Substance-Induced Disorders

The overall category of substance-induced disorders includes intoxication, withdrawal, and other substance/medication-induced mental disorders (e.g., substance-induced psychotic disorder, substance-induced depressive disorder).

Substance Intoxication and Withdrawal

Criteria for substance intoxication are included within the substance-specific sections of this chapter. The essential feature is the development of a reversible substance-specific syndrome due to the recent ingestion of a substance (Criterion A). The clinically significant problematic behavioral or psychological changes associated with intoxication (e.g., belligerence, mood lability, impaired judgment) are attributable to the physiological 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 and are not better explained by another mental disorder (Criterion D). Substance intoxication 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 disturbances of perception, wakefulness, attention, thinking, judgment, psychomotor behavior, and interpersonal behavior. Short-term, or “acute,” intoxications may have different signs and symptoms than 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(O'Brien 2011).

When used in the physiological sense, the term intoxication is broader than substance intoxication as defined here. Many substances may produce physiological or psychological changes that are not necessarily problematic. For example, an individual with tachycardia from substance use has a physiological effect, but if this is the only symptom in the absence of problematic behavior, the diagnosis of intoxication would not apply. Intoxication 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 substance. These longer-term effects of intoxication must be distinguished from withdrawal (i.e., symptoms initiated by a decline in blood or tissue concentrations of a substance).

Criteria for substance withdrawal are included within the substance-specific sections of this chapter. The essential feature is the development of a substance-specific problematic behavioral change, with physiological and cognitive concomitants, that is due to the cessation of, or reduction in, heavy and prolonged substance use (Criterion A). The substance-specific syndrome causes clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). The symptoms are not due to another medical condition and are not better explained by another mental disorder (Criterion D). Withdrawal is usually, but not always, associated with a substance use disorder. Most individuals with withdrawal have an urge to re-administer 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 bloodstream (e.g., intravenous, smoking, intranasal “snorting”) tend to result in a more intense intoxication and an increased likelihood of an escalating pattern of substance use leading to withdrawal. Similarly, rapidly acting substances are more likely than slower-acting substances to produce immediate intoxication(O'Brien 2011).

Duration of Effects

Within the same drug category, relatively short-acting substances tend to have a higher potential for the development of withdrawal than do those with a longer duration of action. However, longer-acting substances tend to have longer withdrawal duration. The half-life of the substance parallels aspects of withdrawal: the longer the duration of action, the longer the time between cessation and the onset of withdrawal symptoms and the longer the withdrawal duration. In general, the longer the acute withdrawal period, the less intense the syndrome tends to be(O'Brien 2011).

Use of Multiple Substances

Substance intoxication and withdrawal often involve several substances used simultaneously 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 does not by itself indicate that the individual has a pattern of substance use that meets criteria for a substance-induced or substance use disorder, and a negative test result does not by itself rule out a diagnosis.

Laboratory tests can be useful in identifying withdrawal. If the individual presents with withdrawal from an unknown substance, laboratory tests may help identify the substance and may also be helpful in differentiating withdrawal from other mental disorders. In addition, normal functioning in the presence of high blood levels of a substance suggests considerable tolerance.

Development and Course

Individuals ages 18–24 years have relatively high prevalence rates for the use of virtually every substance. Intoxication is usually the initial substance-related disorder and often begins 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 should record 292.0 (F13.239) secobarbital withdrawal (rather than sedative, hypnotic, or anxiolytic withdrawal) or 292.89 (F15.129) methamphetamine intoxication (rather than stimulant intoxication). Note that the appropriate ICD-10-CM diagnostic code for intoxication depends on whether there is a comorbid substance use disorder. In this case, the F15.129 code for methamphetamine indicates 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 that all withdrawal codes imply a comorbid moderate to severe substance use disorder for that substance. In the above case, the code for secobarbital withdrawal (F13.239) indicates the comorbid presence of a moderate to severe 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 classes (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 symptoms or problems associated with a particular substance but criteria are not met for any of the substance-specific disorders, the unspecified 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 disorder aspect of the clinical picture and the substance-induced aspect into a single combined code. Thus, if both heroin withdrawal and moderate heroin use disorder are present, the single code F11.23 is given to cover both presentations. In ICD-9-CM, separate diagnostic codes (292.0 and 304.00) are given to indicate withdrawal and a moderate heroin use disorder, respectively. See the individual substance-specific sections for additional coding information.

References: Recording Procedures for Intoxication and Withdrawal

· O’Brien CP : Drug addiction, in Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12th Edition. Edited by Brunton L . New York, McGraw-Hill, 2011, pp 649–668

Substance/Medication-Induced Mental Disorders

The substance/medication-induced mental disorders are potentially severe, usually temporary, but sometimes persisting central nervous system (CNS) syndromes that develop in the context of the effects of substances of abuse, medications, or several toxins. They are distinguished from the substance use disorders, in which a cluster of cognitive, behavioral, and physiological symptoms contribute to the continued use of a substance despite significant substance-related problems. The substance/medication-induced mental disorders may be induced by the 10 classes of substances that produce substance use disorders, or by a great variety of other medications used in medical treatment. Each substance-induced mental disorder is described in the relevant chapter (e.g., “Depressive Disorders,” “Neurocognitive Disorders”), and therefore, only a brief description is offered here. All substance/medication-induced disorders share common characteristics. It is important to recognize these common features to aid in the detection of these disorders. These features are described as follows:

A. The disorder represents a clinically significant 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 capable of producing the mental disorder.

C. The disorder is not better explained by an independent mental disorder (i.e., one that is not substance- or medication-induced). Such evidence of an independent mental disorder could include the following:

3. The disorder preceded the onset of severe intoxication or withdrawal or exposure to the medication; or

3. The full mental disorder persisted for a substantial period of time (e.g., at least 1 month) after the cessation of acute withdrawal or severe intoxication or taking the medication. This criterion does not apply to substance-induced neurocognitive disorders or hallucinogen persisting perception disorder, which persist beyond the cessation of acute intoxication or withdrawal.

1. The disorder does not occur exclusively during the course of a delirium.

1. The disorder causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Features

Some generalizations can be made regarding the categories of substances capable of producing clinically relevant substance-induced mental disorders. In general, the more sedating drugs (sedative, hypnotics, or anxiolytics, and alcohol) can produce prominent and clinically significant depressive disorders during intoxication, while anxiety conditions are likely to be observed during withdrawal syndromes from these substances(Schuckit 2006a). Also, during intoxication, the more stimulating substances (e.g., amphetamines and cocaine) are likely to be associated with substance-induced psychotic disorders and substance-induced anxiety disorders (McLellan et al. 1979), with substance-induced major depressive episodesobserved during withdrawal. Both the more sedating and more stimulating drugs are likely to produce significant but temporary sleep and sexual disturbances(Van Reen et al. 2006). An overview of the relationship between specific categories of substances and specific psychiatric syndromes is presented in Table.

The medication-induced conditions include what are often idiosyncratic CNS reactions or relatively extreme examples of side effects for a wide range of medications taken for a variety of medical concerns. These include neurocognitive complications of anesthetics, antihistamines, antihypertensives, and a variety of other medications and toxins (e.g., organophosphates, insecticides, carbon monoxide), as described in the chapter on neurocognitive disorders. Psychotic syndromes may be temporarily experienced in the context of anticholinergic, cardiovascular, 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 wide 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 temporary anxiety syndromes, sexual dysfunctions, and conditions of disturbed sleep.

In general, to be considered a substance/medication-induced mental disorder, there must be evidence that the disorder 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, continued more than 1 month after cessation of acute withdrawal, severe intoxication, or use of the medications(Caton et al. 2005; Hasin et al. 2002; Schuckit 2006a). When symptoms are only observed during a delirium (e.g., alcohol withdrawal delirium), the mental disorder should be diagnosed as a delirium, and the psychiatric syndrome occurring during the delirium should not also be diagnosed separately, as many symptoms (including disturbances in mood, anxiety, and reality testing) are commonly seen during agitated, confused states. The features associated with each relevant major mental disorder are similar whether observed with independent orsubstance/medication-induced mental disorders. However, individuals with substance/medication-induced mental disordersare likely to also demonstrate the associated features seen with the specific category of substance or medication, as listed in other subsections of this chapter.

Development and Course

Substance-induced mental disorders develop in the context of intoxication or withdrawal from substances of abuse, and medication-induced mental disorders are seen with prescribed or over-the-counter medications that are taken at the suggested doses. Both conditions are usually temporary and likely to disappear within 1 month or so of cessation of acute withdrawal, severe intoxication, or use of the medication. Exceptions to these generalizations occur for certain long-duration substance-induced disorders: substance-associated neurocognitive disorders that relate to conditions such as alcohol-induced neurocognitive disorder, inhalant-induced neurocognitive disorder, and sedative-, hypnotic-, or anxiolytic-induced neurocognitive disorder; and hallucinogen persisting perception disorder (“flashbacks”; see the section “Hallucinogen-Related Disorders” later in this chapter). However, most other substance/medication-induced mental disorders, regardless of the severity of the symptoms, are likely to improve relatively quickly with abstinence and unlikely to remain 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(Alia-Klein et al. 2011; Fu et al. 2002; Nunes et al. 2006; Nurnberger et al. 2004). Similar types of predispositions 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 histories with independent psychiatric syndromes are more likely to develop the induced syndrome once the consideration is made as to whether the quantity and frequency of the substance was sufficient to lead to the development of a substance-induced syndrome.

There are indications that the intake of substances of abuse or some medications with psychiatric side effects in the context of a preexisting mental disorder is likely to result in an intensification of the preexisting independent syndrome(Fu et al. 2002;Swendsen et al. 2010). The risk for substance/medication-induced mental disorders is likely to increase with both the quantity and the frequency of consumption of the relevant substance.

The symptom profiles for the substance/medication-induced mental disorders resemble independent mental disorders(Caton et al. 2005; Hasin et al. 2006; Regier et al. 1990; Schuckit et al. 1997). While the symptoms of substance/medication-induced mental disorders can be identical to those of independent mental disorders (e.g., delusions, hallucinations, psychoses, major depressive episodes, anxiety syndromes), and although they can have the same severe consequences (e.g., suicide)(Aharonovich et al. 2002), most induced mental disorders are likely to improve in a matter of days to weeks of abstinence(Brown et al. 1995; Gilder et al. 2004; Nunes and Rounsaville 2006; Schuckit et al. 2007).

The substance/medication-induced mental disorders are an important part of the differential diagnoses for the independent psychiatric conditions. The importance of recognizing an induced mental disorder is similar to the relevance of identifying the possible role of some medical conditions and medication reactions before diagnosing an independent mental disorder. Symptoms of substance- and medication-induced mental disorders may be identical cross-sectionally to those of independent mental disorders but have different treatments and prognoses from the independent condition.

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/medication-induced mental disorders, but these are likely to disappear within 1 month after abstinence. Similarly, the same functional consequences associated with the relevant substance use disorder are likely to be seen for the substance-induced mental disorders.

Recording Procedures for Substance/Medication-Induced Mental Disorders

Coding notes and separate recording procedures for ICD-9-CM and ICD-10-CM codes for other specific substance/medication-induced mental disorders are provided in other chapters of the manual with disorders with which they share phenomenology (see the substance/medication-induced mental disorders in these chapters: “Schizophrenia Spectrum and Other Psychotic Disorders,” “Bipolar and Related Disorders,” “Depressive Disorders,” “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 diagnostic code is given for the specific substance use disorder, in addition to the code for the substance/medication-induced mental disorder. For ICD-10-CM, a single code combines the substance-induced mental disorder with the substance use disorder. A separate diagnosis of the comorbid substance use disorder is not given, although the name and severity of the specific substance use disorder (when present) are used when recording the substance/medication-induced mental disorder. ICD-10-CM codes are also provided for situations in which the substance/medication-induced mental disorder 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 substance/medication-induced mental disorder is provided in the section “Recording Procedures” for each substance/medication-induced mental disorder in its respective chapter.

References: Recording Procedures for Substance/Medication-Induced Mental Disorders

· Aharonovich E , Liu X , Nunes E , Hasin DS : Suicide attempts in substance abusers: effects of major depression in relation to substance use disorders. Am J Psychiatry 159(9):1600–1602, 2002

· Alia-Klein N , Parvaz MA , Woicik PA , et al: Gene x disease interaction on orbitofrontal gray matter in cocaine addiction. Arch Gen Psychiatry 68(3):283–294, 2011 10.1001/archgenpsychiatry.2011.10

· Brown SA , Inaba RK , Gillin JC , et al: Alcoholism and affective disorder: clinical course of depressive symptoms. Am J Psychiatry 152(1):45–52, 1995

· Caton CL , Drake RE , Hasin DS , et al: Differences between early-phase primary psychotic disorders with concurrent substance use and substance-induced psychoses. Arch Gen Psychiatry 62(2):137–145, 2005 10.1001/archpsyc.62.2.137

· Fu Q , Heath AC , Bucholz KK , et al: Shared genetic risk of major depression, alcohol dependence, and marijuana dependence: contribution of antisocial personality disorder in men. Arch Gen Psychiatry 59(12):1125–1132, 2002

· Gilder DA , Wall TL , Ehlers CL : Comorbidity of select anxiety and affective disorders with alcohol dependence in southwest California Indians. Alcohol Clin Exp Res 28(12):1805–1813, 2004

· Hasin D , Liu X , Nunes E , et al: Effects of major depression on remission and relapse of substance dependence. Arch Gen Psychiatry 59(4):375–380, 2002

· Hasin D , Samet S , Nunes E , et al: Diagnosis of comorbid psychiatric disorders in substance users assessed with the Psychiatric Research Interview for Substance and Mental Disorders for DSM-IV. Am J Psychiatry 163(4):689–696, 2006

· McLellan AT , Woody GE , O’Brien CP : Development of psychiatric illness in drug abusers: possible role of drug preference. N Engl J Med 301(24):1310–1314, 1979

· Nunes EV , Rounsaville BJ : Comorbidity of substance use with depression and other mental disorders: from Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) to DSM-V. Addiction 101(suppl 1):89–96, 2006

· Nunes EV , Liu X , Samet S , et al: Independent versus substance-induced major depressive disorder in substance-dependent patients: observational study of course during follow-up. J Clin Psychiatry 67(10):1561–1567, 2006

· Nurnberger JI Jr , Wiegand R , Bucholz K , et al: A family study of alcohol dependence: coaggregation of multiple disorders in relatives of alcohol-dependent probands. Arch Gen Psychiatry 61(12):1246–1256, 2004 10.1001/archpsyc.61.12.1246

· Regier DA , Farmer ME , Rae DS , et al: Comorbidity of mental disorders with alcohol and other drug abuse: results from the Epidemiologic Catchment Area (ECA) study. JAMA 264(19):2511–2518, 1990

· Schuckit MA : Comorbidity between substance use disorders and psychiatric conditions. Addiction 101(suppl 1):76–88,2006a 10.1111/j.1360-0443.2006.01592.x

· Schuckit MA : Drug and Alcohol Abuse: A Clinical Guide to Diagnosis and Treatment, 6th Edition. New York, Springer,2006b

· Schuckit MA , Tipp JE , Bergman M , et al: Comparison of induced and independent major depressive disorders in 2,945 alcoholics. Am J Psychiatry 154(7):948–957, 1997

· Schuckit MA , Smith TL , Danko GP , et al: A comparison of factors associated with substance-induced versus independent depressions. J Stud Alcohol Drugs 68(6):805–812, 2007

· Swendsen J , Conway KP , Degenhardt L , et al: Mental disorders as risk factors for substance use, abuse and dependence: results from the 10-year follow-up of the National Comorbidity Survey. Addiction 105(6):1117–1128, 2010 10.1111/j.1360-0443.2010.02902.x

· Van Reen E , Jenni OG , Carskadon MA : Effects of alcohol on sleep and the sleep electroencephalogram in healthy young women. Alcoholism Clin Exp Res 30(6):974–981, 2006

Alcohol-Related Disorders

1. Alcohol Use Disorder

2. Alcohol Intoxication

3. Alcohol Withdrawal

4. Other Alcohol-Induced Disorders

5. Unspecified Alcohol-Related Disorder

Alcohol Use Disorder

Diagnostic Criteria

A. A problematic pattern of alcohol use leading to clinically significant impairment or distress, 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.

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 persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol.

7. Important social, occupational, or recreational activities are given up or reduced because 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 desired effect.

b. A markedly diminished effect with continued use of the same amount of alcohol.

11. Withdrawal, as manifested by either of the following:

11. The characteristic withdrawal syndrome for alcohol (refer to Criteria A and B of the criteria set for alcohol withdrawal, pp. 499–500).

11. 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 use 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).

· 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 controlled environment: This additional specifier is used if the individual is in an environment where access to alcohol is restricted.

Code based on current severity /remission : Note for ICD-10-CM codes: If an alcohol intoxication, alcohol withdrawal, or another alcohol-induced mental 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 alcohol-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 moderate or severe alcohol use disorder with alcohol intoxication.

Specify current severity /remission :

· 305.00 (F10.10) Mild: Presence of 2–3 symptoms.

· (F10.11) Mild, In early remission

· (F10.11) Mild, In sustained remission

· 303.90 (F10.20) Moderate: Presence of 4–5 symptoms.

· (F10.21) Moderate, In early remission

· (F10.21) Moderate, In sustained remission

· 303.90 (F10.20) Severe: Presence of 6 or more symptoms.

· (F10.21) Severe, In early remission

· (F10.21) Severe, In sustained remission

Specifiers

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Severity of the disorder is based on the number of diagnostic criteria endorsed. For a given individual, changes in severity ofalcohol use disorder across time 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 knowledgeable others, clinician observations, and, when practical, biological testing (e.g., elevations in blood tests as described in the section “Diagnostic Markers” for this disorder).

Diagnostic Features

Alcohol use disorder is defined by a cluster of behavioral and physical symptoms, which can include withdrawal, tolerance, and craving. Alcohol withdrawal is characterized by withdrawal symptoms that develop approximately 4–12 hours after the reduction of intake following prolonged, heavy alcohol ingestion(Schuckit 2012). 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 symptoms (e.g., sleep problems) can persist at lower intensities for months and can contribute to relapse. Once a pattern of repetitive and intense use develops, individuals with alcohol 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(Hintzen et al. 2011). School and job performance may also suffer either from the aftereffects of drinking or from actual intoxication at school or on the job; child care or household responsibilities may be neglected; and alcohol-related absences may occur from school or work. The individual may use alcohol in physically hazardous circumstances (e.g., driving an automobile, swimming, operating machinery while intoxicated). Finally, individuals with analcohol use disorder may continue to consume alcohol despite the knowledge that continued consumption poses significant physical (e.g., blackouts, liver disease), psychological (e.g., depression), social, or interpersonal problems (e.g., violent arguments with spouse while intoxicated, child abuse).

Associated Features Supporting Diagnosis

Alcohol use disorder is often associated with problems similar to those associated with other substances (e.g., cannabis; cocaine; heroin; amphetamines; 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 available. 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, especially the gastrointestinal tract, cardiovascular system, and the central and peripheral nervous systems(Schuckit 2006b; Schuckit 2011). Gastrointestinal effects include gastritis, stomach or duodenal ulcers, and, in about 15% of individuals who use alcohol heavily, 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 commonly associated conditions is low-grade hypertension. Cardiomyopathy and other myopathies are less common but occur at an increased rate among those who drink very heavily. These factors, along with marked increases in levels of triglycerides and low-density lipoprotein cholesterol, contribute to an elevated risk of heart disease. Peripheral neuropathy may be evidenced by muscular weakness, paresthesias, and decreased peripheral sensation. More persistent central nervous system effects include cognitive deficits, severe memory impairment, and degenerative changes in the cerebellum. These effects are related to the direct effects of alcohol or of trauma and to vitamin deficiencies (particularly of the B vitamins, including thiamine). One devastating central nervous system effect is the relatively rare alcohol-induced persisting 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 chapter “Neurocognitive Disorders” and would be termed asubstance/medication-induced neurocognitive disorder.

Alcohol use disorder is an important contributor to suicide risk during severe intoxication and in the context of a temporary alcohol-induced depressive and bipolar disorder. There is an increased rate of suicidal behavior as well as of completed suicide among individuals 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 States. Rates of the disorder are greater among adult men (12.4%) than among adult women (4.9%). Twelve-month prevalence of alcohol use disorderamong adults decreases in middle 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 are greatest among Hispanics (6.0%) and Native Americans and Alaska Natives (5.7%) relative to whites (5.0%), African Americans (1.8%), and Asian Americans and Pacific Islanders (1.6%). In contrast, among adults, the 12-month prevalence ofalcohol use disorder 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 intoxication is likely to occur during the mid-teens. Alcohol-related problems that do not meet full criteria for a use disorder or isolated problems may occur prior to age 20 years, but the age at onset of an alcohol use disorderwith two or more of the criteria clustered together peaks in the late teens or early to mid 20s(Schuckit 2009a; Trim et al. 2009). The large majority of individuals who develop alcohol-related 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 adolescents with preexisting conduct problems and those with an earlier onset of intoxication(Sartor et al. 2009).

Alcohol use disorder has a variable course that is characterized by periods of remission and relapse(Moos and Moos 2006;Rumpf et al. 2006; Schuckit and Smith 2011). 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 perceived as an intractable condition, perhaps based on the fact that individuals who present for treatment typically have a history of many years of severe alcohol-related problems. However, these most severe cases represent only a small proportion of individuals with this disorder, and the typical individual with the disorder has a much more promising prognosis.

Among adolescents, conduct disorder and repeated antisocial behavior often co-occur with alcohol- and with other substance-related disorders (Dick et al. 2006). While most individuals with alcohol use disorder develop the condition before age 40 years, perhaps 10% have later onset(Gossop and Moos 2008; Schuckit and Smith 2011). Age-related physical changes in older individuals result in increased brain susceptibility to the depressant effects of alcohol; decreased rates of liver metabolism of a variety of substances, including alcohol; and decreased percentages of body water. These changes can cause older people to develop more severe intoxication and subsequent problems at lower levels of consumption. Alcohol-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 attitudes toward drinking and intoxication, the availability of alcohol (including price), acquired personal experiences with alcohol, and stress levels. Additional potential mediators 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(Schuckit et al. 2011).

Genetic and physiological

Alcohol use disorder runs in families, with 40%–60% of the variance of risk explained by genetic influences(Nurnberger and Bierut 2007; Schuckit 2009b). 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 number 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 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 phenotypes) to affect the risk of alcohol use disorder can help to identify individuals who might be at particularly low or high risk for alcohol use disorder (Schuckit 2009b). 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 disorder, as well as impulsivity (producing enhanced 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 account for low response to alcohol or modulate the dopamine reward systems; it is important to note, however, that any one gene variation 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 contributes to considerable morbidity and mortality. An estimated 3.8% of all global deaths and 4.6% of global disability-adjusted life-years are attributable to alcohol(Rehm et al. 2009). In the United States, 80% of adults (age 18 years and older) have consumed alcohol at some time in their lives, and 65% are current drinkers (last 12 months)(Pleis et al. 2010). An estimated 3.6% of the world population (15–64 years old) has a current (12-month) alcohol use disorder, with a lower prevalence (1.1%) found in the African region, a higher rate (5.2%) found in the American region (North, South, and Central America and the Caribbean), and the highest rate (10.9%) found in the Eastern Europe region(Rehm et al. 2009).

Polymorphisms of genes for the alcohol-metabolizing enzymes alcohol dehydrogenase and aldehyde dehydrogenase are most often seen in Asians and affect the response to alcohol. When consuming alcohol, individuals with these gene variations can experience a flushed face and palpitations, reactions that can be so severe as to limit or preclude future alcohol consumption and diminish the risk for 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(Eng et al. 2007; Tan et al. 2010).

Despite small variations regarding individual criterion items, the diagnostic criteria perform equally well across most race/ethnicity groups(Borges et al. 2010; Harford et al. 2009; Saha et al. 2007).

Gender-Related Diagnostic Issues

Males have higher rates of drinking and related disorders than females. 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, including liver disease.

Diagnostic Markers

Individuals whose heavier drinking places them at elevated risk for alcohol use disorder can be identified both through standardized questionnaires and by elevations in blood test results likely to be seen with regular heavier 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. The most direct test available to measure alcohol consumption cross-sectionally is blood alcohol concentration, which can also be used to judge tolerance to alcohol. For example, an individual with a concentration of 150 mg of ethanol per deciliter (dL) of blood who does not show signs of intoxication can be presumed to have acquired at least some degree of tolerance to alcohol. At 200 mg/dL, most nontolerant individuals demonstrate severe intoxication.

Regarding laboratory tests(Conigrave et al. 2002; Niemelä 2007), one sensitive laboratory 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 individuals with a high GGT level are persistent heavy drinkers (i.e., consuming eight or more drinks daily on a regular basis). A second test with comparable or even higher levels of sensitivity and specificity is carbohydrate-deficient transferrin (CDT), with levels of 20 units or higher useful in identifying individuals who regularly consume 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, especially when the clinician observes increases, rather than decreases, in these 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 sensitivity and specificity than either test used alone. Additional useful tests include the mean corpuscular volume (MCV), which may be elevated to high-normal values in individuals who drink heavily—a change that is due to the direct toxic effects of alcohol on erythropoiesis. Although the MCV can be used to help identify those who drink heavily, it is a poor method of monitoring abstinence because of the long half-life of red blood cells. Liver function tests (e.g., alanine aminotransferase [ALT] and alkaline phosphatase) can reveal liver injury that is a consequence of heavy drinking. Other potential markers of heavy drinking that are more nonspecific for alcohol but can help the clinician think of the possible effects of alcohol include elevations in blood levels or lipids (e.g., triglycerides and high-density lipoprotein cholesterol) and high-normal levels of uric acid.

Additional diagnostic markers relate to signs and symptoms that reflect the consequences often associated with persistent heavy drinking. For example, dyspepsia, nausea, and bloating 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 dysfunction. Males with chronic alcohol use disorder may exhibit decreased testicular size and feminizing effects associated with reduced testosterone levels. Repeated heavy drinking in females is associated with menstrual irregularities and, during pregnancy, spontaneous abortion and fetal alcohol syndrome. Individuals with preexisting histories of epilepsy or severe head trauma are more likely to develop alcohol-related seizures. Alcohol withdrawalmay be associated with nausea, vomiting, gastritis, hematemesis, dry mouth, puffy blotchy complexion, and mild peripheral edema.

Functional Consequences of Alcohol Use Disorder

The diagnostic features of alcohol use disorder highlight major areas of life functioning likely to be impaired. These include driving and operating machinery, school and work, interpersonal relationships and communication, and health. Alcohol-related disorders contribute to absenteeism from work, job-related accidents, and low employee productivity. Rates are elevated in homeless individuals, 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, violence, and suicide(Hill et al. 2009). It is estimated that one in five intensive care unit admissions in some urban hospitals is related to alcohol and that 40% of individuals in the United States experience an alcohol-related adverse event at some time in their lives, with alcohol accounting 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 disinhibition and feelings of sadness and irritability, 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 add 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 functioning. While most drinkers sometimes consume enough alcohol to feel intoxicated, only a minority (less than 20%) ever develop alcohol 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 course may be different, especially in relation to medical problems.

Conduct disorder in childhood and adult antisocial personality disorder

Alcohol use disorder, along with other substance 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 important 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 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, alcohol-induced comorbid depressive symptoms resulting from the acute effects of intoxication or withdrawal(Schuckit 2006a). Severe, repeated alcohol intoxication may also suppress immune mechanisms and predispose individuals to infections and increase the risk for cancers.

References: Alcohol Use Disorder

· Borges G , Ye Y , Bond J , et al: The dimensionality of alcohol use disorders and alcohol consumption in a cross-national perspective. Addiction 105(2):240–254, 2010 10.1111/j.1360-0443.2009.02778.x

· Conigrave KM , Degenhardt LJ , Whitfield JB , et al: CDT, GGT, and AST as markers of alcohol use: the WHO/ISBRA collaborative project. Alcohol Clin Exp Res 26(3):332–339, 2002

· Dick DM , Bierut L , Hinrichs A , et al: The role of GABRA2 in risk for conduct disorder and alcohol and drug dependence across developmental stages. Behav Genet 36(4):577–590, 2006 10.1007/s10519-005-9041-8

· Eng MY , Luczak SE , Wall TL : ALDH2, ADH1B, and ADH1C genotypes in Asians: a literature review. Alcohol Res Health30(1):22–27, 2007

· Gossop M , Moos R : Substance misuse among older adults: a neglected but treatable problem. Addiction 103(3):347–348,2008 10.1111/j.1360-0443.2007.02096.x

· Harford TC , Yi HY , Faden VB , Chen CM : The dimensionality of DSM-IV alcohol use disorders among adolescent and adult drinkers and symptom patterns by age, gender, and race/ethnicity. Alcohol Clin Exp Res 33(5):868–878, 200910.1111/j.1530-0277.2009.00910.x

· Hill SY , Steinhauer SR , Locke-Wellman J , Ulrich R : Childhood risk factors for young adult substance dependence outcome in offspring from multiplex alcohol dependence families: a prospective study. Biol Psychiatry 66(8):750–757, 2009

· Hintzen AK , Cramer J , Karagülle D , et al: Does alcohol craving decrease with increasing age? Results from a cross-sectional study. J Stud Alcohol Drugs 72(1):158–162, 2011

· Moos RJ , Moos BS : Rates and predictors of relapse after natural and treated remission from alcohol use disorders.Addiction 101(2):212–222, 2006 10.1111/j.1360-0443.2006.01310.x

· Niemelä O : Biomarkers in alcoholism. Clin Chim Acta 377(1–2):39–49, 2007 10.1016/j.cca.2006.08.035

· Nurnberger JI Jr , Bierut LJ : Seeking the connections: alcoholism and our genes. Sci Am 296(4):46–53, 2007

· Pleis JR , Ward BW , Lucas JW : Summary health statistics for U.S. adults: National Health Interview Survey, 2009. National Center for Health Statistics. Vital Health Stat 10 249:1–207, 2010, Tables 26 and 27

· Rehm J , Mathers C , Popova S , et al: Global burden of disease and injury and economic cost attributable to alcohol use and alcohol-use disorders. Lancet 373(9682):2223–2233, 2009 10.1016/S0140-6736(09)60746-7

· Rumpf HJ , Bischof G , Hapke U , et al: Stability of remission from alcohol dependence without formal help. Alcohol Alcohol41(3):311–314, 2006 10.1093/alcalc/agl008

· Saha TD , Stinson FS , Grant BF : The role of alcohol consumption in future classifications of alcohol use disorders. Drug Alcohol Depend 89(1):82–92, 2007 10.1016/j.drugalcdep.2006.12.003

· Sartor CE , Lynskey MT , Bucholz KK , et al: Timing of first alcohol use and alcohol dependence: evidence of common genetic influences. Addiction 104(9):1512–1518, 2009 10.1111/j.1360-0443.2009.02648.x

· Schuckit MA : Comorbidity between substance use disorders and psychiatric conditions. Addiction 101(suppl 1):76–88,2006a 10.1111/j.1360-0443.2006.01592.x

· Schuckit MA : Drug and Alcohol Abuse: A Clinical Guide to Diagnosis and Treatment, 6th Edition. New York, Springer, 2006b

· Schuckit MA : Alcohol-use disorders. Lancet 373(9662):492–501, 2009a 10.1016/S0140-6736(09)60009-x

· Schuckit MA : An overview of genetic influences in alcoholism. J Subst Abuse Treat 36(1):S5–14, 2009b

· Schuckit MA : Ethanol and methanol, in Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12th Edition. Edited by Brunton L , Chabner B , Knollmann BC . New York, McGraw-Hill, 2011, pp 629–647

· Schuckit MA : Alcohol and alcoholism, in Harrison’s Principles of Internal Medicine, 18th Edition. Edited by Fauci AS , Braunwald E , Kasper DL , et al. New York, McGraw-Hill, 2012, pp 3446–3552

· Schuckit MA , Smith TL : Onset and course of alcoholism over 25 years in middle class men. Drug Alcohol Depend 113(1):21–28, 2011 10.1016/j.drugalcdep.2010.06.017

· Schuckit MA , Smith TL , Heron J , et al: Testing a level of response to alcohol-based model of heavy drinking and alcohol problems in 1,905 17-year-olds. Alcohol Clin Exp Res 35(10):1897–1904, 2011 10.1111/j.1530-0277.2011.01536.x

· Tan EC , Lim L , Leong JY , et al: Alcohol and aldehyde dehydrogenase polymorphisms in Chinese and Indian populations. Subst Use Misuse 45(1–2):1–14, 2010 10.3109/10826080802490584

· Trim RS , Schuckit MA , Smith TL : The relationships of the level of response to alcohol and additional characteristics to alcohol use disorders across adulthood: a discrete-time survival analysis. Alcohol Clin Exp Res 33(9):1562–1570, 200910.1111/j.1530-0277.2009.00984.x

Alcohol Intoxication

Diagnostic Criteria

A. Recent ingestion of alcohol.

B. Clinically significant problematic behavioral or psychological changes (e.g., inappropriate 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, including 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

The essential feature of alcohol intoxication is the presence of clinically significant problematic behavioral or psychological changes (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 judgment and, if intoxication is intense, can result in a life-threatening coma. The symptoms must not be attributable to another medical condition (e.g., diabetic ketoacidosis), are not a reflection of conditions such as delirium, and are not related to intoxication with other depressant drugs (e.g., benzodiazepines) (Criterion D). The levels of incoordination 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 individual’s breath, eliciting a history from the individual 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 (“blackouts”)(Nelson et al. 2004). This phenomenon may be related to the presence of a high blood alcohol level and, perhaps, to the rapidity with which this level is reached. During even mild alcohol intoxication, different symptoms are likely to be observed at different time points. Evidence of mild intoxication with alcohol can be seen in most individuals after approximately two drinks (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, especially when blood alcohol levels are falling, the individual is likely to become progressively more depressed, withdrawn, and cognitively impaired. 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 intoxication depends on how much alcohol was consumed over what period of time. In general, the body is able to metabolize approximately 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 intoxication are likely to be more intense when the blood alcohol level is rising than when it is falling.

Alcohol intoxication is an important contributor to suicidal behavior. There appears to be an increased rate of suicidal behavior, as well as of completed suicide, among persons intoxicated by alcohol.

Prevalence

The large majority of alcohol consumers are likely to have been intoxicated to some degree at some point in their lives. For example, in 2010, 44% of 12th-grade students admitted to having been “drunk in the past year,” with more than 70% of college students reporting the same(Johnston et al. 2009).

Development and Course

Intoxication usually occurs as an episode usually developing over minutes to hours and typically lasting several hours. In the United States, the average age at first intoxication is approximately 15 years, with the highest prevalence at approximately 18–25 years. Frequency and intensity usually decrease with further advancing age. The earlier the onset of regular intoxication, the greater the likelihood the individual will go on to develop alcohol use disorder(Dawson et al. 2008).

Risk and Prognostic Factors

Temperamental

Episodes of alcohol intoxication increase with personality characteristics of sensation seeking and impulsivity.

Environmental

Episodes of alcohol intoxication increase with a heavy drinking environment.

Culture-Related Diagnostic Issues

The major issues parallel the cultural differences regarding the use of alcohol overall. Thus, college fraternities and sororities may encourage alcohol intoxication. This condition is also frequent on certain dates of cultural significance (e.g., New Year’s Eve) and, for some subgroups, during specific 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, fundamentalist Christians, and Muslims).

Gender-Related Diagnostic Issues

Historically, in many Western societies, acceptance 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.

Diagnostic Markers

Intoxication is usually established by observing an individual’s behavior and smelling alcohol on the breath. The degree of intoxication increases with an individual’s blood or breath alcohol level and with the ingestion of other substances, 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 conditions (e.g., cerebellar ataxia, multiple sclerosis) can temporarily resemble alcohol intoxication.

Sedative, hypnotic, or anxiolytic intoxication

Intoxication with sedative, hypnotic, or anxiolytic drugs or with other sedating substances (e.g., antihistamines, anticholinergic drugs) can be mistaken for alcohol intoxication. The differential requires observing alcohol 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 alcohol and include similar problematic behavioral or psychological changes. These changes are accompanied by evidence of impaired functioning and judgment—which, if intense, can result in a life-threatening 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 evidence of misuse of the depressant drug in the blood or urine toxicology analyses.

Comorbidity

Alcohol intoxication may occur comorbidly with other substance intoxication, especially in individuals with conduct disorder or antisocial personality disorder.

References: Alcohol Intoxication

· Dawson DA , Goldstein RB , Chou SP , et al: Age at first drink and the first incidence of adult-onset DSM-IV alcohol use disorders. Alcohol Clin Exp Res 32(12):2149–2160, 2008

· Johnston LD , O’Malley PM , Bachman JG , Schulenberg JE : Monitoring the Future: National Survey Results on Drug Use, 1975–2008:: Volume 1: Secondary School Students. NIH Publ No 09-7402. Bethesda, MD, National Institute on Drug Abuse, 2009

· Nelson EC , Heath AC , Bucholz KK , et al: Genetic epidemiology of alcohol-induced blackouts. Arch Gen Psychiatry61(3):257–263, 2004

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.

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 hallucinations (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 comorbid presence of a moderate or severe alcohol use disorder, reflecting the fact that alcohol withdrawal 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 clear sensorium), a diagnosis of substance/medication-induced psychotic disorder should be considered.

Diagnostic Features

The essential feature of alcohol withdrawal is the presence of a characteristic withdrawal syndrome that develops within several hours to a few days after the cessation of (or reduction in) heavy and prolonged alcohol use (Criteria A and B)(Sannibale et al. 2005). The withdrawal syndrome includes two or more of the symptoms reflecting autonomic hyperactivity and anxiety listed in Criterion B, along with gastrointestinal symptoms(Schuckit 2009).

Withdrawal symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). The symptoms must not be attributable to another medical condition and are not better explained by another mental disorder (e.g., generalized anxiety disorder), 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 use has been stopped or reduced. Reflecting the relatively fast metabolism of alcohol, symptoms of alcohol withdrawal usually peak in intensity during the second day of abstinence and are likely to improve markedly by the fourth or fifth day. Following acute withdrawal, however, symptoms of anxiety, insomnia, and autonomic 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 dramatic symptoms (e.g., severe autonomic hyperactivity, tremors, alcohol withdrawal delirium). 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 withdrawal, alcohol withdrawal delirium (see “Delirium” in the chapter “Neurocognitive Disorders”) 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 consciousness and cognition, withdrawal delirium can include visual, tactile, or (rarely) auditory hallucinations (delirium tremens). When alcohol withdrawal delirium develops, it is likely that a clinically relevant medical condition may be present (e.g., liver failure, pneumonia, gastrointestinal bleeding, sequelae of head trauma, hypoglycemia, an electrolyte imbalance, postoperative status).

Prevalence

It is estimated that approximately 50% of middle-class, highly functional individuals with alcohol use disorder have ever experienced a full alcohol withdrawal syndrome. Among individuals with alcohol use disorder who are hospitalized or homeless, the rate of alcohol withdrawal may be greater than 80%. Less than 10% of individuals in withdrawal ever demonstrate alcohol 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 severity increase with increasing age.

Risk and Prognostic Factors

Environmental

The probability of developing alcohol withdrawal increases with the quantity and frequency of alcohol consumption. Most individuals with this condition are drinking daily, consuming large amounts (approximately 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 alcohol withdrawal (i.e., a genetic component), those with prior withdrawals, and individuals who consume sedative, hypnotic, 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 indicate a likelihood of alcohol withdrawal.

Functional Consequences of Alcohol Withdrawal

Symptoms of withdrawal may serve to perpetuate drinking behaviors and contribute to relapse, resulting in persistently impaired social 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 functional 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 erroneously suggest the tremulousness associated with alcohol withdrawal.

Sedative, hypnotic, or anxiolytic withdrawal

Sedative, hypnotic, or anxiolytic withdrawal produces a syndrome very similar to that of alcohol withdrawal.

Comorbidity

Withdrawal is more likely to occur with heavier alcohol intake, and that might be most often observed in individuals withconduct disorder and antisocial personality disorder. Withdrawal states are also more severe in older individuals, individuals who are also dependent on other depressant drugs (sedative-hypnotics), and individuals who have had more alcohol withdrawal experiences in the past.

References: Alcohol Withdrawal

· Sannibale C , Fucito L , O’Connor D , Curry K : Process evaluation of an out-patient detoxification service. Drug Alcohol Rev24(6):475–481, 2005

· Schuckit MA : Alcohol-use disorders. Lancet 373(9662):492–501, 2009

Other Alcohol-Induced Disorders

The following alcohol-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): alcohol-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); alcohol-induced bipolar disorder (“Bipolar and Related Disorders”); alcohol-induced depressive disorder (“Depressive Disorders”); alcohol-induced anxiety disorder (“Anxiety Disorders”); alcohol-induced sleep disorder (“Sleep-Wake Disorders”); alcohol-induced sexual dysfunction (“Sexual Dysfunctions”); and alcohol-induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For alcohol intoxication delirium and alcohol withdrawal delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These alcohol-induced disorders are diagnosed 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 alcohol-induced condition resemble independent mental disorders as described elsewhere in DSM-5(Caton et al. 2005; Schuckit et al. 1997). However, the alcohol-induced disorder is temporary and observed after severe intoxication with and/or withdrawal from alcohol. While the symptoms can be identical to those of independent mental disorders (e.g., psychoses, major depressive disorder), and while they can have the same severe consequences (e.g., suicide attempts), alcohol-induced conditions are likely to improve without formal treatment in a matter of days to weeks after cessation of severe intoxication and/or withdrawal(Brown et al. 1995; Gilder et al. 2004).

Each alcohol-induced mental disorder is listed in the relevant diagnostic section and therefore only a brief description is offered here. Alcohol-induced disorders must have developed in the context of severe intoxication and/or withdrawal from the substance capable of producing the mental disorder. In addition, there must be evidence that the disorder being observed is not likely to be better explained by another non-alcohol-induced mental disorder. The latter is likely to occur if the mental disorder was present before the severe intoxication or withdrawal, or continued more than 1 month after the cessation of severe intoxication and/or withdrawal(Caton et al. 2005; Schuckit 2006). 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 testing) are commonly seen during agitated, confused states. The alcohol-induced disorder must be clinically relevant, causing significant levels of distress or significant 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(Fu et al. 2002; Swendsen et al. 2010).

The features associated with each relevant major mental disorder (e.g., psychotic episodes, major depressive disorder) are similar whether observed with an independent or an alcohol-induced condition. However, individuals with alcohol-induced disorders are likely to also demonstrate the associated features seen with an alcohol use disorder, as listed in the subsections of this chapter.

Rates of alcohol-induced disorders vary somewhat by diagnostic category. For example, the lifetime risk for major depressive episodes 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 anxiety conditions are likely, but alcohol-induced psychotic episodes are fairly rare.

Development and Course

Once present, the symptoms of an alcohol-induced condition are likely to remain clinically relevant as long as the individual continues to experience severe intoxication and/or withdrawal. 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 consequences (e.g., suicide attempts), all alcohol-induced syndromes other than alcohol-induced neurocognitive disorder, amnestic confabulatory type (alcohol-induced persisting amnestic disorder), regardless of the severity of the symptoms, are likely to improve relatively quickly and unlikely to remain clinically 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. Independent schizophrenia, major depressive disorder, bipolar disorder, and anxiety disorders, such as panic disorder, are likely to be associated 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 cessation 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 endocrine conditions and medication reactions before 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 considered before independent mental disorders are diagnosed.

References: Other Alcohol-Induced Disorders

· Brown SA , Inaba RK , Gillin JC , et al: Alcoholism and affective disorder: clinical course of depressive symptoms. Am J Psychiatry 152(1):45–52, 1995

· Caton CL , Drake RE , Hasin DS , et al: Differences between early-phase primary psychotic disorders with concurrent substance use and substance-induced psychoses. Arch Gen Psychiatry 62(2):137–145, 2005 10.1001/archpsyc.62.2.137

· Fu Q , Heath AC , Bucholz KK , et al: Shared genetic risk of major depression, alcohol dependence, and marijuana dependence: contribution of antisocial personality disorder in men. Arch Gen Psychiatry 59(12):1125–1132, 2002

· Gilder DA , Wall TL , Ehlers CL : Comorbidity of select anxiety and affective disorders with alcohol dependence in southwest California Indians. Alcohol Clin Exp Res 28(12):1805–1813, 2004

· Schuckit MA : Comorbidity between substance use disorders and psychiatric conditions. Addiction 101(suppl 1):76–88, 200610.1111/j.1360-0443.2006.01592.x

· Schuckit MA , Tipp JE , Bergman M , et al: Comparison of induced and independent major depressive disorders in 2,945 alcoholics. Am J Psychiatry 154(7):948–957, 1997

· Swendsen J , Conway KP , Degenhardt L , et al: Mental disorders as risk factors for substance use, abuse and dependence: results from the 10-year follow-up of the National Comorbidity Survey. Addiction 105(6):1117–1128, 2010 10.1111/j.1360-0443.2010.02902.x

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, occupational, 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

1. Caffeine Intoxication

2. Caffeine Withdrawal

3. Other Caffeine-Induced Disorders

4. 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.

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 better explained by another mental disorder, including intoxication with another substance.

Diagnostic Features

Caffeine can be consumed from a number of different sources, including coffee, tea, caffeinated soda, “energy” drinks, over-the-counter analgesics and cold remedies, energy aids (e.g., drinks), weight-loss aids, and chocolate. Caffeine is also increasingly being used as an additive to vitamins and to food products. More than 85% of children and adults consume caffeine regularly(Juliano and Griffiths 2009; Reissig et al. 2009). Some caffeine users display symptoms consistent with problematic 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 prevalence. In contrast, there is evidence that caffeine withdrawal and caffeine intoxication are clinically significant and sufficiently prevalent(Juliano and Griffiths 2004).

The essential feature of caffeine intoxication is recent consumption of caffeine and five or more signs or symptoms that 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 elderly, or individuals who have not been exposed to caffeine previously. Symptoms that generally appear at levels of more than 1 g/day include muscle twitching, rambling flow of thought and speech, tachycardia or cardiac arrhythmia, periods of inexhaustibility, and psychomotor agitation. Caffeine intoxication may not occur despite high caffeine intake because of the development of tolerance. The signs or symptoms must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). The signs or symptoms must not be attributable to another medical condition and are not better explained by another mental disorder (e.g., an anxiety disorder) or intoxication 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, sweating, 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.

Prevalence

The prevalence of caffeine intoxication in the general population is unclear. In the United States, approximately 7% of individuals in the population may experience five or more symptoms along with functional impairment consistent with a diagnosis of caffeine intoxication(Hughes et al. 1998).

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 consume very high doses of caffeine (i.e., 5–10 g) may require immediate medical attention, as such doses can be lethal(Lai et al. 2006).

With advancing age, individuals are likely to demonstrate increasingly intense reactions to caffeine, with greater complaints of interference with sleep or feelings of hyperarousal. Caffeine intoxication among young individuals after consumption of highly caffeinated products, including energy drinks, has been observed(McCarthy et al. 2008; Walsh et al. 2006). Children and adolescents may be at increased risk for caffeine intoxication because of low body weight, lack of tolerance, and lack of knowledge about the pharmacological 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 substantial amount. Furthermore, oral contraceptives significantly decrease the elimination of caffeine and consequently may increase the risk of intoxication.

Genetic and physiological

Genetic factors may affect risk of caffeine intoxication (Kendler et al. 2006).

Functional Consequences of Caffeine Intoxication

Impairment from caffeine intoxication may have serious consequences, including dysfunction at work or school, social indiscretions, or failure to fulfill role obligations. Moreover, extremely high doses of caffeine can be fatal. 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 disorders. To meet criteria for caffeine intoxication, the symptoms must not be associated with another medical condition or another mental disorder, such as an anxiety disorder, that could better explain them. Manic episodes; panic disorder; generalized anxiety disorder; amphetamine intoxication; sedative, hypnotic, or anxiolytic withdrawal or tobacco withdrawal; sleep disorders; and medication-induced side effects (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 helps to establish the diagnosis. Caffeine intoxication is differentiated from caffeine-induced anxiety disorder, with onset during intoxication (see “Substance/Medication-Induced Anxiety Disorder” in the chapter “Anxiety Disorders”), and caffeine-induced sleep disorder, with onset during intoxication (see “Substance/Medication-Induced Sleep Disorder” in the chapter “Sleep-Wake Disorders”), by the fact that the symptoms in these latter disorders are in excess of those usually associated with caffeine intoxication and are severe enough to warrant independent clinical attention.

Comorbidity

Typical dietary doses of caffeine have not been consistently associated with medical problems. However, heavy use (e.g., >400 mg) can cause or exacerbate anxiety and somatic symptoms and gastrointestinal distress(Juliano and Griffiths 2009). With acute, extremely high doses of caffeine, grand mal seizures and respiratory failure may result in death. Excessive caffeine use is associated with depressive disorders, bipolar disorders, eating disorders, psychotic disorders, sleep disorders, and substance-related disorders, whereas individuals with anxiety disorders are more likely to avoid caffeine(Juliano and Griffiths 2009).

References: Caffeine Intoxication

· Hughes JR , Oliveto AH , Liguori A , et al: Endorsement of DSM-IV dependence criteria among caffeine users. Drug Alcohol Depend 52(2):99–107, 1998

· Juliano LM , Griffiths RR : A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features. Psychopharmacology (Berl) 176(1):1–29, 2004

· Juliano LM , Griffiths RR : Caffeine-related disorders, in Kaplan and Sadock’s Comprehensive Textbook of Psychiatry, 9th Edition. Edited by Sadock BJ , Sadock VA , Ruiz P . Philadelphia, PA, Lippincott Williams & Wilkins, 2009, pp 1296–1308

· Kendler KS , Myers J , O Gardner C : Caffeine intake, toxicity and dependence and lifetime risk for psychiatric and substance use disorders: an epidemiologic and co-twin control analysis. Psychol Med 36(12):1717–1725, 2006

· Lai MW , Klein-Schwartz W , Rodgers GC , et al: 2005 Annual Report of the American Association of Poison Control Centers’ national poisoning and exposure database. Clin Toxicol 44(6–7):803–932, 2006

· McCarthy DM , Mycyk MB , DesLauriers CA : Hospitalization for caffeine abuse is associated with abuse of other pharmaceutical products. Am J Emerg Med 26(7):799–802, 2008

· Reissig CJ , Strain EC , Griffiths RR : Caffeinated energy drinks—a growing problem. Drug Alcohol Depend 99(1–3):1–10,2009

· Walsh MJ , Marquardt KA , Albertson TE : Adverse effects from the ingestion of Redline energy drinks. Clin Toxicol 44:642,2006

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) prolonged daily caffeine ingestion (Criterion B). The caffeine withdrawal syndrome is indicated 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 syndrome 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 condition and are not better explained by another mental disorder (Criterion D).

Headache is the hallmark feature of caffeine withdrawal and may be diffuse, gradual in development, throbbing, severe, and sensitive to movement(Juliano and Griffiths 2004). However, other symptoms of caffeine withdrawal can occur in the absence of headache(Juliano and Griffiths 2004; Juliano and Griffiths 2009). Caffeine is the most widely used behaviorally active drug in the world and is present in many different types of beverages (e.g., coffee, tea, maté, soft drinks, energy drinks), foods, energy aids, medications, and dietary supplements(James 1997). 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 unexpected and misattributed to other causes (e.g., the flu, migraine). Furthermore, caffeine withdrawal symptoms may occur when individuals are required to abstain from foods and beverages prior to medical procedures or when a usual caffeine dose is missed because of a change in routine (e.g., during travel, weekends).

The probability and severity of caffeine withdrawal 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(Hughes et al. 1993; Juliano and Griffiths 2004). Caffeine withdrawal symptoms 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 associated with impaired behavioral and cognitive performance (e.g., sustained attention)(Juliano and Griffiths 2004). Electroencephalographic studies have shown that caffeine withdrawal symptoms are significantly associated with increases in theta power and decreases in beta-2 power. Decreased motivation to work and decreased sociability have also been reported during caffeine withdrawal. Increased analgesic use during caffeine withdrawalhas been documented.

Prevalence

More than 85% of adults and children in the United States regularly consume caffeine, with adult caffeine consumers ingesting about 280 mg/day on average. The incidence and prevalence of the caffeine withdrawal syndrome in the general population are unclear. In the United States, headache may occur in approximately 50% of cases of caffeine abstinence(Juliano and Griffiths 2004). In attempts to permanently stop caffeine use, more than 70% of individuals may experience at least one caffeine withdrawal symptom (47% may experience headache), and 24% may experience headache plus one or more other symptoms as well as functional impairment due to withdrawal(Hughes et al. 1998). Among individuals who abstain from caffeine for at least 24 hours but are not trying to permanently stop caffeine use, 11% may experience headache plus one or more other symptoms as well as functional impairment(Hughes et al. 1998). Caffeine consumers can decrease the incidence of caffeine withdrawal by using caffeine daily or only infrequently (e.g., no more than 2 consecutive days). Gradual reduction 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(Griffths et al. 1986) 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 behaviorally active drug that is consumed by individuals of nearly all ages. Rates of caffeine consumption and overall level of caffeine consumption 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 observed among individuals with mental disorders, including eating disorders; smokers; 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 incipient withdrawal symptoms. While caffeine is legal and usually widely available, there are conditions in which caffeine use may be restricted, such as during medical procedures, pregnancy, hospitalizations, religious observances, wartime, travel, and research participation. These external environmental circumstances may precipitate a withdrawal syndrome in vulnerable individuals.

Genetic and physiological factors

Genetic factors appear to increase vulnerability to caffeine withdrawal, but no specific genes have been identified(Kendler and Prescott 1999).

Course modifiers

Caffeine withdrawal symptoms usually 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 symptoms (e.g., consumption of 25 mg by an individual who typically consumes 300 mg).

Culture-Related Diagnostic Issues

Habitual caffeine consumers who fast for religious reasons may be at increased risk for caffeine 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%)(Juliano and Griffiths 2004), with rates as high as 73% found among individuals who also show other problematic features of caffeine use(Strain et al. 1994). Examples of functional impairment include being unable to work, exercise, or care for children; staying in bed all day; missing religious services; ending a vacation early; and cancelling a social gathering(Strain et al. 1994). Caffeine withdrawal headaches may be described by individuals as “the worst headaches” ever experienced. Decrements in cognitive and motor performance have also been observed.

Differential Diagnosis

Other medical disorders and medical side effects

Several disorders should be considered in the differential diagnosis of caffeine withdrawal. Caffeine withdrawal can mimic migraine and other headache disorders, viral illnesses, sinus conditions, tension, other drug withdrawal states (e.g., from amphetamines, cocaine), and medication side effects. The final determination of caffeine withdrawal should rest on a determination of the pattern and amount consumed, the time interval between caffeine abstinence and onset of symptoms, and the particular clinical features presented by the individual. A challenge dose of caffeine followed by symptom remission may be used to confirm the diagnosis.

Comorbidity

Caffeine withdrawal may be associated with major depressive disorder, generalized anxiety disorder, panic disorder, antisocial personality disorder in adults, moderate to severe alcohol use disorder, and cannabis and cocaine use(Kendler et al. 2006).

References: Caffeine Withdrawal

· Griffiths RR , Bigelow GE , Liebson IA : Human coffee drinking: reinforcing and physical dependence producing effects of caffeine. J Pharmacol Exp Ther 239(2):416–425, 1986

· Hughes JR , Oliveto AH , Bickel WK , et al: Caffeine self-administration and withdrawal: incidence, individual differences and interrelationships. Drug Alcohol Depend 32(3):239–246, 1993

· Hughes JR , Oliveto AH , Liguori A , et al: Endorsement of DSM-IV dependence criteria among caffeine users. Drug Alcohol Depend 52(2):99–107, 1998

· James JE : Understanding Caffeine. Thousand Oaks, CA, Sage, 1997

· Juliano LM , Griffiths RR : A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features. Psychopharmacology (Berl) 176(1):1–29, 2004

· Juliano LM , Griffiths RR : Caffeine-related disorders, in Comprehensive Textbook of Psychiatry, 9th Edition. Edited by Sadock BJ , Sadock VA , Ruiz P . Philadelphia, PA, Lippincott Williams & Wilkins, 2009, pp 1296–1308

· Kendler KS , Prescott CA : Caffeine intake, tolerance, and withdrawal in women: a population-based twin study. Am J Psychiatry 156(2):223–228, 1999

· Kendler KS , Myers JO , Gardner C : Caffeine intake, toxicity and dependence and lifetime risk for psychiatric and substance use disorders: an epidemiologic and co-twin control analysis. Psychol Med 36(12):1717–1725, 2006

· Strain EC , Mumford GK , Silverman K , Griffiths RR : Caffeine dependence syndrome: evidence from case histories and experimental evaluations. JAMA 272(13):1043–1048, 1994

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-induced sleep disorder (“Sleep-Wake Disorders”). These caffeine-induced disorders are diagnosed instead of caffeine intoxication or caffeine withdrawal only when the symptoms are sufficiently severe to warrant independent clinical attention.

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, occupational, 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

1. Cannabis Use Disorder

2. Cannabis Intoxication

3. Cannabis Withdrawal

4. Other Cannabis-Induced Disorders

5. Unspecified Cannabis-Related Disorder

Cannabis Use Disorder

Diagnostic Criteria

A. A problematic pattern of cannabis use leading to clinically significant impairment or distress, 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 cannabis, 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 persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of cannabis.

7. Important social, occupational, or recreational activities are given up or reduced because 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 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:

11. The characteristic withdrawal syndrome for cannabis (refer to Criteria A and B of the criteria set for cannabis withdrawal, pp. 517–518).

11. Cannabis (or a closely related substance) is taken to relieve or avoid withdrawal symptoms.

Specify if:

· In early remission: After full criteria for cannabis use 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 desire 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 /remission : 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 disorder). 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 for a moderate or severe cannabis use disorder with cannabis-induced anxiety disorder.

Specify current severity /remission :

· 305.20 (F12.10) Mild: Presence of 2–3 symptoms.

· (F12.11) Mild, In early remission

· (F12.11) Mild, In sustained remission

· 304.30 (F12.20) Moderate: Presence of 4–5 symptoms.

· (F12.21) Moderate, In early remission

· (F12.21) Moderate, In sustained remission

· 304.30 (F12.20) Severe: Presence of 6 or more symptoms.

· (F12.21) Severe, In early remission

· (F12.21) Severe, In sustained remission

Specifiers

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-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 times used per day) and/or dose (e.g., amount used per episode) of cannabis, as assessed by individual self-report, report of knowledgeable others, clinician’s observations, and biological testing.

Diagnostic Features

Cannabis use disorder and the other cannabis-related disorders include problems that are associated with substances derived from the cannabis plant and chemically similar synthetic compounds. Over time, this plant material has accumulated many names (e.g., weed, pot, herb, grass, reefer, mary jane, dagga, 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 psychoactive substance(s) derived from the plant, and as such it is used in this manual to refer to all forms of cannabis-like substances, including synthetic cannabinoid compounds(Budney et al. 2011; Roffman and Stephens 2006).

Synthetic oral formulations (pill/capsules) of delta-9-tetrahydrocannabinol (delta-9-THC) are available by prescription 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 compounds have been manufactured and distributed for nonmedical use in the form of plant material that has been sprayed with a cannabinoid formulation (e.g., K2, Spice, JWH-018, JWH-073)(Seely et al. 2011).

The cannabinoids have diverse effects in the brain, prominent among which are actions on CB1 and CB2 cannabinoid receptors that are found throughout the central nervous system(Tanda and Goldberg 2003). Endogenous ligands for these receptors 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 decades, a steady increase in the potency of seized cannabis has been observed(Mehmedic et al. 2010).

Cannabis is most commonly smoked via a variety of methods: pipes, water pipes (bongs or hookahs), cigarettes (joints or reefers), or, most recently, in the paper from hollowed out cigars (blunts). Cannabis is also sometimes ingested orally, typically by mixing it into food. More recently, devices have been developed in which cannabis is “vaporized.” Vaporization involves heating the plant material to release psychoactive cannabinoids 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 general diagnostic features of a substance use disorder (Budney 2006). Cannabis use disorder is commonly observed as the only substance use disorder experienced by the individual; however, it also frequently occurs concurrently with other types of substance use disorders (i.e., alcohol, cocaine, opioid)(Stinson et al. 2006). 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 effects of cannabis has been reported in individuals who use cannabis persistently(Lichtman and Martin 2005). Generally, tolerance is lost when cannabis use is discontinued 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 aggression, anxiety, depressed mood, restlessness, sleep difficulty, and decreased appetite or weight loss(Budney et al. 2004; Levin et al. 2010). Although typically not as severe as alcohol or opioid withdrawal, the cannabis withdrawal syndrome can cause significant distress and contribute to difficulty quitting or relapse among those trying to abstain(Budney et al. 2008).

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 day under the influence(Roffman and Stephens 2006). 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 family 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). Arguments with spouses or parents over the use of cannabis in the home, or its use in the presence of children, can adversely impact family functioning and are common features of those with cannabis use disorder. Last, individuals with cannabis use disorder may continue using despite knowledge of physical problems (e.g., chronic cough related to smoking) or psychological problems (e.g., excessive sedation or exacerbation of other mental 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 tolerance and withdrawal will naturally occur and should not be used as the primary criteria 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(Stinson et al. 2006). Careful assessment typically reveals reports of cannabis use contributing to exacerbation of these same symptoms, as well as other reasons for frequent use (e.g., to experience euphoria, to forget about problems, in response to anger, as an enjoyable social activity). Related to this issue, some individuals who use cannabis multiple 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 being 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 consequences to other valued activities or relationships (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 intoxication so as to better assess the extent of use. As with other substances, experienced users of cannabis develop behavioral and pharmacological tolerance such that it can be difficult to detect when they are under the influence. Signs of acute and chronic use include red eyes (conjunctival injection), cannabis odor on clothing, 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 cannabis, are the most widely used illicit psychoactive substances in the United States. The 12-month prevalence of cannabis use disorder (DSM-IV abuse and dependence rates combined) is approximately 3.4% among 12- to 17-year-olds and 1.5% among adults age 18 years and older(Stinson et al. 2006). 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 among individuals age 65 years and older (0.01%). The high prevalence of cannabis use disorder likely reflects the much more widespread use of cannabis relative to other illicit drugs 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 highest among Native American and Alaska Natives (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 cannabis use disorder is also highest among Native Americans and Alaska Natives (3.4%) relative 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 disorder has increased among adults and adolescents. Gender differences in cannabis use disorder 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.

Development and Course

The onset of cannabis use disorder can occur at any time during or following adolescence, but onset is most commonly during adolescence or young adulthood(Anthony 2006; Compton et al. 2004). 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 use 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 adolescents, particularly those with pervasive conduct problems(Compton et al. 2004; Stinson et al. 2006). 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 traditionally the first substance that adolescents try. Many perceive cannabis use as less harmful than alcohol or tobacco use, and this perception likely contributes to increased use. Moreover, cannabis intoxication does not typically result in as severe behavioral and cognitive dysfunction as does significant alcohol intoxication, which may increase the probability of more frequent use in more diverse situations than with alcohol. These factors likely contribute to the potential rapid transition from cannabis use to a cannabis use disorder among some adolescents and the common pattern of using throughout the day that is commonly observed among those with more severe cannabis use disorder.

Cannabis use disorder among preteens, adolescents, and young adults is typically expressed as excessive use with peers that is a component of a pattern of other delinquent behaviors usually associated with conduct problems. Milder cases primarily reflect continued use despite clear problems related to disapproval of use by other peers, school administration, 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 throughout the day such that use interferes with daily functioning and takes the place of previously established, prosocial activities.

With adolescent users, changes in mood stability, energy level, and eating patterns are commonly observed. These signs and symptoms are likely due to the direct effects of cannabis use (intoxication) and the subsequent effects following acute intoxication (coming down), as well as attempts to conceal use from others. School-related problems are commonly associated with cannabis use disorder in adolescents, particularly a dramatic drop in grades, truancy, and reduced interest in general school activities and outcomes(Lynskey et al. 2003).

Cannabis use disorder among adults typically involves well-established patterns of daily cannabis use that continue despite clear psychosocial or medical problems. Many adults have experienced repeated desire to stop 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 potential significant consequences of sustained use. The rate of use among middle-age and older adults appears to be increasing, likely because of a cohort effect resulting from high prevalence of use in the late 1960s and the 1970s.

Early onset of cannabis use (e.g., prior to age 15 years) is a robust predictor of the development of cannabis use disorder and other types of substance use disorders and mental disorders during young adulthood(Fergusson et al. 2006; Lynskey et al. 2003). Such early onset is likely related to concurrent other externalizing problems, most notably conduct 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(de Graaf et al. 2010).

Risk and Prognostic Factors

Temperamental

A history of conduct disorder in childhood or adolescence and antisocial personality disorder are risk factors for the development of many substance-related disorders, including cannabis-related disorders. Other risk factors include externalizing or internalizing disorders during childhood or adolescence. Youths with high behavioral disinhibition scores show early-onset substance use disorders, including cannabis use disorder, multiple substance involvement, and early conduct problems(Iacono et al. 2008).

Environmental

Risk factors include academic failure, tobacco smoking, unstable or abusive family situation, use of cannabis among immediate family members, a family history of a substance use disorder, and low socioeconomic status. As with all substances of abuse, the ease of availability of the substance is a risk 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 cannabis use disorders (Agrawal and Lynskey 2009). 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 environmental influences between cannabis and other types of substance use disorders suggest a common genetic basis for adolescent substance use and conduct problems.

Culture-Related Diagnostic Issues

Cannabis is probably the world’s most commonly used illicit substance(Degenhardt et al. 2008). Occurrence of cannabis use disorder across countries is unknown, but the prevalence rates are likely similar among developed countries(Hall and Degenhardt 2007). It is frequently among the first drugs of experimentation (often in the teens) of all cultural groups in the United States(Degenhardt et al. 2010).

Acceptance of cannabis for medical purposes varies widely across and within cultures. Cultural factors (acceptability and legal status) that might impact diagnosis relate to differential consequences across cultures for detection of use (i.e., arrest, school suspensions, or employment suspension). The general change in substance use disorder diagnostic criteria from DSM-IV to DSM-5 (i.e., removal of the recurrent substance-related legal problems criterion) mitigates this concern to some degree.

Diagnostic Markers

Biological tests for cannabinoid metabolites are useful for determining if an individual has recently used cannabis. Such testing is helpful in making a diagnosis, particularly in milder cases if an individual denies using while others (family, work, school) purport concern about a substance use problem. Because cannabinoids are fat soluble, they persist in bodily fluids for extended periods of time and are excreted slowly. Expertise in urine testing methods is needed to reliably interpret results.

Functional Consequences of Cannabis Use Disorder

Functional consequences of cannabis use disorder are part of the diagnostic criteria. Many areas of psychosocial, cognitive, and health functioning may be compromised in relation to cannabis use disorder(Budney et al. 2011). Cognitive function, particularly higher executive function, appears to be compromised in cannabis users, and this relationship appears to be dose dependent (both acutely and chronically)(Grant et al. 2003; Vandrey and Mintzer 2009). This may contribute to increased difficulty at school or work. Cannabis use has been related to a reduction in prosocial goal-directed activity, which some have labeled an amotivational syndrome, that manifests itself in poor school performance and employment problems. These problems may be related to pervasive intoxication or recovery from the effects of intoxication. Similarly, cannabis-associated problems with social relationships are commonly reported in those with cannabis use disorder. Accidents due to engagement in potentially dangerous behaviors while under the influence (e.g., driving, sport, recreational or employment activities) are also of concern. Cannabis smoke contains high levels of carcinogenic compounds that place chronic users at risk for respiratory illnesses similar to those experienced by tobacco smokers. Chronic cannabis use may contribute to the onset or exacerbation of many other mental disorders. In particular, concern has been raised about cannabis use as a causal factor inschizophrenia and other psychotic disorders. Cannabis use can contribute to the onset of an acute psychotic episode, can exacerbate some symptoms, and can adversely affect treatment of a major psychotic illness.

Differential Diagnosis

Nonproblematic use of cannabis

The distinction between nonproblematic use of cannabis and cannabis use disorder can be difficult to make because social, behavioral, or psychological problems may be difficult to attribute to the substance, especially in the context of use of other substances. Also, denial of heavy cannabis use and the attribution that cannabis is related to or causing substantial problems are common among individuals who are referred to treatment by others (i.e., school, family, employer, criminal justice system).

Other mental disorders

Cannabis-induced disorder may be characterized by symptoms (e.g., anxiety) that resemble primary mental disorders (e.g., generalized anxiety disorder vs. cannabis-induced anxiety disorder, with generalized anxiety, with onset during intoxication). Chronic intake of cannabis can produce a lack of motivation that resembles persistent depressive disorder (dysthymia). Acute adverse reactions to cannabis should be differentiated from the symptoms of panic disorder, major depressive disorder,delusional disorder, bipolar disorder, or schizophrenia, paranoid type. Physical examination will usually show an increased pulse and conjunctival injection. Urine toxicological testing can be helpful in making a diagnosis.

Comorbidity

Cannabis has been commonly thought of as a “gateway” drug because individuals who frequently use cannabis have a much greater lifetime probability than nonusers of using what are commonly considered more dangerous substances, like opioids or cocaine(Degenhardt et al. 2010). Cannabis use and cannabis use disorder are highly comorbid with other substance use disorders (Stinson et al. 2006). Co-occurring mental conditions are common in cannabis use disorder (Budney et al. 2011). Cannabis use has been associated with poorer life satisfaction; increased mental health treatment and hospitalization; and higher rates of depression, anxiety disorders, suicide attempts, and conduct disorder. Individuals with past-year or lifetime cannabis use disorder have high rates of alcohol use disorder (greater than 50%) and tobacco use disorder (53%). Rates of other substance use disorders are also likely to be high among individuals with cannabis use disorder. Among those seeking treatment for a cannabis use disorder, 74% report problematic use of a secondary or tertiary substance: alcohol (40%), cocaine (12%), methamphetamine (6%), and heroin or other opiates (2%). Among those younger than 18 years, 61% reported problematic use of a secondary substance: alcohol (48%), cocaine (4%), methamphetamine (2%), and heroin or other opiates (2%). Cannabis use disorder is also often observed as a secondary problem among those with a primary diagnosis of othersubstance use disorders, with approximately 25%–80% of those in treatment for another substance use disorder reporting use of cannabis.

Individuals with past-year or lifetime diagnoses of cannabis use disorder also have high rates of concurrent mental disorders other than substance use disorders(Budney et al. 2011). Major depressive disorder (11%), any anxiety disorder (24%), andbipolar I disorder (13%) are quite common among individuals with a past-year diagnosis of a cannabis use disorder, as are antisocial (30%), obsessive-compulsive, (19%), and paranoid (18%) personality disorders. Approximately 33% of adolescents with cannabis use disorder have internalizing disorders (e.g., anxiety, depression, posttraumatic stress disorder), and 60% have externalizing disorders (e.g., conduct disorder, attention-deficit/hyperactivity disorder).

Although cannabis use can impact multiple aspects of normal human functioning, including the cardiovascular, immune, neuromuscular, ocular, reproductive, and respiratory systems, as well as appetite and cognition/perception, there are few clear medical conditions that commonly co-occur with cannabis use disorder. The most significant health effects of cannabis involve the respiratory system, and chronic cannabis smokers exhibit high rates of respiratory symptoms of bronchitis, sputum production, shortness of breath, and wheezing(Tashkin et al. 2002).

References: Cannabis Use Disorder

· Agrawal A , Lynskey MT : Candidate genes for cannabis use disorders: findings, challenges and directions. Addiction104(4):518–532, 2009

· Anthony JC : The epidemiology of cannabis dependence, in Cannabis Dependence: Its Nature, Consequences and Treatment. Edited by Roffman RA , Stephens RS . Cambridge, UK, Cambridge University Press, 2006, pp 58–95

· Budney AJ : Are specific dependence criteria necessary for different substances: how can research on cannabis inform this issue? Addiction 101(suppl 1):125–133, 2006

· Budney AJ , Hughes JR , Moore BA , Vandrey R : Review of the validity and significance of the cannabis withdrawal syndrome. Am J Psychiatry 161(11):1967–1977, 2004

· Budney AJ , Vandrey RG , Hughes JR , et al: Comparison of cannabis and tobacco withdrawal: severity and contribution to relapse. J Subst Abuse Treat 35(4):362–368, 2008

· Budney A , Vandrey R , Fearer SA : Cannabis (marijuana), in Lowenson and Ruiz’s Substance Abuse: A Comprehensive Textbook, 5th Edition. Edited by Ruiz P , Strain E . Baltimore, MD, Lippincott Williams & Wilkins, 2011, pp 214–237

· Compton WM , Grant BF , Colliver JD , et al: Prevalence of marijuana use disorders in the United States: 1991–1992 and 2001–2002. JAMA 291(17):2114–2121, 2004

· de Graaf R , Radovanovic M , van Laar M , et al: Early cannabis use and estimated risk of later onset of depression spells: epidemiologic evidence from the population-based World Health Organization World Mental Health Survey Initiative. Am J Epidemiol 172(2):149–159, 2010

· Degenhardt L , Chiu WT , Sampson N , et al: Toward a global view of alcohol, tobacco, cannabis, and cocaine use: findings from the WHO World Mental Health Surveys. PLoS Med 5(7):e141, 2008

· Degenhardt L , Dierker L , Chiu WT , et al: Evaluating the drug use “gateway” theory using cross-national data: consistency and associations of the order of initiation of drug use among participants in the WHO World Mental Health Surveys. Drug Alcohol Depend 108(1–2):84–97, 2010

· Fergusson DM , Boden JM , Horwood LJ : Cannabis use and other illicit drug use: testing the cannabis gateway hypothesis.Addiction 101(4):556–569, 2006

· Grant I , Gonzalez R , Carey CL , et al: Non-acute (residual) neurocognitive effects of cannabis use: a meta-analytic study. J Int Neuropsychol Soc 9(5):679–689, 2003

· Hall W , Degenhardt L : Prevalence and correlates of cannabis use in developed and developing countries. Curr Opin Psychiatry 20(4):393–397, 2007

· Iacono WG , Malone SM , McGue M : Behavioral disinhibition and the development of early-onset addiction: common and specific influences. Annu Rev Clin Psychol 4:325–348, 2008

· Levin KH , Copersino ML , Heishman SJ , et al: Cannabis withdrawal symptoms in non-treatment-seeking adult cannabis smokers. Drug Alcohol Depend 111(1–2):120–127, 2010

· Lichtman AH , Martin BR : Cannabinoid tolerance and dependence, in Handbook of Experimental Pharmacology: Cannabinoids. Edited by Pertwee RG . Berlin, Springer-Verlag, 2005, pp 691–717

· Lynskey MT , Hall W : The effects of adolescent cannabis use on educational attainment: a review. Addiction 95(11):1621–1630, 2000

· Lynskey MT , Heath AC , Bucholz KK , et al: Escalation of drug use in early-onset cannabis users vs co-twin controls. JAMA289(4):427–433, 2003

· Mehmedic Z , Chandra S , Slade D , et al: Potency trends of delta9-THC and other cannabinoids in confiscated cannabis preparations from 1993 to 2008. J Forensic Sci 55(5):1209–1217, 2010 10.1111/j.1556-4029.2010.01441.x

· Roffman R , Stephens R (eds): Cannabis Dependence: Its Nature, Consequences, and Treatment. Cambridge, UK, Cambridge University Press, 2006

· Seely KA , Prather PL , James LP , Moran JH : Marijuana-based drugs: innovative therapeutics or designer drugs of abuse?Mol Interv 11(1):36–51, 2011

· Stinson FS , Ruan WJ , Pickering R , Grant BF : Cannabis use disorders in the USA: prevalence, correlates and co-morbidity.Psychol Med 36(10):1447–1460, 2006

· Tanda G , Goldberg SR : Cannabinoids: reward, dependence, and underlying neurochemical mechanisms—a review of recent preclinical data. Psychopharmacology (Berl) 169(2):115–134, 2003

· Tashkin DP , Baldwin GC , Sarafian T , et al: Respiratory and immunologic consequences of marijuana smoking. J Clin Pharmacol 42(11 suppl):71S–81S, 2002

· Vandrey R , Mintzer MZ : Performance and cognitive alterations, in The Pharmacology and Treatment of Substance Abuse: An Evidence-Based Approach. Edited by Cohen L , Collins FL , Young AM , et al. Mahwah, NJ, Erlbaum, 2009, pp 41–62

Cannabis Intoxication

Diagnostic Criteria

A. Recent use of cannabis.

B. Clinically significant problematic behavioral or psychological changes (e.g., impaired motor coordination, euphoria, anxiety, sensation of slowed time, impaired judgment, social withdrawal) that developed during, or shortly after, cannabis use.

C. Two (or more) of the following signs or symptoms developing within 2 hours of cannabis use:

1. Conjunctival injection.

2. Increased appetite.

3. Dry mouth.

4. Tachycardia.

D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication with another substance.

Specify if:

· With perceptual disturbances: Hallucinations with intact reality testing or auditory, visual, or tactile illusions occur in the absence of a delirium.

Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether or not there is a comorbid cannabis use disorder and whether or not there are perceptual disturbances.

· For cannabis intoxication, without perceptual disturbances: If a mild cannabis use disorder is comorbid, the ICD-10-CM code is F12.129, and if a moderate or severe cannabis use disorder is comorbid, the ICD-10-CM code is F12.229. If there is no comorbid cannabis use disorder, then the ICD-10-CM code is F12.929.

· For cannabis intoxication, with perceptual disturbances: If a mild cannabis use disorder is comorbid, the ICD-10-CM code is F12.122, and if a moderate or severe cannabis use disorder is comorbid, the ICD-10-CM code isF12.222. If there is no comorbid cannabis use disorder, then the ICD-10-CM code is F12.922.

Specifiers

When hallucinations occur in the absence of intact reality testing, a diagnosis of substance/medication-induced psychotic disorder should be considered.

Diagnostic Features

The essential feature of cannabis intoxication is the presence of clinically significant problematic behavioral or psychological changes that develop during, or shortly after, cannabis use (Criterion B)(Schuckit 2005). Intoxication typically begins with a “high” feeling followed by symptoms that include euphoria with inappropriate laughter and grandiosity, sedation, lethargy, impairment in short-term memory, difficulty carrying out complex mental processes, impaired judgment, distorted sensory perceptions, impaired motor performance, and the sensation that time is passing slowly. Occasionally, anxiety (which can be severe), dysphoria, or social withdrawal occurs. These psychoactive effects are accompanied by two or more of the following signs, developing within 2 hours of cannabis use: conjunctival injection, increased appetite, dry mouth, and tachycardia (Criterion C).

Intoxication develops within minutes if the cannabis is smoked but may take a few hours to develop if the cannabis is ingested orally. The effects usually last 3–4 hours, with the duration being somewhat longer when the substance is ingested orally. The magnitude of the behavioral and physiological changes depends on the dose, the method of administration, and the characteristics of the individual using the substance, such as rate of absorption, tolerance, and sensitivity to the effects of the substance. Because most cannabinoids, including delta-9-tetrahydrocannabinol (delta-9-THC), are fat soluble, the effects of cannabis or hashish may occasionally persist or reoccur for 12–24 hours because of the slow release of psychoactive substances from fatty tissue or to enterohepatic circulation.

Prevalence

The prevalence of actual episodes of cannabis intoxication in the general population is unknown. However, it is probable that most cannabis users would at some time meet criteria for cannabis intoxication. Given this, the prevalence of cannabis users and the prevalence of individuals experiencing cannabis intoxication are likely similar.

Functional Consequences of Cannabis Intoxication

Impairment from cannabis intoxication may have serious consequences, including dysfunction at work or school, social indiscretions, failure to fulfill role obligations, traffic accidents, and having unprotected sex. In rare cases, cannabis intoxication may precipitate a psychosis that may vary in duration.

Differential Diagnosis

Note that if the clinical presentation includes hallucinations in the absence of intact reality testing, a diagnosis of substance/medication-induced psychotic disorder should be considered.

Other substance intoxication

Cannabis intoxication may resemble intoxication with other types of substances. However, in contrast to cannabis intoxication, alcohol intoxication and sedative, hypnotic, or anxiolytic intoxication frequently decrease appetite, increase aggressive behavior, and produce nystagmus or ataxia. Hallucinogens in low doses may cause a clinical picture that resembles cannabis intoxication. Phencyclidine, like cannabis, can be smoked and also causes perceptual changes, but phencyclidine intoxication is much more likely to cause ataxia and aggressive behavior.

Other cannabis-induced disorders

Cannabis intoxication is distinguished from the other cannabis-induced disorders (e.g., cannabis-induced anxiety disorder, with onset during intoxication) because the symptoms in these latter disorders predominate the clinical presentation and are severe enough to warrant independent clinical attention.

References: Cannabis Intoxication

· Schuckit MA : Drug and Alcohol Abuse: A Clinical Guide to Diagnosis and Treatment, 6th Edition. New York, Springer, 2005, pp 192–209

Cannabis Withdrawal

Diagnostic Criteria

292.0 (F12.288)

A. Cessation of cannabis use that has been heavy and prolonged (i.e., usually daily or almost daily use over a period of at least a few months).

B. Three (or more) of the following signs and symptoms develop within approximately 1 week after Criterion A:

1. Irritability, anger, or aggression.

2. Nervousness or anxiety.

3. Sleep difficulty (e.g., insomnia, disturbing dreams).

4. Decreased appetite or weight loss.

5. Restlessness.

6. Depressed mood.

7. At least one of the following physical symptoms causing significant discomfort: abdominal pain, shakiness/tremors, sweating, fever, chills, or headache.

C. The signs or symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication or withdrawal from another substance.

Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for cannabis withdrawal is F12.288. Note that the ICD-10-CM code indicates the comorbid presence of a moderate or severe cannabis use disorder, reflecting the fact that cannabis withdrawal can only occur in the presence of a moderate or severe cannabis use disorder. It is not permissible to code a comorbid mild cannabis use disorder with cannabis withdrawal.

Diagnostic Features

The essential feature of cannabis withdrawal is the presence of a characteristic withdrawal syndrome that develops after the cessation of or substantial reduction in heavy and prolonged cannabis use. In addition to the symptoms in Criterion B, the following may also be observed postabstinence: fatigue, yawning, difficulty concentrating, and rebound periods of increased appetite and hypersomnia that follow initial periods of loss of appetite and insomnia(Budney et al. 2004; Levin et al. 2010). For the diagnosis, withdrawal symptoms must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). Many cannabis users report smoking cannabis or taking other substances to help relieve withdrawal symptoms, and many report that withdrawal symptoms make quitting difficult or have contributed to relapse(Budney et al. 2008; Copersino et al. 2006). The symptoms typically are not of sufficient severity to require medical attention, but medication or behavioral strategies may help alleviate symptoms and improve prognosis in those trying to quit using cannabis.

Cannabis withdrawal is commonly observed in individuals seeking treatment for cannabis use as well as in heavy cannabis users who are not seeking treatment. Among individuals who have used cannabis regularly during some period of their lifetime, up to one-third report having experienced cannabis withdrawal (Agrawal et al. 2008; Budney and Hughes 2006;Hasin et al. 2008). Among adults and adolescents enrolled in treatment or heavy cannabis users, 50%–95% report cannabis withdrawal (Budney and Hughes 2006; Chung et al. 2008; Copersino et al. 2006; Cornelius et al. 2008; Levin et al. 2010). These findings indicate that cannabis withdrawal occurs among a substantial subset of regular cannabis users who try to quit.

Development and Course

The amount, duration, and frequency of cannabis smoking that is required to produce an associated withdrawal disorder during a quit attempt are unknown. Most symptoms have their onset within the first 24–72 hours of cessation, peak within the first week, and last approximately 1–2 weeks. Sleep difficulties may last more than 30 days. Cannabis withdrawal has been documented among adolescents and adults. Withdrawal tends to be more common and severe among adults, most likely related to the more persistent and greater frequency and quantity of use among adults.

Risk and Prognostic Factors

Environmental

Most likely, the prevalence and severity of cannabis withdrawal are greater among heavier cannabis users, and particularly among those seeking treatment for cannabis use disorders(Budney and Hughes 2006). Withdrawal severity also appears to be positively related to the severity of comorbid symptoms of mental disorders.

Functional Consequences of Cannabis Withdrawal

Cannabis users report using cannabis to relieve withdrawal symptoms, suggesting that withdrawal might contribute to ongoing expression of cannabis use disorder. Worse outcomes may be associated with greater withdrawal(Chung et al. 2008;Cornelius et al. 2008). A substantial proportion of adults and adolescents in treatment for moderate to severe cannabis use disorder acknowledge moderate to severe withdrawal symptoms, and many complain that these symptoms make cessation more difficult. Cannabis users report having relapsed to cannabis use or initiating use of other drugs (e.g., tranquilizers) to provide relief from cannabis withdrawal symptoms. Last, individuals living with cannabis users observe significant withdrawal effects, suggesting that such symptoms are disruptive to daily living.

Differential Diagnosis

Because many of the symptoms of cannabis withdrawal are also symptoms of other substance withdrawal syndromes or of depressive or bipolar disorders, careful evaluation should focus on ensuring that the symptoms are not better explained by cessation from another substance (e.g., tobacco or alcohol withdrawal), another mental disorder (generalized anxiety disorder,major depressive disorder), or another medical condition.

References: Cannabis Withdrawal

· Agrawal A , Pergadia ML , Lynskey MT : Is there evidence for symptoms of cannabis withdrawal in the national epidemiologic survey of alcohol and related conditions? Am J Addict 17(3):199–208, 2008

· Allsop DJ , Norberg MM , Copeland J , et al: The Cannabis Withdrawal Scale development: patterns and predictors of cannabis withdrawal and distress. Drug Alcohol Depend 119(1–2):123–129, 2011

· Budney AJ , Hughes JR : The cannabis withdrawal syndrome. Curr Opin Psychiatry 19(3):233–238, 2006

· Budney AJ , Hughes JR , Moore BA , Vandrey RA : Review of the validity and significance of the cannabis withdrawal syndrome. Am J Psychiatry 161(11):1967–1977, 2004

· Budney A , Moore BA , Vandrey R : Health consequences of marijuana use, in Handbook of the Medical Consequences of Alcohol and Drug Abuse. Edited by Brick J . Philadelphia, PA, Haworth Press/Taylor & Francis, 2008, pp 251–282

· Chung T , Martin CS , Cornelius JR , Clark DB : Cannabis withdrawal predicts severity of cannabis involvement at 1-year follow-up among treated adolescents. Addiction 103(5):787–799, 2008

· Copersino ML , Boyd SJ , Tashkin DP , et al: Cannabis withdrawal among non-treatment-seeking adult cannabis users. Am J Addict 15(1):8–14, 2006

· Cornelius JR , Chung T , Martin C , et al: Cannabis withdrawal is common among treatment-seeking adolescents with cannabis dependence and major depression, and is associated with rapid relapse to dependence. Addict Behav 33(11):1500–1505, 2008

· Hasin DS , Keyes KM , Alderson D , et al: Cannabis withdrawal in the United States: results from NESARC. J Clin Psychiatry69(9):1354–1363, 2008

· Levin KH , Copersino ML , Heishman SJ , et al: Cannabis withdrawal symptoms in non-treatment-seeking adult cannabis smokers. Drug Alcohol Depend 111(1–2):120–127, 2010

Other Cannabis-Induced Disorders

The following cannabis-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): cannabis-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); cannabis-induced anxiety disorder (“Anxiety Disorders”); and cannabis-induced sleep disorder (“Sleep-Wake Disorders”). For cannabis intoxication delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These cannabis-induced disorders are diagnosed instead of cannabis intoxication or cannabis withdrawal when the symptoms are sufficiently severe to warrant independent clinical attention.

Unspecified Cannabis-Related Disorder

292.9 (F12.99)

This category applies to presentations in which symptoms characteristic of a cannabis-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific cannabis-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Hallucinogen-Related Disorders

1. Phencyclidine Use Disorder

2. Other Hallucinogen Use Disorder

3. Phencyclidine Intoxication

4. Other Hallucinogen Intoxication

5. Hallucinogen Persisting Perception Disorder

6. Other Phencyclidine-Induced Disorders

7. Other Hallucinogen-Induced Disorders

8. Unspecified Phencyclidine-Related Disorder

9. Unspecified Hallucinogen-Related Disorder

Phencyclidine Use Disorder

Diagnostic Criteria

A. A pattern of phencyclidine (or a pharmacologically similar substance) use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. Phencyclidine 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 phencyclidine use.

3. A great deal of time is spent in activities necessary to obtain phencyclidine, use the phencyclidine, or recover from its effects.

4. Craving, or a strong desire or urge to use phencyclidine.

5. Recurrent phencyclidine use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences from work or poor work performance related to phencyclidine use; phencyclidine-related absences, suspensions, or expulsions from school; neglect of children or household).

6. Continued phencyclidine use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the phencyclidine (e.g., arguments with a spouse about consequences of intoxication; physical fights).

7. Important social, occupational, or recreational activities are given up or reduced because of phencyclidine use.

8. Recurrent phencyclidine use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by a phencyclidine). 

9. Phencyclidine use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the phencyclidine.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of the phencyclidine to achieve intoxication or desired effect.

b. A markedly diminished effect with continued use of the same amount of the phencyclidine.

Note: Withdrawal symptoms and signs are not established for phencyclidines, and so this criterion does not apply. (Withdrawal from phencyclidines has been reported in animals but not documented in human users.)

Specify if:

· In early remission: After full criteria for phencyclidine use disorder were previously met, none of the criteria for phencyclidine use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the phencyclidine,” may be met).

· In sustained remission: After full criteria for phencyclidine use disorder were previously met, none of the criteria for phencyclidine use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the phencyclidine,” may be met).

Specify if:

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to phencyclidines is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If a phencyclidine intoxication or another phencyclidine-induced mental disorder is also present, do not use the codes below for phencyclidine use disorder. Instead, the comorbid phencyclidine use disorder is indicated in the 4th character of the phencyclidine-induced disorder code (see the coding note for phencyclidine intoxication or a specific phencyclidine-induced mental disorder). For example, if there is comorbid phencyclidine-induced psychotic disorder, only the phencyclidine-induced psychotic disorder code is given, with the 4th character indicating whether the comorbid phencyclidine use disorder is mild, moderate, or severe: F16.159 for mild phencyclidine use disorder with phencyclidine-induced psychotic disorder or F16.259 for a moderate or severe phencyclidine use disorder with phencyclidine-induced psychotic disorder.

Specify current severity /remission :

· 305.90 (F16.10) Mild: Presence of 2–3 symptoms.

· (F16.11) Mild, In early remission

· (F16.11) Mild, In sustained remission

· 304.60 (F16.20) Moderate: Presence of 4–5 symptoms.

· (F16.21) Moderate, In early remission

· (F16.21) Moderate, In sustained remission

· 304.60 (F16.20) Severe: Presence of 6 or more symptoms.

· (F16.21) Severe, In early remission

· (F16.21) Severe, In sustained remission

Specifiers

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Diagnostic Features

The phencyclidines (or phencyclidine-like substances) include phencyclidine (e.g., PCP, “angel dust”) and less potent but similarly acting compounds such as ketamine, cyclohexamine, and dizocilpine. These substances were first developed as dissociative anesthetics in the 1950s and became street drugs in the 1960s. They produce feelings of separation from mind and body (hence “dissociative”) in low doses, and at high doses, stupor and coma can result. These substances are most commonly smoked or taken orally, but they may also be snorted or injected. Although the primary psychoactive effects of PCP last for a few hours, the total elimination rate of this drug from the body typically extends 8 days or longer. The hallucinogenic effects in vulnerable individuals may last for weeks and may precipitate a persistent psychotic episode resembling schizophrenia(Luscher 2009). Ketamine has been observed to have utility in the treatment of major depressive disorder(Aan Het Rot et al. 2012). Withdrawal symptoms have not been clearly established in humans, and therefore the withdrawal criterion is not included in the diagnosis of phencyclidine use disorder.

Associated Features Supporting Diagnosis

Phencyclidine may be detected in urine for up to 8 days or even longer at very high doses(Martin 2008). In addition to laboratory tests to detect its presence, characteristic symptoms resulting from intoxication with phencyclidine or related substances may aid in its diagnosis. Phencyclidine is likely to produce dissociative symptoms, analgesia, nystagmus, and hypertension, with risk of hypotension and shock. Violent behavior can also occur with phencyclidine use, as intoxicated persons may believe that they are being attacked. Residual symptoms following use may resemble schizophrenia.

Prevalence

The prevalence of phencyclidine use disorder is unknown. Approximately 2.5% of the population reports having ever used phencyclidine. The proportion of users increases with age, from 0.3% of 12- to 17-year-olds, to 1.3% of 18- to 25-year-olds, to 2.9% of those age 26 years and older reporting ever using phencyclidine(Substance Abuse and Mental Health Services Administration 2012). There appears to have been an increase among 12th graders in both ever used (to 2.3% from 1.8%) and past-year use (to 1.3% from 1.0%) of phencyclidine(Johnson et al. 2012). Past-year use of ketamine appears relatively stable among 12th graders (1.6%–1.7% over the past 3 years).

Risk and Prognostic Factors

There is little information about risk factors for phencyclidine use disorder. Among individuals admitted to substance abuse treatment, those for whom phencyclidine was the primary substance were younger than those admitted for other substance use, had lower educational levels, and were more likely to be located in the West and Northeast regions of the United States, compared with other admissions(Substance Abuse and Mental Health Services Administration 2004).

Culture-Related Diagnostic Issues

Ketamine use in youths ages 16–23 years has been reported to be more common among whites (0.5%) than among other ethnic groups (range 0%–0.3%)(Wu et al. 2006). Among individuals admitted to substance abuse treatment, those for whom phencyclidine was the primary substance were predominantly black (49%) or Hispanic (29%)(Substance Abuse and Mental Health Services Administration 2004).

Gender-Related Diagnostic Issues

Males make up about three-quarters of those with phencyclidine-related emergency room visits(Thombs 1989).

Diagnostic Markers

Laboratory testing may be useful, as phencyclidine is present in the urine in intoxicated individuals up to 8 days after ingestion(Martin 2008). The individual’s history, along with certain physical signs, such as nystagmus, analgesia and prominent hypertension, may aid in distinguishing the phencyclidine clinical picture from that of other hallucinogens.

Functional Consequences of Phencyclidine Use Disorder

In individuals with phencyclidine use disorder, there may be physical evidence of injuries from accidents, fights, and falls. Chronic use of phencyclidine may lead to deficits in memory, speech, and cognition that may last for months(Hanson et al. 2012). Cardiovascular and neurological toxicities (e.g., seizures, dystonias, dyskinesias, catalepsy, hypothermia or hyperthermia) may result from intoxication with phencyclidine(O'Brien 2011). Other consequences include intracranial hemorrhage, rhabdomyolysis, respiratory problems, and (occasionally) cardiac arrest(Baldridge and Bessen 1990).

Differential Diagnosis

Other substance use disorders

Distinguishing the effects of phencyclidine from those of other substances is important, since it may be a common additive to other substances (e.g., cannabis, cocaine).

Schizophrenia and other mental disorders

Some of the effects of phencyclidine and related substance use may resemble symptoms of other psychiatric disorders, such as psychosis (schizophrenia), low mood (major depressive disorder), violent aggressive behaviors (conduct disorder, antisocial personality disorder). Discerning whether these behaviors occurred before the intake of the drug is important in the differentiation of acute drug effects from preexisting mental disorder. Phencyclidine-induced psychotic disorder should be considered when there is impaired reality testing in individuals experiencing disturbances in perception resulting from ingestion of phencyclidine.

References: Phencyclidine Use Disorder

· Aan Het Rot M , Zarate CA Jr , Charney DS , Mathew SJ : Ketamine for depression: where do we go from here? Biol Psychiatry 72(7):537–547, 2012

· Baldridge EB , Bessen HA : Phencyclidine. Emerg Med Clin North Am 8(3):541–550, 1990

· Hanson GR , Venturelli PJ , Fleckenstein AE : Drugs and Society, 11th Edition. Burlington, MA, Jones & Bartlett Learning,2012, pp 368–371

· Johnston LD , O’Malley PM , Bachman JG , Schulenberger JE : Monitoring the Future national results on adolescent drug use: overview of key findings, 2011. Ann Arbor, Institute for Social Research, The University of Michigan, 2012

· Luscher C : Drugs of abuse, in Basic and Clinical Pharmacology, 11th Edition. Edited by Katzung BG , Masters SB , Trevor AJ. Chicago, IL, McGraw-Hill Medical, 2009, pp 553–558

· Martin PR : Substance-related disorders, in Current Diagnosis and Treatment: Psychiatry, 2nd Edition. Edited by Ebert MH , Loosen PT , Nurcombe B , Leckman JF . New York, McGraw-Hill Medical, 2008, pp 230–260

· O’Brien CP : Drug addiction, in Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12th Edition. Edited by Brunton L , Chabner B , Knollman B . New York, McGraw-Hill Professional, 2011, pp 649–668

· Substance Abuse and Mental Health Services Administration, Office of Applied Studies : Characteristics of primary phencyclidine (PCP) admissions, 2001. The DASIS Report, May 7, 2004

· Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality : National Survey on Drug Use and Health (NSDUH) series. 2009 and 2010. Available at:http://www.icpsr.umich.edu.ezp.waldenulibrary.org/icpsrweb/SAMHDA/series/64. Accessed September 20, 2012.

· Thombs DL : A review of PCP abuse trends and perceptions. Public Health Rep 104(4):325–328, 1989

· Wu LT , Schlenger WE , Galvin DM : Concurrent use of methamphetamine, MDMA, LSD, ketamine, GHB, and flunitrazepam among American youths. Drug Alcohol Depend 84(1):102–113, 2006

Other Hallucinogen Use Disorder

Diagnostic Criteria

A. A problematic pattern of hallucinogen (other than phencyclidine) use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. The hallucinogen is often taken in larger amounts or over a longer period than was intended.

2. There is a persistent desire or unsuccessful efforts to cut down or control hallucinogen use.

3. A great deal of time is spent in activities necessary to obtain the hallucinogen, use the hallucinogen, or recover from its effects.

4. Craving, or a strong desire or urge to use the hallucinogen.

5. Recurrent hallucinogen use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences from work or poor work performance related to hallucinogen use; hallucinogen-related absences, suspensions, or expulsions from school; neglect of children or household).

6. Continued hallucinogen use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the hallucinogen (e.g., arguments with a spouse about consequences of intoxication; physical fights).

7. Important social, occupational, or recreational activities are given up or reduced because of hallucinogen use.

8. Recurrent hallucinogen use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by the hallucinogen).

9. Hallucinogen 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 the hallucinogen.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of the hallucinogen to achieve intoxication or desired effect.

b. A markedly diminished effect with continued use of the same amount of the hallucinogen.

Note: Withdrawal symptoms and signs are not established for hallucinogens, and so this criterion does not apply.

Specify the particular hallucinogen.

Specify if:

· In early remission: After full criteria for other hallucinogen use disorder were previously met, none of the criteria for other hallucinogen use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the hallucinogen,” may be met).

· In sustained remission: After full criteria for other hallucinogen use disorder were previously met, none of the criteria for other hallucinogen use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the hallucinogen,” may be met).

Specify if:

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to hallucinogens is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If a hallucinogen intoxication or another hallucinogen-induced mental disorder is also present, do not use the codes below for hallucinogen use disorder. Instead, the comorbid hallucinogen use disorder is indicated in the 4th character of the hallucinogen-induced disorder code (see the coding note for hallucinogen intoxication or specific hallucinogen-induced mental disorder). For example, if there is comorbid hallucinogen-induced psychotic disorder and hallucinogen use disorder, only the hallucinogen-induced psychotic disorder code is given, with the 4th character indicating whether the comorbid hallucinogen use disorder is mild, moderate, or severe: F16.159 for mild hallucinogen use disorder with hallucinogen-induced psychotic disorder or F16.259 for a moderate or severe hallucinogen use disorder with hallucinogen-induced psychotic disorder.

Specify current severity /remission :

· 305.30 (F16.10) Mild: Presence of 2–3 symptoms.

· (F16.11) Mild, In early remission

· (F16.11) Mild, In sustained remission

· 304.50 (F16.20) Moderate: Presence of 4–5 symptoms.

· (F16.21) Moderate, In early remission

· (F16.21) Moderate, In sustained remission

· 304.50 (F16.20) Severe: Presence of 6 or more symptoms.

· (F16.21) Severe, In early remission

· (F16.21) Severe, In sustained remission

Specifiers

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Diagnostic Features

Hallucinogens comprise a diverse group of substances that, despite having different chemical structures and possibly involving different molecular mechanisms, produce similar alterations of perception, mood, and cognition in users. Hallucinogens included are phenylalkylamines (e.g., mescaline, DOM [2,5-dimethoxy-4-methylamphetamine], and MDMA [3,4-methylenedioxymethamphetamine; also called “ecstasy”]); the indoleamines, including psilocybin (i.e., psilocin) and dimethyltryptamine (DMT); and the ergolines, such as LSD (lysergic acid diethylamide) and morning glory seeds. In addition, miscellaneous other ethnobotanical compounds are classified as “hallucinogens,” of which Salvia divinorum and jimsonweed are two examples. Excluded from the hallucinogen group are cannabis and its active compound, delta-9-tetrahydrocannabinol (THC) (see the section “Cannabis-Related Disorders”). These substances can have hallucinogenic effects but are diagnosed separately because of significant differences in their psychological and behavioral effects.

Hallucinogens are usually taken orally, although some forms are smoked (e.g., DMT, salvia) or (rarely) taken intranasally or by injection (e.g., ecstasy). Duration of effects varies across types of hallucinogens. Some of these substances (i.e., LSD, MDMA) have a long half-life and extended duration such that users may spend hours to days using and/or recovering from the effects of these drugs. However, other hallucinogenic drugs (e.g., DMT, salvia) are short acting. Tolerance to hallucinogens develops with repeated use and has been reported to have both autonomic and psychological effects(Passie et al. 2008). Cross-tolerance exists between LSD and other hallucinogens (e.g., psilocybin, mescaline) but does not extend to other drug categories such as amphetamines and cannabis(Passie et al. 2008).

MDMA/ecstasy as a hallucinogen may have distinctive effects attributable to both its hallucinogenic and its stimulant properties. Among heavy ecstasy users, continued use despite physical or psychological problems, tolerance, hazardous use, and spending a great deal of time obtaining the substance are the most commonly reported criteria—over 50% in adults(Cottler et al. 2009) and over 30% in a younger sample(Cottler et al. 2001), while legal problems related to substance use and persistent desire/inability to quit are rarely reported. As found for other substances, diagnostic criteria for other hallucinogen use disorder are arrayed along a single continuum of severity(Kerridge et al. 2011; L. T. Wu et al. 2010).

One of the generic criteria for substance use disorders, a clinically significant withdrawal syndrome, has not been consistently documented in humans, and therefore the diagnosis of hallucinogen withdrawal syndrome is not included in DSM-5. However, there is evidence of withdrawal from MDMA, with endorsement of two or more withdrawal symptoms observed in 59%–98% in selected samples of ecstasy users. Both psychological and physical problems have been commonly reported as withdrawal problems(Cottler et al. 2001; Cottler et al. 2009).

Associated Features Supporting Diagnosis

The characteristic symptom features of some of the hallucinogens can aid in diagnosis if urine or blood toxicology results are not available. For example, individuals who use LSD tend to experience visual hallucinations that can be frightening. Individuals intoxicated with hallucinogens may exhibit a temporary increase in suicidality(Halpern 2003).

Prevalence

Of all substance use disorders, other hallucinogen use disorder is one of the rarest. The 12-month prevalence is estimated to be 0.5% among 12- to 17-year-olds(Substance Abuse and Mental Health Services Administration 2011) and 0.1% among adults age 18 and older in the United States(Compton et al. 2007). Rates are higher in adult males (0.2%) compared with females (0.1%), but the opposite is observed in adolescent samples ages 12–17, in which the 12-month rate is slightly higher in females (0.6%) than in males (0.4%). Rates are highest in individuals younger than 30 years, with the peak occurring in individuals ages 18–29 years (0.6%) and decreasing to virtually 0.0% among individuals age 45 and older.

There are marked ethnic differences in 12-month prevalence of other hallucinogen use disorder. Among youths ages 12–17 years, 12-month prevalence is higher among Native Americans and Alaska Natives (1.2%) than among Hispanics (0.6%), whites (0.6%), African Americans (0.2%), and Asian Americans and Pacific Islanders (0.2%). Among adults, 12-month prevalence of other hallucinogen use disorder is similar for Native Americans and Alaska Natives, whites, and Hispanics (all 0.2%) but somewhat lower for Asian Americans and Pacific Islanders (0.07%) and African Americans (0.03%). Past-year prevalence is higher in clinical samples (e.g., 19% in adolescents in treatment)(Chung and Martin 2005). Among individuals currently using hallucinogens in the general population, 7.8% (adult) to 17% (adolescent) had a problematic pattern of use that met criteria for past-year other hallucinogen use disorder (Wu et al. 2008; Wu et al. 2009b). Among select groups of individuals who use hallucinogens (e.g., recent heavy ecstasy use), 73.5% of adults and 77% of adolescents have a problematic pattern of use that may meet other hallucinogen use disorder criteria(Cottler et al. 2001; Cottler et al. 2009).

Development and Course

Unlike most substances where an early age at onset is associated with elevations in risk for the corresponding use disorder, it is unclear whether there is an association of an early age at onset with elevations in risk for other hallucinogen use disorder. However, patterns of drug consumption have been found to differ by age at onset, with early-onset ecstasy users more likely to be polydrug users than their later-onset counterparts(Wu et al. 2009c). There may be a disproportionate influence of use of specific hallucinogens on risk of developing other hallucinogen use disorder, with use of ecstasy/MDMA increasing the risk of the disorder relative to use of other hallucinogens(Wu et al. 2009b).

Little is known regarding the course of other hallucinogen use disorder, but it is generally thought to have low incidence, low persistence, and high rates of recovery. Adolescents are especially at risk for using these drugs, and it is estimated that 2.7% of youths ages 12–17 years have used one or more of these drugs in the past 12 months, with 44% having used ecstasy/MDMA(Wu et al. 2009b). Other hallucinogen use disorder is a disorder observed primarily in individuals younger than 30 years, with rates vanishingly rare among older adults.

Risk and Prognostic Factors

Temperamental

In adolescents but not consistently in adults, MDMA use is associated with an elevated rate of other hallucinogen use disorder(Wu et al. 2008; Wu et al. 2009a; Wu et al. 2009b). Other substance use disorders, particularly alcohol, tobacco, and cannabis, and major depressive disorder are associated with elevated rates of other hallucinogen use disorder (Wu et al. 2008; Wu et al. 2009b). Antisocial personality disorder may be elevated among individuals who use more than two other drugs in addition to hallucinogens, compared with their counterparts with less extensive use history(Wu et al. 2009c). The influence of adult antisocial behaviors—but not conduct disorder or antisocial personality disorder—on other hallucinogen use disorder may be stronger in females than in males(Compton et al. 2005). Use of specific hallucinogens (e.g., salvia) is prominent among individuals ages 18–25 years with other risk-taking behaviors and illegal activities(Perron et al. 2012). Cannabis use has also been implicated as a precursor to initiation of use of hallucinogens (e.g., ecstasy)(Zimmermann et al. 2005), along with early use of alcohol and tobacco(P. Wu et al. 2010). Higher drug use by peers and high sensation seeking have also been associated with elevated rates of ecstasy use(Martins et al. 2008). MDMA/ecstasy use appears to signify a more severe group of hallucinogen users.

Genetic and physiological

Among male twins, total variance due to additive genetics has been estimated to range from 26% to 79%, with inconsistent evidence for shared environmental influences(Kendler et al. 2000; Tsuang et al. 1998).

Culture-Related Diagnostic Issues

Historically, hallucinogens have been used as part of established religious practices, such as the use of peyote in the Native American Church and in Mexico. Ritual use by indigenous populations of psilocybin obtained from certain types of mushrooms has occurred in South America, Mexico, and some areas in the United States, or of ayahuasca in the Santo Daime and União de Vegetal sects(El-Mallakh et al. 2008). Regular use of peyote as part of religious rituals is not linked to neuropsychological or psychological deficits(Halpern et al. 2005). For adults, no race or ethnicity differences for the full criteria or for any individual criterion are apparent at this time.

Gender-Related Diagnostic Issues

In adolescents, females may be less likely than males to endorse “hazardous use,” and female gender may be associated with increased odds of other hallucinogen use disorder (L. T. Wu et al. 2010).

Diagnostic Markers

Laboratory testing can be useful in distinguishing among the different hallucinogens. However, because some agents (e.g., LSD) are so potent that as little as 75 micrograms can produce severe reactions, typical toxicological examination will not always reveal which substance has been used.

Functional Consequences of Other Hallucinogen Use Disorder

There is evidence for long-term neurotoxic effects of MDMA/ecstasy use, including impairments in memory, psychological function, and neuroendocrine function; serotonin system dysfunction; and sleep disturbance; as well as adverse effects on brain microvasculature, white matter maturation, and damage to axons(Gouzoulis-Mayfrank and Daumann 2009). Use of MDMA/ecstasy may diminish functional connectivity among brain regions(Salomon et al. 2011).

Differential Diagnosis

Other substance use disorders

The effects of hallucinogens must be distinguished from those of other substances (e.g., amphetamines), especially because contamination of the hallucinogens with other drugs is relatively common.

Schizophrenia

Schizophrenia also must be ruled out, as some affected individuals (e.g., individuals with schizophrenia who exhibit paranoia) may falsely attribute their symptoms to use of hallucinogens(El-Mallakh et al. 2008).

Other mental disorders or medical conditions

Other potential disorders or conditions to consider include panic disorder, depressive and bipolar disorders, alcohol or sedative withdrawal, hypoglycemia and other metabolic conditions, seizure disorder, stroke, ophthalmological disorder, and central nervous system tumors(El-Mallakh et al. 2008). Careful history of drug taking, collateral reports from family and friends (if possible), age, clinical history, physical examination, and toxicology reports should be useful in arriving at the final diagnostic decision.

Comorbidity

Adolescents who use MDMA/ecstasy and other hallucinogens, as well as adults who have recently used ecstasy, have a higher prevalence of other substance use disorders compared with nonhallucinogen substance users(Wu et al. 2009a; Wu et al. 2009b). Individuals who use hallucinogens exhibit elevations of nonsubstance mental disorders (especially anxiety, depressive, and bipolar disorders), particularly with use of ecstasy and salvia(Perron et al. 2012; Wu et al. 2009a; Wu et al. 2009c). Rates of antisocial personality disorder (but not conduct disorder) are significantly elevated among individuals with other hallucinogen use disorder, as are rates of adult antisocial behavior(Compton et al. 2005). However, it is unclear whether the mental illnesses may be precursors to rather than consequences of other hallucinogen use disorder (see the section “Risk and Prognostic Factors” for this disorder). Both adults and adolescents who use ecstasy are more likely than other drug users to be polydrug users and to have other drug use disorders(Wu et al. 2009a; Wu et al. 2009b).

References: Other Hallucinogen Use Disorder

· Chung T , Martin CS : Classification and short-term course of DSM-IV cannabis, hallucinogen, cocaine, and opioid disorders in treated adolescents. J Consult Clin Psychol 73(6):995–1004, 2005

· Compton WM , Conway KP , Stinson FS , et al: Prevalence, correlates, and comorbidity of DSM-IV antisocial personality syndromes and alcohol and specific drug use disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions. J Clin Psychiatry 66(6):677–685, 2005

· Compton WM , Thomas YF , Stinson FS , Grant BF : Prevalence, correlates, disability, and comorbidity of DSM-IV drug abuse and dependence in the United States: results from the national epidemiologic survey on alcohol and related conditions. Arch Gen Psychiatry 64(5):566–576, 2007

· Cottler LB , Womack SB , Compton WM , Ben-Abdallah A : Ecstasy abuse and dependence among adolescents and young adults: applicability and reliability of DSM-IV criteria. Hum Psychopharmacol 16(8):599–606, 2001

· Cottler LB , Leung KS , Abdallah AB : Test-re-test reliability of DSM-IV adopted criteria for 3,4-methylenedioxymethamphetamine (MDMA) abuse and dependence: a cross-national study. Addiction 104(10):1670–1690,2009

· El-Mallakh RS , Halpern JH , Abraham HD : Substance abuse: hallucinogen- and MDMA-related disorders, in Psychiatry,, 3rd Edition. Edited by Tasman A , Kay J , Lieberman JA , et al. London, Wiley, 2008, pp 1100–1126

· Gouzoulis-Mayfrank E , Daumann J : Neurotoxicity of drugs of abuse—the case of methylenedioxyamphetamines (MDMA, ecstasy) and amphetamines. Dialogues Clin Neurosci 11(3):305–317, 2009

· Halpern JH : Hallucinogens: an update. Curr Psychiatry Rep 5(5):347–354, 2003

· Halpern JH , Sherwood AR , Hudson JI , et al: Psychological and cognitive effects of long-term peyote use among Native Americans. Biol Psychiatry 58(8):624–631, 2005

· Kendler KS , Karkowski LM , Neale MC , Prescott CA : Illicit psychoactive substance use, heavy use, abuse and dependence in a US population-based sample of male twins. Arch Gen Psychiatry 57(3):261–269, 2000

· Kerridge BT , Saha TD , Smith S , et al: Dimensionality of hallucinogen and inhalant/solvent abuse and dependence criteria: implications for the Diagnostic and Statistical Manual of Mental Disorders—Fifth Edition. Addict Behav 36(9):912–918, 2011doi.10.1016/j.addbeh.2011.04.006

· Martins SS , Storr CL , Alexandre PK , Chilcoat HD : Adolescent ecstasy and other drug use in the National Survey of Parents and Youth: the role of sensation-seeking, parental monitoring and peer’s drug use. Addict Behav 33(7):919–933, 2008

· Passie T , Halpern JH , Stichtenoth DO , et al: The pharmacology of lysergic acid diethylamide: a review. CNS Neurosci Ther14(4):295–314, 2008

· Perron BE , Ahmedani BK , Vaughn MG , et al: Use of Salvia divinorum in a nationally representative sample. Am J Drug Alcohol Abuse 38(1):108–113, 2012 10.3109/00952990.2011.600397

· Salomon RM , Karageorgiou J , Dietrich MS , et al: MDMA (Ecstasy) association with impaired fMRI BOLD thalamic coherence and functional connectivity. Drug Alcohol Depend 120(1–3):41–47, 2011 10.1016/j.drugalcdep.2011.06.022

· Substance Abuse and Mental Health Services Administration : Results From the 2010 National Survey on Drug Use and Health: Summary of National Findings. NSDUH Series H-41, HHS Publication No (SMA) 11-4658. Rockville, MD, Substance Abuse and Mental Health Services Administration, September 2011. Available at:http://www.samhsa.gov/data/NSDUH/2k10Results/Web/HTML/2k10Results.htm. Accessed March 20, 2012.

· Tsuang MT , Lyons MJ , Meyer JM , et al: Co-occurrence of abuse of different drugs in men: the role of drug-specific and shared vulnerabilities. Arch Gen Psychiatry 55(11):967–972, 1998

· Wu LT , Ringwalt CL , Mannelli P , Patkar AA : Hallucinogen use disorders among adult users of MDMA and other hallucinogens. Am J Addict 17(5):354–363, 2008

· Wu LT , Parrott AC , Ringwalt CL , et al: The high prevalence of substance use disorders among recent MDMA users compared with other drug users: implications for intervention. Addict Behav 34(8):654–661, 2009a

· Wu LT , Ringwalt CL , Weiss RD , Blazer DG : Hallucinogen-related disorders in a national sample of adolescents: the influence of ecstasy/MDMA use. Drug Alcohol Dep 104(1–2):156–166, 2009b

· Wu LT , Parrott AC , Ringwalt CL , et al: The variety of ecstasy/MDMA users: results from the National Epidemiologic Survey on alcohol and related conditions. Am J Addict 18(6):452–461, 2009c

· Wu LT , Pan JJ , Yang C , et al: An item response theory analysis of DSM-IV criteria for hallucinogen abuse and dependence in adolescents. Addict Behav 35(3):273–277, 2010

· Wu P , Liu X , Fan B : Factors associated with initiation of ecstasy use among US adolescents: findings from a national survey. Drug Alcohol Depend 106(2–3):193–198, 2010

· Zimmermann P , Wittchen HU , Waszak F , et al: Pathways into ecstasy use: the role of prior cannabis use and ecstasy availability. Drug Alcohol Depend 79(3):331–341, 2005

Phencyclidine Intoxication

Diagnostic Criteria

A. Recent use of phencyclidine (or a pharmacologically similar substance).

B. Clinically significant problematic behavioral changes (e.g., belligerence, assaultiveness, impulsiveness, unpredictability, psychomotor agitation, impaired judgment) that developed during, or shortly after, phencyclidine use.

C. Within 1 hour, two (or more) of the following signs or symptoms:

Note: When the drug is smoked, “snorted,” or used intravenously, the onset may be particularly rapid.

1. Vertical or horizontal nystagmus.

2. Hypertension or tachycardia.

3. Numbness or diminished responsiveness to pain.

4. Ataxia.

5. Dysarthria.

6. Muscle rigidity.

7. Seizures or coma.

8. Hyperacusis.

D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication with another substance.

Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether there is a comorbid phencyclidine use disorder. If a mild phencyclidine use disorder is comorbid, the ICD-10-CM code is F16.129, and if a moderate or severe phencyclidine use disorder is comorbid, the ICD-10-CM code is F16.229. If there is no comorbid phencyclidine use disorder, then the ICD-10-CM code is F16.929.

Note: In addition to the section “Functional Consequences of Phencyclidine Intoxication,” see the corresponding section in phencyclidine use disorder.

Diagnostic Features

Phencyclidine intoxication reflects the clinically significant behavioral changes that occur shortly after ingestion of this substance (or a pharmacologically similar substance). The most common clinical presentations of phencyclidine intoxicationinclude disorientation, confusion without hallucinations, hallucinations or delusions, a catatonic-like syndrome, and coma of varying severity(McCarron et al. 1981a). The intoxication typically lasts for several hours but, depending on the type of clinical presentation and whether other drugs besides phencyclidine were consumed, may last for several days or longer(McCarron et al. 1981a).

Prevalence

Use of phencyclidine or related substances may be taken as an estimate of the prevalence of intoxication. Approximately 2.5% of the population reports having ever used phencyclidine(Substance Abuse and Mental Health Services Administration 2011). Among high school students, 2.3% of 12th graders report ever using phencyclidine, with 57% having used in the past 12 months(Johnston et al. 2012). This represents an increase from prior to 2011. Past-year use of ketamine, which is assessed separately from other substances, has remained stable over time, with about 1.7% of 12th graders reporting use.

Diagnostic Markers

Laboratory testing may be useful, as phencyclidine is detectable in urine for up to 8 days following use, although the levels are only weakly associated with an individual’s clinical presentation and may therefore not be useful for case management. Creatine phosphokinase and aspartate aminotransferase levels may be elevated.

Functional Consequences of Phencyclidine Intoxication

Phencyclidine intoxication produces extensive cardiovascular and neurological (e.g., seizures, dystonias, dyskinesias, catalepsy, hypothermia or hyperthermia) toxicity.

Differential Diagnosis

In particular, in the absence of intact reality testing (i.e., without insight into any perceptual abnormalities), an additional diagnosis of phencyclidine-induced psychotic disorder should be considered.

Other substance intoxication

Phencyclidine intoxication should be differentiated from intoxication due to other substances, including other hallucinogens; amphetamine, cocaine, or other stimulants; and anticholinergics, as well as withdrawal from benzodiazepines(Bey and Patel 2007). Nystagmus and bizarre and violent behavior may distinguish intoxication due to phencyclidine from that due to other substances(Baldridge and Bessen 1990; McCarron et al. 1981b). Toxicological tests may be useful in making this distinction, since phencyclidine is detectable in urine for up to 8 days after use. However, there is a weak correlation between quantitative toxicology levels of phencyclidine and clinical presentation that diminishes the utility of the laboratory findings for patient management(Baldridge and Bessen 1990; Bey and Patel 2007; McCarron et al. 1981b).

Other conditions

Other conditions to be considered include schizophrenia, depression, withdrawal from other drugs (e.g., sedatives, alcohol), certain metabolic disorders like hypoglycemia and hyponatremia, central nervous system tumors, seizure disorders, sepsis, neuroleptic malignant syndrome, and vascular insults(Bey and Patel 2007).

References: Phencyclidine Intoxication

· Baldridge EB , Bessen HA : Phencyclidine. Emerg Med Clin North Am 8(3):541–550, 1990

· Bey T , Patel A : Phencyclidine intoxicatiaon and adverse effects: a clinical and pharmacological review of an illicit drug. Cal J Emerg Med 8(1):9–14, 2007

· Johnston LD , O’Malley PM , Bachman JG , Schulenberger JE : Monitoring the Future National Results on Adolescent Drug Use: overview of key findings, 2011. Ann Arbor, Institute for Social Research, The University of Michigan, 2012

· McCarron MM , Schulze BW , Thompson GA , et al: Acute phencyclidine intoxication: clinical patterns, complications, and treatment. Ann Emerg Med 10(6):290–297, 1981a

· McCarron MM , Schulze BW , Thompson GA , et al: Acute phencyclidine intoxication: incidence of clinical findings in 1,000 cases. Ann Emerg Med 10(5):237–242, 1981b

· Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality : National Survey on Drug Use and Health (NSDUH) series. 2009 and 2010. Available at:http://www.icpsr.umich.edu.ezp.waldenulibrary.org/icpsrweb/SAMHDA/series/64. Accessed September 20, 2012.

Other Hallucinogen Intoxication

Diagnostic Criteria

A. Recent use of a hallucinogen (other than phencyclidine).

B. Clinically significant problematic behavioral or psychological changes (e.g., marked anxiety or depression, ideas of reference, fear of “losing one’s mind,” paranoid ideation, impaired judgment) that developed during, or shortly after, hallucinogen use.

C. Perceptual changes occurring in a state of full wakefulness and alertness (e.g., subjective intensification of perceptions, depersonalization, derealization, illusions, hallucinations, synesthesias) that developed during, or shortly after, hallucinogen use.

D. Two (or more) of the following signs developing during, or shortly after, hallucinogen use:

1. Pupillary dilation.

2. Tachycardia.

3. Sweating.

4. Palpitations.

5. Blurring of vision.

6. Tremors.

7. Incoordination.

E. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication with another substance.

Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether there is a comorbid hallucinogen use disorder. If a mild hallucinogen use disorder is comorbid, the ICD-10-CM code is F16.129, and if a moderate or severe hallucinogen use disorder is comorbid, the ICD-10-CM code is F16.229. If there is no comorbid hallucinogen use disorder, then the ICD-10-CM code is F16.929.

Note: For information on Associated Features Supporting Diagnosis and Culture-Related Diagnostic Issues, see the corresponding sections in other hallucinogen use disorder.

Diagnostic Features

Other hallucinogen intoxication reflects the clinically significant behavioral or psychological changes that occur shortly after ingestion of a hallucinogen. Depending on the specific hallucinogen, the intoxication may last only minutes (e.g., for salvia) or several hours or longer (e.g., for LSD [lysergic acid diethylamide] or MDMA [3,4-methylenedioxymethamphetamine]).

Prevalence

The prevalence of other hallucinogen intoxication may be estimated by use of those substances. In the United States, 1.8% of individuals age 12 years or older report using hallucinogens in the past year. Use is more prevalent among younger individuals, with 3.1% of 12- to 17-year-olds and 7.1% of 18- to 25-year-olds using hallucinogens in the past year, compared with only 0.7% of individuals age 26 years or older(Substance Abuse and Mental Health Services Administration 2011). Twelve-month prevalence for hallucinogen use is more common in males (2.4%) than in females (1.2%), and even more so among 18- to 25-year-olds (9.2% for males vs. 5.0% for females). In contrast, among individuals ages 12–17 years, there are no gender differences (3.1% for both genders). These figures may be used as proxy estimates for gender-related differences in the prevalence of other hallucinogen intoxication.

Suicide Risk

Other hallucinogen intoxication may lead to increased suicidality, although suicide is rare among users of hallucinogens(Halpern 2003; Martin 2008).

Functional Consequences of Other Hallucinogen Intoxication

Other hallucinogen intoxication can have serious consequences. The perceptual disturbances and impaired judgment associated with other hallucinogen intoxication can result in injuries or fatalities from automobile crashes, physical fights, or unintentional self-injury (e.g., attempts to “fly” from high places). Environmental factors and the personality and expectations of the individual using the hallucinogen may contribute to the nature of and severity of hallucinogen intoxication. Continued use of hallucinogens, particularly MDMA, has also been linked with neurotoxic effects(de Win et al. 2008).

Differential Diagnosis

Other substance intoxication

Other hallucinogen intoxication should be differentiated from intoxication with amphetamines, cocaine, or other stimulants; anticholinergics; inhalants; and phencyclidine. Toxicological tests are useful in making this distinction, and determining the route of administration may also be useful.

Other conditions

Other disorders and conditions to be considered include schizophrenia, depression, withdrawal from other drugs (e.g., sedatives, alcohol), certain metabolic disorders (e.g., hypoglycemia), seizure disorders, tumors of the central nervous system, and vascular insults(El-Mallakh et al. 2008).

Hallucinogen persisting perception disorder

Other hallucinogen intoxication is distinguished from hallucinogen persisting perception disorder because the symptoms in the latter continue episodically or continuously for weeks (or longer) after the most recent intoxication.

Other hallucinogen-induced disorders

Other hallucinogen intoxication is distinguished from the other hallucinogen-induced disorders (e.g., hallucinogen-induced anxiety disorder, with onset during intoxication) because the symptoms in these latter disorders predominate the clinical presentation and are severe enough to warrant independent clinical attention.

References: Other Hallucinogen Intoxication

· de Win MM , Jager G , Booij J , et al: :Neurotoxic effects of ecstasy on the thalamus. Br J Psychiatry 193(4):289–296, 2008

· El-Mallakh RS , Halpern JH , Abraham HD : Substance abuse: hallucinogen- and MDMA-related disorders, in Psychiatry, 3rd Edition. Edited by Tasman A , Kay J , Lieberman JA , et al. London, Wiley, 2008, pp 1100–1126

· Halpern JH : Hallucinogens: an update. Curr Psychiatry Rep 5(5):347–354, 2003

· Martin PR : Substance-related disorders, in Current Diagnosis and Treatment: Psychiatry, 2nd Edition. Edited by Ebert MH , Loosen PT , Nurcombe B , Leckman JF . New York, McGraw-Hill Medical, 2008, pp 230–260

· Substance Abuse and Mental Health Services Administration : Results from the 2010 National Survey on Drug Use and Health: summary of national findings. NSDUH Series H-41, HHS Publ No (SMA) 11-4658. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2011. Available at:http://www.samhsa.gov/data/NSDUH/2k10Results/Web/HTML/2k10Results.htm. Accessed March 20, 2012.

Hallucinogen Persisting Perception Disorder

Diagnostic Criteria

292.89 (F16.983)

A. Following cessation of use of a hallucinogen, the reexperiencing of one or more of the perceptual symptoms that were experienced while intoxicated with the hallucinogen (e.g., geometric hallucinations, false perceptions of movement in the peripheral visual fields, flashes of color, intensified colors, trails of images of moving objects, positive afterimages, halos around objects, macropsia and micropsia).

B. The symptoms in Criterion A cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

C. The symptoms are not attributable to another medical condition (e.g., anatomical lesions and infections of the brain, visual epilepsies) and are not better explained by another mental disorder (e.g., delirium, major neurocognitive disorder, schizophrenia) or hypnopompic hallucinations.

Diagnostic Features

The hallmark of hallucinogen persisting perception disorder is the reexperiencing, when the individual is sober, of the perceptual disturbances that were experienced while the individual was intoxicated with the hallucinogen (Criterion A). The symptoms may include any perceptual perturbations, but visual disturbances tend to be predominant(Halpern and Pope 2003). Typical of the abnormal visual perceptions are geometric hallucinations, false perceptions of movement in the peripheral visual fields, flashes of color, intensified colors, trails of images of moving objects (i.e., images left suspended in the path of a moving object as seen in stroboscopic photography), perceptions of entire objects, positive afterimages (i.e., a same-colored or complementary-colored “shadow” of an object remaining after removal of the object), halos around objects, or misperception of images as too large (macropsia) or too small (micropsia). Duration of the visual disturbances may be episodic or nearly continuous and must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion B). The disturbances may last for weeks, months, or years. Other explanations for the disturbances (e.g., brain lesions, preexisting psychosis, seizure disorders, migraine aura without headaches) must be ruled out (Criterion C).

Hallucinogen persisting perception disorder occurs primarily after LSD (lysergic acid diethylamide) use, but not exclusively(El-Mallakh et al. 2008). There does not appear to be a strong correlation between hallucinogen persisting perception disorder and number of occasions of hallucinogen use, with some instances of hallucinogen persisting perception disorder occurring in individuals with minimal exposure to hallucinogens. Some instances of hallucinogen persisting perception disorder may be triggered by use of other substances (e.g., cannabis or alcohol) or in adaptation to dark environments(Abraham 1983).

Associated Features Supporting Diagnosis

Reality testing remains intact in individuals with hallucinogen persisting perception disorder (i.e., the individual is aware that the disturbance is linked to the effect of the drug). If this is not the case, another disorder might better explain the abnormal perceptions.

Prevalence

Prevalence estimates of hallucinogen persisting perception disorder are unknown. Initial prevalence estimates of the disorder among individuals who use hallucinogens is approximately 4.2%(Baggott et al. 2011).

Development and Course

Little is known about the development of hallucinogen persisting perception disorder. Its course, as suggested by its name, is persistent, lasting for weeks, months, or even years in certain individuals.

Risk and Prognostic Factors

There is little evidence regarding risk factors for hallucinogen persisting perception disorder, although genetic factors have been suggested as a possible explanation underlying the susceptibility to LSD effects in this condition(Abraham 1983).

Functional Consequences of Hallucinogen Persisting Perception Disorder

Although hallucinogen persisting perception disorder remains a chronic condition in some cases, many individuals with the disorder are able to suppress the disturbances and continue to function normally(Abraham 1983).

Differential Diagnosis

Conditions to be ruled out include schizophrenia, other drug effects, neurodegenerative disorders, stroke, brain tumors, infections, and head trauma(El-Mallakh et al. 2008). Neuroimaging results in hallucinogen persisting perception disorder cases are typically negative. As noted earlier, reality testing remains intact (i.e., the individual is aware that the disturbance is linked to the effect of the drug); if this is not the case, another disorder (e.g., psychotic disorder, another medical condition) might better explain the abnormal perceptions.

Comorbidity

Common comorbid mental disorders accompanying hallucinogen persisting perception disorder are panic disorder, alcohol use disorder, and major depressive disorder (El-Mallakh et al. 2008).

References: Hallucinogen Persisting Perception Disorder

· Abraham HD : Visual phenomenology of the LSD flashback. Arch Gen Psychiatry 40(8):884–889, 1983

· Baggott MJ , Coyle JR , Erowid E , et al: Abnormal visual experiences in individuals with histories of hallucinogen use: a Web-based questionnaire. Drug Alcohol Depend 114(1):61–67, 2011

· El-Mallakh RS , Halpern JH , Abraham HD : Substance abuse: hallucinogen- and MDMA- related disorders, in Psychiatry, 3rd Edition. Edited by Tasman A , Kay J , Lieberman JA , et al. London, Wiley, 2008, pp 1100–1126

· Halpern JH , Pope HG Jr : Hallucinogen persisting perception disorder: what do we know after 50 years? Drug Alcohol Depend 69(2):109–119, 2003

Other Phencyclidine-Induced Disorders

Other phencyclidine-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): phencyclidine-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); phencyclidine-induced bipolar disorder (“Bipolar and Related Disorders”); phencyclidine-induced depressive disorder (“Depressive Disorders”); and phencyclidine-induced anxiety disorder (“Anxiety Disorders”). For phencyclidine-induced intoxication delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These phencyclidine-induced disorders are diagnosed instead of phencyclidine intoxication only when the symptoms are sufficiently severe to warrant independent clinical attention.

Other Hallucinogen-Induced Disorders

The following other hallucinogen-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): other hallucinogen–induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); other hallucinogen–induced bipolar disorder (“Bipolar and Related Disorders”); other hallucinogen–induced depressive disorder (“Depressive Disorders”); and other hallucinogen–induced anxiety disorder (“Anxiety Disorders”). For other hallucinogen intoxication delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These hallucinogen-induced disorders are diagnosed instead of other hallucinogen intoxication only when the symptoms are sufficiently severe to warrant independent clinical attention.

Unspecified Phencyclidine-Related Disorder

292.9 (F16.99)

This category applies to presentations in which symptoms characteristic of a phencyclidine-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific phencyclidine-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Unspecified Hallucinogen-Related Disorder

292.9 (F16.99)

This category applies to presentations in which symptoms characteristic of a hallucinogen-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific hallucinogen-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Inhalant-Related Disorders

1. Inhalant Use Disorder

2. Inhalant Intoxication

3. Other Inhalant-Induced Disorders

4. Unspecified Inhalant-Related Disorder

Inhalant Use Disorder

Diagnostic Criteria

A. A problematic pattern of use of a hydrocarbon-based inhalant substance leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. The inhalant substance 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 use of the inhalant substance.

3. A great deal of time is spent in activities necessary to obtain the inhalant substance, use it, or recover from its effects.

4. Craving, or a strong desire or urge to use the inhalant substance.

5. Recurrent use of the inhalant substance resulting in a failure to fulfill major role obligations at work, school, or home.

6. Continued use of the inhalant substance despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of its use.

7. Important social, occupational, or recreational activities are given up or reduced because of use of the inhalant substance.

8. Recurrent use of the inhalant substance in situations in which it is physically hazardous.

9. Use of the inhalant substance is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of the inhalant substance to achieve intoxication or desired effect.

b. A markedly diminished effect with continued use of the same amount of the inhalant substance.

Specify the particular inhalant: When possible, the particular substance involved should be named (e.g., “solvent use disorder”).

Specify if:

· In early remission: After full criteria for inhalant use disorder were previously met, none of the criteria for inhalant use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the inhalant substance,” may be met).

· In sustained remission: After full criteria for inhalant use disorder were previously met, none of the criteria for inhalant use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the inhalant substance,” may be met).

Specify if:

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to inhalant substances is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If an inhalant intoxication or another inhalant-induced mental disorder is also present, do not use the codes below for inhalant use disorder. Instead, the comorbid inhalant use disorder is indicated in the 4th character of the inhalant-induced disorder code (see the coding note for inhalant intoxication or a specific inhalant-induced mental disorder). For example, if there is comorbid inhalant-induced depressive disorder and inhalant use disorder, only the inhalant-induced depressive disorder code is given, with the 4th character indicating whether the comorbid inhalant use disorder is mild, moderate, or severe: F18.14 for mild inhalant use disorder with inhalant-induced depressive disorder or F18.24 for a moderate or severe inhalant use disorder with inhalant-induced depressive disorder.

Specify current severity /remission :

· 305.90 (F18.10) Mild: Presence of 2–3 symptoms.

· (F18.11) Mild, In early remission

· (F18.11) Mild, In sustained remission

· 304.60 (F18.20) Moderate: Presence of 4–5 symptoms.

· (F18.21) Moderate, In early remission

· (F18.21) Moderate, In sustained remission

· 304.60 (F18.20) Severe: Presence of 6 or more symptoms.

· (F18.21) Severe, In early remission

· (F18.21) Severe, In sustained remission

Specifiers

This manual recognizes volatile hydrocarbon use meeting the above diagnostic criteria as inhalant use disorder. Volatile hydrocarbons are toxic gases from glues, fuels, paints, and other volatile compounds. When possible, the particular substance involved should be named (e.g., “toluene use disorder”). However, most compounds that are inhaled are a mixture of several substances that can produce psychoactive effects, and it is often difficult to ascertain the exact substance responsible for the disorder. Unless there is clear evidence that a single, unmixed substance has been used, the general term inhalant should be used in recording the diagnosis. Disorders arising from inhalation of nitrous oxide or of amyl-, butyl-, or isobutylnitrite are considered as other (or unknown) substance use disorder.

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

The severity of individuals’ inhalant use disorder is assessed by the number of diagnostic criteria endorsed. Changing severity of individuals’ inhalant use disorder across time is reflected by reductions in the frequency (e.g., days used per month) and/or dose (e.g., tubes of glue per day) used, as assessed by the individual’s self-report, report of others, clinician’s observations, and biological testing (when practical).

Diagnostic Features

Features of inhalant use disorder include repeated use of an inhalant substance despite the individual’s knowing that the substance is causing serious problems for the individual (Criterion A9). Those problems are reflected in the diagnostic criteria.

Missing work or school or inability to perform typical responsibilities at work or school (Criterion A5), and continued use of the inhalant substance even though it causes arguments with family or friends, fights, and other social or interpersonal problems (Criterion A6), may be seen in inhalant use disorder. Limiting family contact, work or school obligations, or recreational activities (e.g., sports, games, hobbies) may also occur (Criterion A7). Use of inhalants when driving or operating dangerous equipment (Criterion A8) is also seen.

Tolerance (Criterion A10) and mild withdrawal are each reported by about 10% of individuals who use inhalants, and a few individuals use inhalants to avoid withdrawal(Ridenour et al. 2007). However, because the withdrawal symptoms are mild(Miyata et al. 2004), this manual neither recognizes a diagnosis of inhalant withdrawal nor counts withdrawal complaints as a diagnostic criterion for inhalant use disorder.

Associated Features Supporting Diagnosis

A diagnosis of inhalant use disorder is supported by recurring episodes of intoxication with negative results in standard drug screens (which do not detect inhalants); possession, or lingering odors, of inhalant substances; peri-oral or peri-nasal “glue-sniffer’s rash”; association with other individuals known to use inhalants; membership in groups with prevalent inhalant use (e.g., some native or aboriginal communities, homeless children in street gangs); easy access to certain inhalant substances; paraphernalia possession; presence of the disorder’s characteristic medical complications (e.g., brain white matter pathology, rhabdomyolysis); and the presence of multiple substance use disorders(Wu et al. 2008). Inhalant use and inhalant use disorder are associated with past suicide attempts, especially among adults reporting previous episodes of low mood or anhedonia(Botnick et al. 2002; Howard et al. 2010).

Prevalence

About 0.4% of Americans ages 12–17 years have a pattern of use that meets criteria for inhalant use disorder in the past 12 months(Substance Abuse and Mental Health Services Administration 2010). Among those youths, the prevalence is highest in Native Americans and lowest in African Americans. Prevalence falls to about 0.1% among Americans ages 18–29 years, and only 0.02% when all Americans 18 years or older are considered, with almost no females and a preponderance of European Americans. Of course, in isolated subgroups, prevalence may differ considerably from these overall rates.

Development and Course

About 10% of 13-year-old American children report having used inhalants at least once; that percentage remains stable through age 17 years(Substance Abuse and Mental Health Services Administration 2008). Among those 12- to 17-year-olds who use inhalants, the more-used substances include glue, shoe polish, or toluene; gasoline or lighter fluid; or spray paints(Substance Abuse and Mental Health Services Administration 2010).

Only 0.4% of 12- to 17-year-olds progress to inhalant use disorder; those youths tend to exhibit multiple other problems(Wu et al. 2004). The declining prevalence of inhalant use disorder after adolescence indicates that this disorder usually remits in early adulthood.

Volatile hydrocarbon use disorder is rare in prepubertal children, most common in adolescents and young adults, and uncommon in older persons. Calls to poison-control centers for “intentional abuse” of inhalants peak with calls involving individuals at age 14 years(Marsolek et al. 2010). Of adolescents who use inhalants, perhaps one-fifth develop inhalant use disorder (Perron et al. 2009); a few die from inhalant-related accidents, or “sudden sniffing death”(Pfeiffer et al. 2006). But the disorder apparently remits in many individuals after adolescence. Prevalence declines dramatically among individuals in their 20s. Those with inhalant use disorder extending into adulthood often have severe problems: substance use disorders, antisocial personality disorder, and suicidal ideation with attempts(Howard et al. 2010).

Risk and Prognostic Factors

Temperamental

Predictors of progression from nonuse of inhalants, to use, to inhalant use disorder include comorbid non-inhalant substance use disorders and either conduct disorder or antisocial personality disorder. Other predictors are earlier onset of inhalant use and prior use of mental health services(Compton et al. 2005; Howard et al. 2010; Wu et al. 2004).

Environmental

Inhalant gases are widely and legally available, increasing the risk of misuse. Childhood maltreatment or trauma also is associated with youthful progression from inhalant non-use to inhalant use disorder (Perron and Howard 2009).

Genetic and physiological

Behavioral disinhibition is a highly heritable general propensity to not constrain behavior in socially acceptable ways, to break social norms and rules, and to take dangerous risks, pursuing rewards excessively despite dangers of adverse consequences. Youths with strong behavioral disinhibition show risk factors for inhalant use disorder: early-onset substance use disorder, multiple substance involvement, and early conduct problems(Iacono et al. 2008). Because behavioral disinhibition is under strong genetic influence, youths in families with substance and antisocial problems are at elevated risk for inhalant use disorder (Perron et al. 2009).

Culture-Related Diagnostic Issues

Certain native or aboriginal communities have experienced a high prevalence of inhalant problems(Cairney and Dingwall 2010; Mitchell et al. 2003). Also, in some countries, groups of homeless children in street gangs have extensive inhalant use problems(Seth et al. 2005).

Gender-Related Diagnostic Issues

Although the prevalence of inhalant use disorder is almost identical in adolescent males and females, the disorder is very rare among adult females.

Diagnostic Markers

Urine, breath, or saliva tests may be valuable for assessing concurrent use of non-inhalant substances by individuals withinhalant use disorder. However, technical problems and the considerable expense of analyses make frequent biological testing for inhalants themselves impractical(Sakai and Crowley 2009).

Functional Consequences of Inhalant Use Disorder

Because of inherent toxicity, use of butane or propane is not infrequently fatal(Marsolek et al. 2010). Moreover, any inhaled volatile hydrocarbons may produce “sudden sniffing death” from cardiac arrhythmia(Sakai and Crowley 2009). Fatalities may occur even on the first inhalant exposure and are not thought to be dose-related. Volatile hydrocarbon use impairs neurobehavioral function and causes various neurological, gastrointestinal, cardiovascular, and pulmonary problems(Sakai and Crowley 2009).

Long-term inhalant users are at increased risk for tuberculosis, HIV/AIDS, sexually transmitted diseases, depression, anxiety, bronchitis, asthma, and sinusitis(Han et al. 2010). Deaths may occur from respiratory depression, arrhythmias, asphyxiation, aspiration of vomitus, or accident and injury(Sakai and Crowley 2009).

Differential Diagnosis

Inhalant exposure (unintentional) from industrial or other accidents

This designation is used when findings suggest repeated or continuous inhalant exposure but the involved individual and other informants deny any history of purposeful inhalant use.

Inhalant use (intentional), without meeting criteria for inhalant use disorder

Inhalant use is common among adolescents, but for most of those individuals, the inhalant use does not meet the diagnostic standard of two or more Criterion A items for inhalant use disorder in the past year.

Inhalant intoxication, without meeting criteria for inhalant use disorder

Inhalant intoxication occurs frequently during inhalant use disorder but also may occur among individuals whose use does not meet criteria for inhalant use disorder, which requires at least two of the 10 diagnostic criteria in the past year.

Inhalant-induced disorders (i.e., inhalant-induced psychotic disorder, depressive disorder, anxiety disorder, neurocognitive disorder, other inhalant-induced disorders) without meeting criteria for inhalant use disorder

Criteria are met for a psychotic, depressive, anxiety, or major neurocognitive disorder, and there is evidence from history, physical examination, or laboratory findings that the deficits are etiologically related to the effects of inhalant substances. Yet, criteria for inhalant use disorder may not be met (i.e., fewer than 2 of the 10 criteria were present).

Other substance use disorders, especially those involving sedating substances (e.g., alcohol, benzodiazepines, barbiturates)

Inhalant use disorder commonly co-occurs with other substance use disorders, and the symptoms of the disorders may be similar and overlapping. To disentangle symptom patterns, it is helpful to inquire about which symptoms persisted during periods when some of the substances were not being used.

Other toxic, metabolic, traumatic, neoplastic, or infectious disorders impairing central or peripheral nervous system function

Individuals with inhalant use disorder may present with symptoms of pernicious anemia, subacute combined degeneration of the spinal cord, psychosis, major or minor cognitive disorder, brain atrophy, leukoencephalopathy, and many other nervous system disorders(Sakai and Crowley 2009). Of course, these disorders also may occur in the absence of inhalant use disorder. A history of little or no inhalant use helps to exclude inhalant use disorder as the source of these problems.

Disorders of other organ systems

Individuals with inhalant use disorder may present with symptoms of hepatic or renal damage, rhabdomyolysis, methemoglobinemia, or symptoms of other gastrointestinal, cardiovascular, or pulmonary diseases(Sakai and Crowley 2009). A history of little or no inhalant use helps to exclude inhalant use disorder as the source of such medical problems.

Comorbidity

Individuals with inhalant use disorder receiving clinical care often have numerous other substance use disorders (Wu et al. 2008). Inhalant use disorder commonly co-occurs with adolescent conduct disorder and adult antisocial personality disorder. Adult inhalant use and inhalant use disorder also are strongly associated with suicidal ideation and suicide attempts(Howard et al. 2010).

References: Inhalant Use Disorder

· Botnick MR , Heath KV , Cornelisse PG , et al: Correlates of suicide attempts in an open cohort of young men who have sex with men. Can J Public Health 93(1):59–62, 2002

· Cairney S , Dingwall K : The mysterious practice of petrol sniffing in isolated indigenous communities. J Paediatr Child Health 46(9):510–515, 2010 10.1111/j.1440-1754.2010.01850.x

· Compton WM , Conway KP , Stinson FS , et al: Prevalence, correlates, and comorbidity of DSM-IV antisocial personality syndromes and alcohol and specific drug use disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions. J Clin Psychiatry 66(6):677–685, 2005

· Han B , Gfroerer JC , Colliver JD : Associations between duration of illicit drug use and health conditions: results from the 2005–2007 national surveys on drug use and health. Ann Epidemiol 20(4):289–297, 2010

· Howard MO , Perron BE , Sacco P , et al: Suicide ideation and attempts among inhalant users: results from the national epidemiologic survey on alcohol and related conditions. Suicide Life Threat Behav 40(3):276–286, 2010

· Iacono WG , Malone SM , McGue M : Behavioral disinhibition and the development of early-onset addiction: common and specific influences. Ann Rev Clin Psychol 4:325–348, 2008

· Marsolek MR , White NC , Litovitz TL : Inhalant abuse: monitoring trends by using poison control data. Pediatrics125(5):906–913, 2010

· Mitchell CM , Beals J , Novins DK , et al: Drug use among two American Indian populations: prevalence of lifetime use and DSM-IV substance use disorders. Drug Alcohol Depend 69(1):29–41, 2003

· Miyata H , Kono J , Ushijima S , et al: Clinical features of nicotine dependence compared with those of alcohol, methamphetamine, and inhalant dependence. Ann N Y Acad Sci 1025:481–488, 2004

· Perron BE , Howard MO : Adolescent inhalant use, abuse and dependence. Addiction 104(7):1185–1192, 2009

· Perron B , Howard MO , Maitra S , Vaughn MG : Prevalence, timing, and predictors of transitions from inhalant use to inhalant use disorders. Drug Alcohol Depend 100(3):277–284, 2009

· Pfeiffer H , Al Khaddam M , Brinkmann B , et al: Sudden death after isobutane sniffing: a report of two forensic cases. Int J Legal Med 120(3):168–173, 2006

· Ridenour TA , Bray BC , Cottler LB : Reliability of use, abuse, and dependence of four types of inhalants in adolescents and young adults. Drug Alcohol Depend 91(1):40–49, 2007

· Sakai JT , Crowley TJ : Inhalant-related disorders, in Comprehensive Textbook of Psychiatry, 9th Edition, Vol 1. Edited by Sadock BJ , Sadock VA , Ruiz P . Baltimore, MD, Williams & Wilkins, 2009, pp 1341–1352

· Seth R , Kotwal A , Ganguly KK : Street and working children of Delhi, India, misusing toluene: an ethnographic exploration.Subst Use Misuse 40(11):1659–1679, 2005

· Substance Abuse and Mental Health Services Administration, Office of Applied Studies : Inhalant use across the adolescent years. The NSDUH Report,, March 13, 2008. Available at: http://www.samhsa.gov/data/2k8/inhalants/inhalants.htm. Accessed June 15, 2012..

· Substance Abuse and Mental Health Services Administration, Office of Applied Studies : Table 9 in Prevalence of Substance Use Disorders by Sex and Race-Ethnicity (12–17 year olds): 2009 National Survey on Drug Use and Health. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2010

· Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality : 2010 National Survey on Drug Use and Health: Table 5.2B Substance dependence or abuse for specific substances in the past year, by age group: percentages 2009–2010. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2011. Available at: http:oas.samhsa.gov/nsduh/2K10NSDUH/tabs/Sect5peTabs1to56.htm#tab5.2B. Accessed June 15, 2012..

· Wu LT , Pilowsky DJ , Schlenger WE : Inhalant abuse and dependence among adolescents in the United States. J Am Acad Child Adolesc Psychiatry 43(10):1206–1214, 2004

· Wu LT , Howard MO , Pilowsky DJ : Substance use disorders among inhalant users: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Addict Behav 33(7):968–973, 2008

Inhalant Intoxication

Diagnostic Criteria

A. Recent intended or unintended short-term, high-dose exposure to inhalant substances, including volatile hydrocarbons such as toluene or gasoline.

B. Clinically significant problematic behavioral or psychological changes (e.g., belligerence, assaultiveness, apathy, impaired judgment) that developed during, or shortly after, exposure to inhalants.

C. Two (or more) of the following signs or symptoms developing during, or shortly after, inhalant use or exposure:

1. Dizziness.

2. Nystagmus.

3. Incoordination.

4. Slurred speech.

5. Unsteady gait.

6. Lethargy.

7. Depressed reflexes.

8. Psychomotor retardation.

9. Tremor.

10. Generalized muscle weakness.

11. Blurred vision or diplopia.

12. Stupor or coma.

13. Euphoria.

D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication with another substance.

Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether there is a comorbid inhalant use disorder. If a mild inhalant use disorder is comorbid, the ICD-10-CM code is F18.129, and if a moderate or severe inhalant use disorder is comorbid, the ICD-10-CM code is F18.229. If there is no comorbid inhalant use disorder, then the ICD-10-CM code is F18.929.

Note: For information on Development and Course, Risk and Prognostic Factors, Culture-Related Diagnostic Issues, and Diagnostic Markers, see the corresponding sections in inhalant use disorder.

Diagnostic Features

Inhalant intoxication is an inhalant-related, clinically significant mental disorder that develops during, or immediately after, intended or unintended inhalation of a volatile hydrocarbon substance. Volatile hydrocarbons are toxic gases from glues, fuels, paints, and other volatile compounds. When it is possible to do so, the particular substance involved should be named (e.g., toluene intoxication). Among those who do, the intoxication clears within a few minutes to a few hours after the exposure ends. Thus, inhalant intoxication usually occurs in brief episodes that may recur.

Associated Features Supporting Diagnosis

Inhalant intoxication may be indicated by evidence of possession, or lingering odors, of inhalant substances (e.g., glue, paint thinner, gasoline, butane lighters); apparent intoxication occurring in the age range with the highest prevalence of inhalant use (12–17 years); and apparent intoxication with negative results from the standard drug screens that usually fail to identify inhalants.

Prevalence

The prevalence of actual episodes of inhalant intoxication in the general population is unknown, but it is probable that most inhalant users would at some time exhibit use that would meet criteria for inhalant intoxication disorder. Therefore, the prevalence of inhalant use and the prevalence of inhalant intoxication disorder are likely similar. In 2009 and 2010, inhalant use in the past year was reported by 0.8% of all Americans older than 12 years; the prevalence was highest in younger age groups (3.6% for individuals 12 to 17 years old, and 1.7% for individuals 18 to 25 years old)(Substance Abuse and Mental Health Services Administration 2011a).

Gender-Related Diagnostic Issues

Gender differences in the prevalence of inhalant intoxication in the general population are unknown. However, if it is assumed that most inhalant users eventually experience inhalant intoxication, gender differences in the prevalence of inhalant userslikely approximate those in the proportions of males and females experiencing inhalant intoxication. Regarding gender differences in the prevalence of inhalant users in the United States, 1% of males older than 12 years and 0.7% of females older than 12 years have used inhalants in the previous year, but in the younger age groups more females than males have used inhalants (e.g., among 12- to 17-year-olds, 3.6% of males and 4.2% of females)(Substance Abuse and Mental Health Services Administration 2011b).

Functional Consequences of Inhalant Intoxication

Use of inhaled substances in a closed container, such as a plastic bag over the head, may lead to unconsciousness, anoxia, and death. Separately, “sudden sniffing death,” likely from cardiac arrhythmia or arrest, may occur with various volatile inhalants. The enhanced toxicity of certain volatile inhalants, such as butane or propane, also causes fatalities(Marsolek et al. 2010). Although inhalant intoxication itself is of short duration, it may produce persisting medical and neurological problems, especially if the intoxications are frequent.

Differential Diagnosis

Inhalant exposure, without meeting the criteria for inhalant intoxication disorder

The individual intentionally or unintentionally inhaled substances, but the dose was insufficient for the diagnostic criteria for inhalant use disorder to be met.

Intoxication and other substance/medication-induced disorders from other substances, especially from sedating substances (e.g., alcohol, benzodiazepines, barbiturates)

These disorders may have similar signs and symptoms, but the intoxication is attributable to other intoxicants that may be identified via a toxicology screen. Differentiating the source of the intoxication may involve discerning evidence of inhalant exposure as described for inhalant use disorder. A diagnosis of inhalant intoxication may be suggested by possession, or lingering odors, of inhalant substances (e.g., glue, paint thinner, gasoline, butane lighters,); paraphernalia possession (e.g., rags or bags for concentrating glue fumes); perioral or perinasal “glue-sniffer’s rash”; reports from family or friends that the intoxicated individual possesses or uses inhalants; apparent intoxication despite negative results on standard drug screens (which usually fail to identify inhalants); apparent intoxication occurring in that age range with the highest prevalence of inhalant use (12–17 years); association with others known to use inhalants; membership in certain small communities with prevalent inhalant use (e.g., some native or aboriginal communities, homeless street children and adolescents); or unusual access to certain inhalant substances.

Other inhalant-related disorders

Episodes of inhalant intoxication do occur during, but are not identical with, other inhalant-related disorders. Those inhalant-related disorders are recognized by their respective diagnostic criteria: inhalant use disorder, inhalant-induced neurocognitive disorder, inhalant-induced psychotic disorder, inhalant-induced depressive disorder, inhalant-induced anxiety disorder, and other inhalant-induced disorders.

Other toxic, metabolic, traumatic, neoplastic, or infectious disorders that impair brain function and cognition

Numerous neurological and other medical conditions may produce the clinically significant behavioral or psychological changes (e.g., belligerence, assaultiveness, apathy, impaired judgment) that also characterize inhalant intoxication.

References: Inhalant Intoxication

· Marsolek MR , White NC , Litvitz TL : Inhalant abuse: monitoring trends by using poison control data, 1993–2008.Pediatrics 125(5):906–913, 2010

· Substance Abuse and Mental Health Services Administration : Results from the 2010 National Survey on Drug Use and Health: summary of national findings. NSDUH Series H-41, HHS Publ No (SMA) 11-4658.. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2011a

· Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality : 2010 National Survey on Drug Use and Health: Table 1.45B Inhalant use in lifetime, past year, and past month among persons aged 12 to 17, by demographic characteristics: percentages, 2009 and 2010, and Table 1.46B Inhalant use in lifetime, past year, and past month among persons aged 18 to 25, by demographic characteristics: percentages, 2009 and 2010. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2011b. Available at:http:oas.samhsa.gov/nsduh/2K10NSDUH/tabs/Sect1peTabs1to46.htm#tab1.45B and http:oas.samhsa.gov/nsduh/2K10NSDUH/tabs/Sect1peTabs1to46.htm#tab1.46B Accessed June 15, 2012.

Other Inhalant-Induced Disorders

The following inhalant-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): inhalant-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); inhalant-induced depressive disorder (“Depressive Disorders”); inhalant-induced anxiety disorder (“Anxiety Disorders”); and inhalant-induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For inhalant intoxication delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These inhalant-induced disorders are diagnosed instead of inhalant intoxication only when symptoms are sufficiently severe to warrant independent clinical attention.

Unspecified Inhalant-Related Disorder

292.9 (F18.99)

This category applies to presentations in which symptoms characteristic of an inhalant-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific inhalant-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Opioid-Related Disorders

1. Opioid Use Disorder

2. Opioid Intoxication

3. Opioid Withdrawal

4. Other Opioid-Induced Disorders

5. Unspecified Opioid-Related Disorder

Opioid Use Disorder

Diagnostic Criteria

A. A problematic pattern of opioid use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. Opioids are 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 opioid use.

3. A great deal of time is spent in activities necessary to obtain the opioid, use the opioid, or recover from its effects.

4. Craving, or a strong desire or urge to use opioids.

5. Recurrent opioid use resulting in a failure to fulfill major role obligations at work, school, or home.

6. Continued opioid use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of opioids.

7. Important social, occupational, or recreational activities are given up or reduced because of opioid use.

8. Recurrent opioid use in situations in which it is physically hazardous.

9. Continued opioid use despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of opioids to achieve intoxication or desired effect.

b. A markedly diminished effect with continued use of the same amount of an opioid.

10. Note: This criterion is not considered to be met for those taking opioids solely under appropriate medical supervision.

. Withdrawal, as manifested by either of the following:

a. The characteristic opioid withdrawal syndrome (refer to Criteria A and B of the criteria set for opioid withdrawal, pp. 547–548).

b. Opioids (or a closely related substance) are taken to relieve or avoid withdrawal symptoms.

1. Note: This criterion is not considered to be met for those individuals taking opioids solely under appropriate medical supervision.

Specify if:

· In early remission: After full criteria for opioid use disorder were previously met, none of the criteria for opioid 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 opioids,” may be met).

· In sustained remission: After full criteria for opioid use disorder were previously met, none of the criteria for opioid 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 opioids,” may be met).

Specify if:

· On maintenance therapy: This additional specifier is used if the individual is taking a prescribed agonist medication such as methadone or buprenorphine and none of the criteria for opioid use disorder have been met for that class of medication (except tolerance to, or withdrawal from, the agonist). This category also applies to those individuals being maintained on a partial agonist, an agonist/antagonist, or a full antagonist such as oral naltrexone or depot naltrexone.

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to opioids is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If an opioid intoxication, opioid withdrawal, or another opioid-induced mental disorder is also present, do not use the codes below for opioid use disorder. Instead, the comorbid opioid use disorder is indicated in the 4th character of the opioid-induced disorder code (see the coding note for opioid intoxication, opioid withdrawal, or a specific opioid-induced mental disorder). For example, if there is comorbid opioid-induced depressive disorder and opioid use disorder, only the opioid-induced depressive disorder code is given, with the 4th character indicating whether the comorbid opioid use disorder is mild, moderate, or severe: F11.14 for mild opioid use disorder with opioid-induced depressive disorder or F11.24 for a moderate or severe opioid use disorder with opioid-induced depressive disorder.

Specify current severity /remission :

· 305.50 (F11.10) Mild: Presence of 2–3 symptoms.

· (F11.11) Mild, In early remission

· (F11.11) Mild, In sustained remission

· 304.00 (F11.20) Moderate: Presence of 4–5 symptoms.

· (F11.21) Moderate, In early remission

· (F11.21) Moderate, In sustained remission

· 304.00 (F11.20) Severe: Presence of 6 or more symptoms.

· (F11.21) Severe, In early remission

· (F11.21) Severe, In sustained remission

Specifiers

The “on maintenance therapy” specifier applies as a further specifier of remission if the individual is both in remission and receiving maintenance therapy. “In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Changing severity across time in an individual is also reflected by reductions in the frequency (e.g., days of use per month) and/or dose (e.g., injections or number of pills) of an opioid, as assessed by the individual’s self-report, report of knowledgeable others, clinician’s observations, and biological testing.

Diagnostic Features

Opioid use disorder includes signs and symptoms that reflect compulsive, prolonged self-administration of opioid substances that are used for no legitimate medical purpose or, if another medical condition is present that requires opioid treatment, that are used in doses greatly in excess of the amount needed for that medical condition. (For example, an individual prescribed analgesic opioids for pain relief at adequate dosing will use significantly more than prescribed and not only because of persistent pain.) Individuals with opioid use disorder tend to develop such regular patterns of compulsive drug use that daily activities are planned around obtaining and administering opioids. Opioids are usually purchased on the illegal market but may also be obtained from physicians by falsifying or exaggerating general medical problems or by receiving simultaneous prescriptions from several physicians. Health care professionals with opioid use disorder will often obtain opioids by writing prescriptions for themselves or by diverting opioids that have been prescribed for patients or from pharmacy supplies. Most individuals with opioid use disorder have significant levels of tolerance and will experience withdrawal on abrupt discontinuation of opioid substances. Individuals with opioid use disorder often develop conditioned responses to drug-related stimuli (e.g., craving on seeing any heroin powder–like substance)—a phenomenon that occurs with most drugs that cause intense psychological changes. These responses probably contribute to relapse, are difficult to extinguish, and typically persist long after detoxification is completed(Fatseas et al. 2011b).

Associated Features Supporting Diagnosis

Opioid use disorder can be associated with a history of drug-related crimes (e.g., possession or distribution of drugs, forgery, burglary, robbery, larceny, receiving stolen goods). Among health care professionals and individuals who have ready access to controlled substances, there is often a different pattern of illegal activities involving problems with state licensing boards, professional staffs of hospitals, or other administrative agencies. Marital difficulties (including divorce), unemployment, and irregular employment are often associated with opioid use disorder at all socioeconomic levels.

Prevalence

The 12-month prevalence of opioid use disorder is approximately 0.37% among adults age 18 years and older in the community population(Compton et al. 2007). This may be an underestimate because of the large number of incarcerated individuals with opioid use disorders(Compton et al. 2010). Rates are higher in males than in females (0.49% vs. 0.26%), with the male-to-female ratio typically being 1.5:1 for opioids other than heroin (i.e., available by prescription) and 3:1 for heroin. Female adolescents may have a higher likelihood of developing opioid use disorders(Wu et al. 2009). The prevalence decreases with age, with the prevalence highest (0.82%) among adults age 29 years or younger, and decreasing to 0.09% among adults age 65 years and older. Among adults, the prevalence of opioid use disorder is lower among African Americans at 0.18% and overrepresented among Native Americans at 1.25%. It is close to average among whites (0.38%), Asian or Pacific Islanders (0.35%), and Hispanics (0.39%)(Wu et al. 2009).

Among individuals in the United States ages 12–17 years, the overall 12-month prevalence of opioid use disorder in the community population is approximately 1.0%, but the prevalence of heroin use disorder is less than 0.1%. By contrast, analgesic use disorder is prevalent in about 1.0% of those ages 12–17 years, speaking to the importance of opioid analgesics as a group of substances with significant health consequences(Substance Abuse and Mental Health Services Administration 2011).

The 12-month prevalence of problem opioid use in European countries in the community population ages 15–64 years is between 0.1% and 0.8%. The average prevalence of problem opioid use in the European Union and Norway is between 0.36% and 0.44%(European Monitoring Centre for Drugs and Drug Addiction 2010).

Development and Course

Opioid use disorder can begin at any age, but problems associated with opioid use are most commonly first observed in the late teens or early 20s. Once opioid use disorder develops, it usually continues over a period of many years, even though brief periods of abstinence are frequent. In treated populations, relapse following abstinence is common. Even though relapses do occur, and while some long-term mortality rates may be as high as 2% per year, about 20%–30% of individuals with opioid use disorder achieve long-term abstinence. An exception concerns that of military service personnel who became dependent on opioids in Vietnam; over 90% of this population who had been dependent on opioids during deployment in Vietnam achieved abstinence after they returned, but they experienced increased rates of alcohol or amphetamine use disorder as well as increased suicidality(Price et al. 2001).

Increasing age is associated with a decrease in prevalence as a result of early mortality and the remission of symptoms after age 40 years (i.e., “maturing out”). However, many individuals continue have presentations that meet opioid use disordercriteria for decades(Hser et al. 2007).

Risk and Prognostic Factors

Genetic and physiological

The risk for opioid use disorder can be related to individual, family, peer, and social environmental factors(Kendler et al. 2003; Tsuang et al. 1998), but within these domains, genetic factors play a particularly important role both directly and indirectly. For instance, impulsivity and novelty seeking are individual temperaments that relate to the propensity to develop a substance use disorder but may themselves be genetically determined. Peer factors may relate to genetic predisposition in terms of how an individual selects his or her environment.

Culture-Related Diagnostic Issues

Despite small variations regarding individual criterion items, opioid use disorder diagnostic criteria perform equally well across most race/ethnicity groups. Individuals from ethnic minority populations living in economically deprived areas have been overrepresented among individuals with opioid use disorder. However, over time, opioid use disorder is seen more often among white middle-class individuals, especially females, suggesting that differences in use reflect the availability of opioid drugs and that other social factors may impact prevalence. Medical personnel who have ready access to opioids may be at increased risk for opioid use disorder.

Diagnostic Markers

Routine urine toxicology test results are often positive for opioid drugs in individuals with opioid use disorder. Urine test results remain positive for most opioids (e.g., heroin, morphine, codeine, oxycodone, propoxyphene) for 12–36 hours after administration. Fentanyl is not detected by standard urine tests but can be identified by more specialized procedures for several days. Methadone, buprenorphine (or buprenorphine/naloxone combination), and LAAM (l-alpha-acetylmethadol) have to be specifically tested for and will not cause a positive result on routine tests for opiates. They can be detected for several days up to more than 1 week. Laboratory evidence of the presence of other substances (e.g., cocaine, marijuana, alcohol, amphetamines, benzodiazepines) is common. Screening test results for hepatitis A, B, and C virus are positive in as many as 80%–90% of injection opioid users, either for hepatitis antigen (signifying active infection) or for hepatitis antibody (signifying past infection). HIV is prevalent in injection opioid users as well. Mildly elevated liver function test results are common, either as a result of resolving hepatitis or from toxic injury to the liver due to contaminants that have been mixed with the injected opioid. Subtle changes in cortisol secretion patterns and body temperature regulation have been observed for up to 6 months following opioid detoxification.

Suicide Risk

Similar to the risk generally observed for all substance use disorders, opioid use disorder is associated with a heightened risk for suicide attempts and completed suicides. Particularly notable are both accidental and deliberate opioid overdoses. Some suicide risk factors overlap with risk factors for an opioid use disorder. In addition, repeated opioid intoxication or withdrawalmay be associated with severe depressions that, although temporary, can be intense enough to lead to suicide attempts and completed suicides. Available data suggest that nonfatal accidental opioid overdose (which is common) and attempted suicide are distinct clinically significant problems that should not be mistaken for each other.

Functional Consequences of Opioid Use Disorder

Opioid use is associated with a lack of mucous membrane secretions, causing dry mouth and nose. Slowing of gastrointestinal activity and a decrease in gut motility can produce severe constipation. Visual acuity may be impaired as a result of pupillary constriction with acute administration. In individuals who inject opioids, sclerosed veins (“tracks”) and puncture marks on the lower portions of the upper extremities are common. Veins sometimes become so severely sclerosed that peripheral edema develops, and individuals switch to injecting in veins in the legs, neck, or groin. When these veins become unusable, individuals often inject directly into their subcutaneous tissue (“skin-popping”), resulting in cellulitis, abscesses, and circular-appearing scars from healed skin lesions. Tetanus and Clostridium botulinum infections are relatively rare but extremely serious consequences of injecting opioids, especially with contaminated needles. Infections may also occur in other organs and include bacterial endocarditis, hepatitis, and HIV infection. Hepatitis C infections, for example, may occur in up to 90% of persons who inject opioids. In addition, the prevalence of HIV infection can be high among individuals who inject drugs, a large proportion of whom are individuals with opioid use disorder. HIV infection rates have been reported to be as high as 60% among heroin users with opioid use disorder in some areas of the United States or the Russian Federation. However, the incidence may also be 10% or less in other areas, especially those where access to clean injection material and paraphernalia is facilitated(Fatseas et al. 2011a).

Tuberculosis is a particularly serious problem among individuals who use drugs intravenously, especially those who are dependent on heroin; infection is usually asymptomatic and evident only by the presence of a positive tuberculin skin test. However, many cases of active tuberculosis have been found, especially among those who are infected with HIV. These individuals often have a newly acquired infection but also are likely to experience reactivation of a prior infection because of impaired immune function.

Individuals who sniff heroin or other opioids into the nose (“snorting”) often develop irritation of the nasal mucosa, sometimes accompanied by perforation of the nasal septum. Difficulties in sexual functioning are common. Males often experience erectile dysfunction during intoxication or chronic use. Females commonly have disturbances of reproductive function and irregular menses.

In relation to infections such as cellulitis, hepatitis, HIV infection, tuberculosis, and endocarditis, opioid use disorder is associated with a mortality rate as high as 1.5%–2% per year. Death most often results from overdose, accidents, injuries, AIDS, or other general medical complications. Accidents and injuries due to violence that is associated with buying or selling drugs are common. In some areas, violence accounts for more opioid-related deaths than overdose or HIV infection. Physiological dependence on opioids may occur in about half of the infants born to females with opioid use disorder; this can produce a severe withdrawal syndrome requiring medical treatment. Although low birth weight is also seen in children of mothers with opioid use disorder, it is usually not marked and is generally not associated with serious adverse consequences.

Differential Diagnosis

Opioid-induced mental disorders

Opioid-induced disorders occur frequently in individuals with opioid use disorder. Opioid-induced disorders may be characterized by symptoms (e.g., depressed mood) that resemble primary mental disorders (e.g., persistent depressive disorder [dysthymia] vs. opioid-induced depressive disorder, with depressive features, with onset during intoxication). Opioids are less likely to produce symptoms of mental disturbance than are most other drugs of abuse. Opioid intoxicationand opioid withdrawal are distinguished from the other opioid-induced disorders (e.g., opioid-induced depressive disorder, with onset during intoxication) because the symptoms in these latter disorders predominate the clinical presentation and are severe enough to warrant independent clinical attention.

Other substance intoxication

Alcohol intoxication and sedative, hypnotic, or anxiolytic intoxication can cause a clinical picture that resembles that for opioid intoxication. A diagnosis of alcohol or sedative, hypnotic, or anxiolytic intoxication can usually be made based on the absence of pupillary constriction or the lack of a response to naloxone challenge. In some cases, intoxication may be due both to opioids and to alcohol or other sedatives. In these cases, the naloxone challenge will not reverse all of the sedative effects.

Other withdrawal disorders

The anxiety and restlessness associated with opioid withdrawal resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid withdrawal is also accompanied by rhinorrhea, lacrimation, and pupillary dilation, which are not seen in sedative-type withdrawal. Dilated pupils are also seen in hallucinogen intoxication and stimulant intoxication. However, other signs or symptoms of opioid withdrawal, such as nausea, vomiting, diarrhea, abdominal cramps, rhinorrhea, or lacrimation, are not present.

Comorbidity

The most common medical conditions associated with opioid use disorder are viral (e.g., HIV, hepatitis C virus) and bacterial infections, particularly among users of opioids by injection. These infections are less common in opioid use disorder with prescription opioids. Opioid use disorder is often associated with other substance use disorders, especially those involving tobacco, alcohol, cannabis, stimulants, and benzodiazepines, which are often taken to reduce symptoms of opioid withdrawal or craving for opioids, or to enhance the effects of administered opioids. Individuals with opioid use disorder are at risk for the development of mild to moderate depression that meets symptomatic and duration criteria for persistent depressive disorder (dysthymia) or, in some cases, for major depressive disorder(Compton et al. 2005). These symptoms may represent an opioid-induced depressive disorder or an exacerbation of a preexisting primary depressive disorder. Periods of depression are especially common during chronic intoxication or in association with physical or psychosocial stressors that are related to the opioid use disorder. Insomnia is common, especially during withdrawal. Antisocial personality disorder is much more common in individuals with opioid use disorder than in the general population(Compton et al. 2005). Posttraumatic stress disorder is also seen with increased frequency(Price et al. 2004). A history of conduct disorder in childhood or adolescence has been identified as a significant risk factor for substance-related disorders, especially opioid use disorder.

References: Opioid Use Disorder

· Compton WM , Conway KP , Stinson FS , et al: Prevalence, correlates, and comorbidity of DSM-IV antisocial personality syndromes and alcohol and specific substance use disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions. J Clin Psychiatry 66(6):677–685, 2005

· Compton WM , Thomas YF , Stinson FS , Grant BF : Prevalence, correlates, disability, and comorbidity of DSM-IV drug abuse and dependence in the United States: results from the national epidemiologic survey on alcohol and related conditions. Arch Gen Psychiatry 64(5):566–576, 2007

· Compton WM , Dawson D , Duffy SQ , Grant BF : The effect of inmate populations on estimates of DSM-IV alcohol and drug use disorders in the United States. Am J Psychiatry 167(4):473–475, 2010

· Conway KP , Compton WM , Stinson FS , Grant BF : Lifetime comorbidity of DSM-IV mood and anxiety disorders and specific drug use disorders: results from the National Epidemiologic Survey on Alcohol and Related Conditions. J Clin Psychiatry 67(2):247–257, 2006

· European Monitoring Centre for Drugs and Drug Addiction : Opioid use and drug injection, in Annual Report 2010: The States of the Drugs Problem in Europe. Lisbon, European Monitoring Centre for Drugs and Drug Addiction, November 2010. Available at: http://www.emcdda.europa.eu/online/annual-report/2010/opioids. Accessed April 15, 2012..

· Fatseas M , Denis C , Massida Z , et al: Cue-induced reactivity, cortisol response and substance use outcome in treated heroin dependent individuals. Biol Psychiatry 70(8):720–727, 2011a

· Fatseas M , Denis C , Serre F , et al: Change in HIV-HCV risk-taking behavior and seroprevalence among opiate users seeking treatment over an 11-year period and harm reduction policy. AIDS Behav 16(7):2082–2090, 2011b

· Hser YI , Huang D , Chou CP , Anglin MD : Trajectories of heroin addiction: growth mixture modeling results based on a 33-year follow-up study. Eval Rev 31(6):548–563, 2007

· Kendler KS , Jacobson KC , Prescott CA , Neale MC : Specificity of genetic and environmental risk factors for use and abuse/dependence of cannabis, cocaine, hallucinogens, sedatives, stimulants, and opiates in male twins. Am J Psychiatry160(4):687–695, 2003

· Price RK , Risk NK , Spitznagel EL : Remission from drug abuse over a 25-year period: patterns of remission and treatment use. Am J Public Health 91(7):1107–1113, 2001

· Price RK , Risk NK , Haden AH , et al: Post-traumatic stress disorder, drug dependence, and suicidality among male Vietnam veterans with a history of heavy drug use. Drug Alcohol Depend 76(suppl):S31–43, 2004

· Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality : 2010 National Survey on Drug Use and Health:: Table 5.2B Substance dependence or abuse for specific substances in the past year, by age group: percentages 2009–2010. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2011. Available at: http:oas.samhsa.gov/nsduh/2K10NSDUH/tabs/Sect5peTabs1to56.htm#tab5.2B. Accessed June 15, 2012.

· Tsuang MT , Lyons MJ , Meyer JM , et al: Co-occurrence of abuse of different drugs in men: the role of drug-specific and shared vulnerabilities. Arch Gen Psychiatry 55(11):967–972, 1998

· Wu LT , Pan JJ , Blazer DG , et al: The construct and measurement equivalence of cocaine and opioid dependences: a National Drug Abuse Treatment Clinical Trials Network (CTN) study. Drug Alcohol Depend 103(3):114–123, 2009

Opioid Intoxication

Diagnostic Criteria

A. Recent use of an opioid.

B. Clinically significant problematic behavioral or psychological changes (e.g., initial euphoria followed by apathy, dysphoria, psychomotor agitation or retardation, impaired judgment) that developed during, or shortly after, opioid use.

C. Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) and one (or more) of the following signs or symptoms developing during, or shortly after, opioid use:

1. Drowsiness or coma.

2. Slurred speech.

3. Impairment in attention or memory.

D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication with another substance.

Specify if:

· With perceptual disturbances: This specifier may be noted in the rare instance in which hallucinations 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 292.89. The ICD-10-CM code depends on whether or not there is a comorbid opioid use disorder and whether or not there are perceptual disturbances.

· For opioid intoxication without perceptual disturbances: If a mild opioid use disorder is comorbid, the ICD-10-CM code is F11.129, and if a moderate or severe opioid use disorder is comorbid, the ICD-10-CM code isF11.229. If there is no comorbid opioid use disorder, then the ICD-10-CM code is F11.929.

· For opioid intoxication with perceptual disturbances: If a mild opioid use disorder is comorbid, the ICD-10-CM code is F11.122, and if a moderate or severe opioid use disorder is comorbid, the ICD-10-CM code is F11.222. If there is no comorbid opioid use disorder, then the ICD-10-CM code is F11.922.

Diagnostic Features

The essential feature of opioid intoxication is the presence of clinically significant problematic behavioral or psychological changes (e.g., initial euphoria followed by apathy, dysphoria, psychomotor agitation or retardation, impaired judgment) that develop during, or shortly after, opioid use (Criteria A and B)(Boyer 2012). Intoxication is accompanied by pupillary constriction (unless there has been a severe overdose with consequent anoxia and pupillary dilation) and one or more of the following signs: drowsiness (described as being “on the nod”), slurred speech, and impairment in attention or memory (Criterion C); drowsiness may progress to coma. Individuals with opioid intoxication may demonstrate inattention to the environment, even to the point of ignoring potentially harmful events. The signs or symptoms must not be attributable to another medical condition and are not better explained by another mental disorder (Criterion D).

Differential Diagnosis

Other substance intoxication

Alcohol intoxication and sedative-hypnotic intoxication can cause a clinical picture that resembles opioid intoxication. A diagnosis of alcohol or sedative-hypnotic intoxication can usually be made based on the absence of pupillary constriction or the lack of a response to a naloxone challenge. In some cases, intoxication may be due both to opioids and to alcohol or other sedatives. In these cases, the naloxone challenge will not reverse all of the sedative effects.

Other opioid-related disorders

Opioid intoxication is distinguished from the other opioid-induced disorders (e.g., opioid-induced depressive disorder, with onset during intoxication) because the symptoms in the latter disorders predominate in the clinical presentation and meet full criteria for the relevant disorder.

References: Opioid Intoxication

· Boyer EW : Management of opioid analgesic overdose. N Engl J Med 367(2):146–155, 2012

Opioid Withdrawal

Diagnostic Criteria

292.0 (F11.23)

A. Presence of either of the following:

1. Cessation of (or reduction in) opioid use that has been heavy and prolonged (i.e., several weeks or longer).

2. Administration of an opioid antagonist after a period of opioid use.

B. Three (or more) of the following developing within minutes to several days after Criterion A:

2. Dysphoric mood.

2. Nausea or vomiting.

2. Muscle aches.

2. Lacrimation or rhinorrhea.

2. Pupillary dilation, piloerection, or sweating.

2. Diarrhea.

2. Yawning.

2. Fever.

2. Insomnia.

1. The signs or symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

1. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication or withdrawal from another substance.

Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for opioid withdrawal is F11.23. Note that the ICD-10-CM code indicates the comorbid presence of a moderate or severe opioid use disorder, reflecting the fact that opioid withdrawal can only occur in the presence of a moderate or severe opioid use disorder. It is not permissible to code a comorbid mild opioid use disorder with opioid withdrawal.

Diagnostic Features

The essential feature of opioid withdrawal is the presence of a characteristic withdrawal syndrome that develops after the cessation of (or reduction in) opioid use that has been heavy and prolonged (Criterion A1). The withdrawal syndrome can also be precipitated by administration of an opioid antagonist (e.g., naloxone or naltrexone) after a period of opioid use (Criterion A2). This may also occur after administration of an opioid partial agonist such as buprenorphine to a person currently using a full opioid agonist.

Opioid withdrawal is characterized by a pattern of signs and symptoms that are opposite to the acute agonist effects. The first of these are subjective and consist of complaints of anxiety, restlessness, and an “achy feeling” that is often located in the back and legs, along with irritability and increased sensitivity to pain. Three or more of the following must be present to make a diagnosis of opioid withdrawal: dysphoric mood; nausea or vomiting; muscle aches; lacrimation or rhinorrhea; pupillary dilation, piloerection, or increased sweating; diarrhea; yawning; fever; and insomnia (Criterion B). Piloerection and fever are associated with more severe withdrawal and are not often seen in routine clinical practice because individuals with opioid use disorder usually obtain substances before withdrawal becomes that far advanced. These symptoms of opioid withdrawal must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). The symptoms must not be attributable to another medical condition and are not better explained by another mental disorder (Criterion D). Meeting diagnostic criteria for opioid withdrawal alone is not sufficient for a diagnosis of opioid use disorder, but concurrent symptoms of craving and drug-seeking behavior are suggestive of comorbid opioid use disorder. ICD-10-CM codes only allow a diagnosis of opioid withdrawal in the presence of comorbid moderate to severe opioid use disorder.

The speed and severity of withdrawal associated with opioids depend on the half-life of the opioid used. Most individuals who are physiologically dependent on short-acting drugs such as heroin begin to have withdrawal symptoms within 6–12 hours after the last dose. Symptoms may take 2–4 days to emerge in the case of longer-acting drugs such as methadone, LAAM (l-alpha-acetylmethadol), or buprenorphine. Acute withdrawal symptoms for a short-acting opioid such as heroin usually peak within 1–3 days and gradually subside over a period of 5–7 days. Less acute withdrawal symptoms can last for weeks to months. These more chronic symptoms include anxiety, dysphoria, anhedonia, and insomnia.

Associated Features Supporting Diagnosis

Males with opioid withdrawal may experience piloerection, sweating, and spontaneous ejaculations while awake. Opioid withdrawal is distinct from opioid use disorder and does not necessarily occur in the presence of the drug-seeking behavior associated with opioid use disorder. Opioid withdrawal may occur in any individual after cessation of repeated use of an opioid, whether in the setting of medical management of pain, during opioid agonist therapy for opioid use disorder, in the context of private recreational use, or following attempts to self-treat symptoms of mental disorders with opioids.

Prevalence

Among individuals from various clinical settings, opioid withdrawal occurred in 60% of individuals who had used heroin at least once in the prior 12 months(Hasin et al. 2012).

Development and Course

Opioid withdrawal is typical in the course of an opioid use disorder. It can be part of an escalating pattern in which an opioid is used to reduce withdrawal symptoms, in turn leading to more withdrawal at a later time. For persons with an established opioid use disorder, withdrawal and attempts to relieve withdrawal are typical(Koob 2009).

Differential Diagnosis

Other withdrawal disorders

The anxiety and restlessness associated with opioid withdrawal resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid withdrawal is also accompanied by rhinorrhea, lacrimation, and pupillary dilation, which are not seen in sedative-type withdrawal.

Other substance intoxication

Dilated pupils are also seen in hallucinogen intoxication and stimulant intoxication. However, other signs or symptoms of opioid withdrawal, such as nausea, vomiting, diarrhea, abdominal cramps, rhinorrhea, and lacrimation, are not present.

Other opioid-induced disorders

Opioid withdrawal is distinguished from the other opioid-induced disorders (e.g., opioid-induced depressive disorder, with onset during withdrawal) because the symptoms in these latter disorders are in excess of those usually associated with opioid withdrawal and meet full criteria for the relevant disorder.

References: Opioid Withdrawal

· Hasin DS , Fenton MC , Beseler C , et al: Analyses related to the development of DSM-5 criteria for substance use related disorders, 2: proposed DSM-5 criteria for alcohol, cannabis, cocaine and heroin disorders in 663 substance abuse patients.Drug Alcohol Depend 122(1–2):28–37, 2012

· Koob GF : Neurobiological substrates for the dark side of compulsivity in addiction. Neuropsychopharmacology 56(suppl 1):18–31, 2009

Other Opioid-Induced Disorders

The following opioid-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): opioid-induced depressive disorder (“Depressive Disorders”); opioid-induced anxiety disorder (“Anxiety Disorders”); opioid-induced sleep disorder (“Sleep-Wake Disorders”); and opioid-induced sexual dysfunction (“Sexual Dysfunctions”). For opioid intoxication delirium and opioid withdrawal delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These opioid-induced disorders are diagnosed instead of opioid intoxication or opioid withdrawal only when the symptoms are sufficiently severe to warrant independent clinical attention.

Unspecified Opioid-Related Disorder

292.9 (F11.99)

This category applies to presentations in which symptoms characteristic of an opioid-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific opioid-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Sedative-, Hypnotic-, or Anxiolytic-Related Disorders

1. Sedative, Hypnotic, or Anxiolytic Use Disorder

2. Sedative, Hypnotic, or Anxiolytic Intoxication

3. Sedative, Hypnotic, or Anxiolytic Withdrawal

4. Other Sedative-, Hypnotic-, or Anxiolytic-Induced Disorders

5. Unspecified Sedative-, Hypnotic-, or Anxiolytic-Related Disorder

Sedative, Hypnotic, or Anxiolytic Use Disorder

Diagnostic Criteria

A. A problematic pattern of sedative, hypnotic, or anxiolytic use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. Sedatives, hypnotics, or anxiolytics are 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 sedative, hypnotic, or anxiolytic use.

3. A great deal of time is spent in activities necessary to obtain the sedative, hypnotic, or anxiolytic; use the sedative, hypnotic, or anxiolytic; or recover from its effects.

4. Craving, or a strong desire or urge to use the sedative, hypnotic, or anxiolytic.

5. Recurrent sedative, hypnotic, or anxiolytic use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences from work or poor work performance related to sedative, hypnotic, or anxiolytic use; sedative-, hypnotic-, or anxiolytic-related absences, suspensions, or expulsions from school; neglect of children or household).

6. Continued sedative, hypnotic, or anxiolytic use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of sedatives, hypnotics, or anxiolytics (e.g., arguments with a spouse about consequences of intoxication; physical fights).

7. Important social, occupational, or recreational activities are given up or reduced because of sedative, hypnotic, or anxiolytic use.

8. Recurrent sedative, hypnotic, or anxiolytic use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by sedative, hypnotic, or anxiolytic use).

9. Sedative, hypnotic, or anxiolytic 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 the sedative, hypnotic, or anxiolytic.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of the sedative, hypnotic, or anxiolytic to achieve intoxication or desired effect.

b. A markedly diminished effect with continued use of the same amount of the sedative, hypnotic, or anxiolytic.

10. Note: This criterion is not considered to be met for individuals taking sedatives, hypnotics, or anxiolytics under medical supervision.

. Withdrawal, as manifested by either of the following:

a. The characteristic withdrawal syndrome for sedatives, hypnotics, or anxiolytics (refer to Criteria A and B of the criteria set for sedative, hypnotic, or anxiolytic withdrawal, pp. 557–558).

b. Sedatives, hypnotics, or anxiolytics (or a closely related substance, such as alcohol) are taken to relieve or avoid withdrawal symptoms.

1. Note: This criterion is not considered to be met for individuals taking sedatives, hypnotics, or anxiolytics under medical supervision.

Specify if:

· In early remission: After full criteria for sedative, hypnotic, or anxiolytic use disorder were previously met, none of the criteria for sedative, hypnotic, or anxiolytic use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the sedative, hypnotic, or anxiolytic,” may be met).

· In sustained remission: After full criteria for sedative, hypnotic, or anxiolytic use disorder were previously met, none of the criteria for sedative, hypnotic, or anxiolytic use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the sedative, hypnotic, or anxiolytic,” may be met).

Specify if:

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to sedatives, hypnotics, or anxiolytics is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If a sedative, hypnotic, or anxiolytic intoxication; sedative, hypnotic, or anxiolytic withdrawal; or another sedative-, hypnotic-, or anxiolytic-induced mental disorder is also present, do not use the codes below for sedative, hypnotic, or anxiolytic use disorder. Instead the comorbid sedative, hypnotic, or anxiolytic use disorder is indicated in the 4th character of the sedative-, hypnotic-, or anxiolytic-induced disorder (see the coding note for sedative, hypnotic, or anxiolytic intoxication; sedative, hypnotic, or anxiolytic withdrawal; or specific sedative-, hypnotic-, or anxiolytic-induced mental disorder). For example, if there is comorbid sedative-, hypnotic-, or anxiolytic-induced depressive disorder and sedative, hypnotic, or anxiolytic use disorder, only the sedative-, hypnotic-, or anxiolytic-induced depressive disorder code is given with the 4th character indicating whether the comorbid sedative, hypnotic, or anxiolytic use disorder is mild, moderate, or severe: F13.14 for mild sedative, hypnotic, or anxiolytic use disorder with sedative-, hypnotic-, or anxiolytic-induced depressive disorder or F13.24 for a moderate or severe sedative, hypnotic, or anxiolytic use disorder with sedative-, hypnotic-, or anxiolytic-induced depressive disorder.

Specify current severity /remission :

· 305.40 (F13.10) Mild: Presence of 2–3 symptoms.

· (F13.11) Mild, In early remission

· (F13.11) Mild, In sustained remission

· 304.10 (F13.20) Moderate: Presence of 4–5 symptoms.

· (F13.21) Moderate, In early remission

· (F13.21) Moderate, In sustained remission

· 304.10 (F13.20) Severe: Presence of 6 or more symptoms.

· (F13.21) Severe, In early remission

· (F13.21) Severe, In sustained remission

Specifiers

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Diagnostic Features

Sedative, hypnotic, or anxiolytic substances include benzodiazepines, benzodiazepine-like drugs (e.g., zolpidem, zaleplon), carbamates (e.g., glutethimide, meprobamate), barbiturates (e.g., secobarbital), and barbiturate-like hypnotics (e.g., glutethimide, methaqualone). This class of substances includes all prescription sleeping medications and almost all prescription antianxiety medications. Nonbenzodiazepine antianxiety agents (e.g., buspirone, gepirone) are not included in this class because they do not appear to be associated with significant misuse.

Like alcohol, these agents are brain depressants and can produce similar substance/medication-induced and substance use disorders. Sedative, hypnotic, or anxiolytic substances are available both by prescription and illegally. Some individuals who obtain these substances by prescription will develop a sedative, hypnotic, or anxiolytic use disorder, while others who misuse these substances or use them for intoxication will not develop a use disorder. In particular, sedatives, hypnotics, or anxiolytics with rapid onset and/or short to intermediate lengths of action may be taken for intoxication purposes, although longer acting substances in this class may be taken for intoxication as well(Licata and Rowlett 2008).

Craving (Criterion A4), either while using or during a period of abstinence, is a typical feature of sedative, hypnotic, or anxiolytic use disorder. Misuse of substances from this class may occur on its own or in conjunction with use of other substances. For example, individuals may use intoxicating doses of sedatives or benzodiazepines to “come down” from cocaine or amphetamines or use high doses of benzodiazepines in combination with methadone to “boost” its effects(Iguchi et al. 1993).

Repeated absences or poor work performance, school absences, suspensions or expulsions, and neglect of children or household (Criterion A5) may be related to sedative, hypnotic, or anxiolytic use disorder, as may the continued use of the substances despite arguments with a spouse about consequences of intoxication or despite physical fights (Criterion A6). Limiting contact with family or friends, avoiding work or school, or stopping participation in hobbies, sports, or games (Criterion A7) and recurrent sedative, hypnotic, or anxiolytic use when driving an automobile or operating a machine when impaired by sedative, hypnotic, or anxiolytic use (Criterion A8) are also seen in sedative, hypnotic, or anxiolytic use disorder.

Very significant levels of tolerance and withdrawal can develop to the sedative, hypnotic, or anxiolytic. There may be evidence of tolerance and withdrawal in the absence of a diagnosis of a sedative, hypnotic, or anxiolytic use disorder in an individual who has abruptly discontinued use of benzodiazepines that were taken for long periods of time at prescribed and therapeutic doses(O'Brien 2005). In these cases, an additional diagnosis of sedative, hypnotic, or anxiolytic use disorder is made only if other criteria are met. That is, sedative, hypnotic, or anxiolytic medications may be prescribed for appropriate medical purposes, and depending on the dose regimen, these drugs may then produce tolerance and withdrawal. If these drugs are prescribed or recommended for appropriate medical purposes, and if they are used as prescribed, the resulting tolerance or withdrawal does not meet the criteria for diagnosing a substance use disorder. However, it is necessary to determine whether the drugs were appropriately prescribed and used (e.g., falsifying medical symptoms to obtain the medication; using more medication than prescribed; obtaining the medication from several doctors without informing them of the others’ involvement).

Given the unidimensional nature of the symptoms of sedative, hypnotic, or anxiolytic use disorder (Gillespie et al. 2007), severity is based on the number of criteria endorsed.

Associated Features Supporting Diagnosis

Sedative, hypnotic, or anxiolytic use disorder is often associated with other substance use disorders (e.g., alcohol, cannabis, opioid, stimulant use disorders). Sedatives are often used to alleviate the unwanted effects of these other substances. With repeated use of the substance, tolerance develops to the sedative effects, and a progressively higher dose is used. However, tolerance to brain stem depressant effects develops much more slowly, and as the individual takes more substance to achieve euphoria or other desired effects, there may be a sudden onset of respiratory depression and hypotension, which may result in death. Intense or repeated sedative, hypnotic, or anxiolytic intoxication may be associated with severe depression that, although temporary, can lead to suicide attempt and completed suicide.

Prevalence

The 12-month prevalences of DSM-IV sedative, hypnotic, or anxiolytic use disorder are estimated to be 0.3% among 12- to 17-year-olds and 0.2% among adults age 18 years and older(Compton et al. 2007; Substance Abuse and Mental Health ServicesAdministration 2011). Rates of DSM-IV sedative, hypnotic, or anxiolytic use disorder are slightly greater among adult males (0.3%) than among adult females, but for 12- to 17-year-olds, the rate for females (0.4%) exceeds that for males (0.2%). The 12-month prevalence of DSM-IV sedative, hypnotic, or anxiolytic use disorder decreases as a function of age and is greatest among 18- to 29-year-olds (0.5%) and lowest among individuals 65 years and older (0.04%).

Twelve-month prevalence of sedative, hypnotic, or anxiolytic use disorder varies across racial/ethnic subgroups of the U.S. population(Compton et al. 2007; Substance Abuse and Mental Health Services Administration 2011). For 12- to 17-year-olds, rates are greatest among whites (0.3%) relative to African Americans (0.2%), Hispanics (0.2%), Native Americans (0.1%), and Asian Americans and Pacific Islanders (0.1%). Among adults, 12-month prevalence is greatest among Native Americans and Alaska Natives (0.8%), with rates of approximately 0.2% among African Americans, whites, and Hispanics and 0.1% among Asian Americans and Pacific Islanders.

Development and Course

The usual course of sedative, hypnotic, or anxiolytic use disorder involves individuals in their teens or 20s who escalate their occasional use of sedative, hypnotic, or anxiolytic agents to the point at which they develop problems that meet criteria for a diagnosis(Licata and Rowlett 2008). This pattern may be especially likely among individuals who have other substance use disorders (e.g., alcohol, opioids, stimulants). An initial pattern of intermittent use socially (e.g., at parties) can lead to daily use and high levels of tolerance. Once this occurs, an increasing level of interpersonal difficulties, as well as increasingly severe episodes of cognitive dysfunction and physiological withdrawal, can be expected.

The second and less frequently observed clinical course begins with an individual who originally obtained the medication by prescription from a physician, usually for the treatment of anxiety, insomnia, or somatic complaints. As either tolerance or a need for higher doses of the medication develops, there is a gradual increase in the dose and frequency of self-administration. The individual is likely to continue to justify use on the basis of his or her original symptoms of anxiety or insomnia, but substance-seeking behavior becomes more prominent, and the individual may seek out multiple physicians to obtain sufficient supplies of the medication. Tolerance can reach high levels, and withdrawal (including seizures and withdrawal delirium) may occur.

As with many substance use disorders, sedative, hypnotic, or anxiolytic use disorder generally has an onset during adolescence or early adult life. There is an increased risk for misuse and problems from many psychoactive substances as individuals age(Licata and Rowlett 2008). In particular, cognitive impairment increases as a side effect with age, and the metabolism of sedatives, hypnotics, or anxiolytics decreases with age among older individuals. Both acute and chronic toxic effects of these substances, especially effects on cognition, memory, and motor coordination, are likely to increase with age as a consequence of pharmacodynamic and pharmacokinetic age-related changes. Individuals with major neurocognitive disorder (dementia) are more likely to develop intoxication and impaired physiological functioning at lower doses.

Deliberate intoxication to achieve a “high” is most likely to be observed in teenagers and individuals in their 20s(Licata and Rowlett 2008). Problems associated with sedatives, hypnotics, or anxiolytics are also seen in individuals in their 40s and older who escalate the dose of prescribed medications. In older individuals, intoxication can resemble a progressive dementia.

Risk and Prognostic Factors

Temperamental

Impulsivity and novelty seeking are individual temperaments that relate to the propensity to develop a substance use disorder but may themselves be genetically determined.

Environmental

Since sedatives, hypnotics, or anxiolytics are all pharmaceuticals, a key risk factor relates to availability of the substances. In the United States, the historical patterns of sedative, hypnotic, or anxiolytic misuse relate to the broad prescribing patterns. For instance, a marked decrease in prescription of barbiturates was associated with an increase in benzodiazepine prescribing. Peer factors may relate to genetic predisposition in terms of how individuals select their environment. Other individuals at heightened risk might include those with alcohol use disorder who may receive repeated prescriptions in response to their complaints of alcohol-related anxiety or insomnia.

Genetic and physiological

As for other substance use disorders, the risk for sedative, hypnotic, or anxiolytic use disorder can be related to individual, family, peer, social, and environmental factors(Kendler et al. 2003; Tsuang et al. 1998). Within these domains, genetic factors play a particularly important role both directly and indirectly. Overall, across development, genetic factors seem to play a larger role in the onset of sedative, hypnotic, or anxiolytic use disorder as individuals age through puberty into adult life.

Course modifiers

Early onset of use is associated with greater likelihood for developing a sedative, hypnotic, or anxiolytic use disorder (McCabe et al. 2007).

Culture-Related Diagnostic Issues

There are marked variations in prescription patterns (and availability) of this class of substances in different countries, which may lead to variations in prevalence of sedative, hypnotic, or anxiolytic use disorders.

Gender-Related Diagnostic Issues

Females may be at higher risk than males for prescription drug misuse of sedative, hypnotic, or anxiolytic substances.

Diagnostic Markers

Almost all sedative, hypnotic, or anxiolytic substances can be identified through laboratory evaluations of urine or blood (the latter of which can quantify the amounts of these agents in the body). Urine tests are likely to remain positive for up to approximately 1 week after the use of long-acting substances, such as diazepam or flurazepam(Licata and Rowlett 2008).

Functional Consequences of Sedative, Hypnotic, or Anxiolytic Use Disorder

The social and interpersonal consequences of sedative, hypnotic, or anxiolytic use disorder mimic those of alcohol in terms of the potential for disinhibited behavior(Licata and Rowlett 2008). Accidents, interpersonal difficulties (such as arguments or fights), and interference with work or school performance are all common outcomes. Physical examination is likely to reveal evidence of a mild decrease in most aspects of autonomic nervous system functioning, including a slower pulse, a slightly decreased respiratory rate, and a slight drop in blood pressure (most likely to occur with postural changes). At high doses, sedative, hypnotic, or anxiolytic substances can be lethal, particularly when mixed with alcohol, although the lethal dosage varies considerably among the specific substances. Overdoses may be associated with a deterioration in vital signs that signals an impending medical emergency (e.g., respiratory arrest from barbiturates). There may be consequences of trauma (e.g., internal bleeding or a subdural hematoma) from accidents that occur while intoxicated. Intravenous use of these substances can result in medical complications related to the use of contaminated needles (e.g., hepatitis and HIV).

Acute intoxication can result in accidental injuries and automobile accidents. For elderly individuals, even short-term use of these sedating medications at prescribed doses can be associated with an increased risk for cognitive problems and falls. The disinhibiting effects of these agents, like alcohol, may potentially contribute to overly aggressive behavior, with subsequent interpersonal and legal problems. Accidental or deliberate overdoses, similar to those observed for alcohol use disorder or repeated alcohol intoxication, can occur. In contrast to their wide margin of safety when used alone, benzodiazepines taken in combination with alcohol can be particularly dangerous, and accidental overdoses are reported commonly. Accidental overdoses have also been reported in individuals who deliberately misuse barbiturates and other nonbenzodiazepine sedatives (e.g., methaqualone), but since these agents are much less available than the benzodiazepines, the frequency of overdosing is low in most settings.

Differential Diagnosis

Other mental disorders or medical conditions

Individuals with sedative-, hypnotic-, or anxiolytic-induced disorders may present with symptoms (e.g., anxiety) that resemble primary mental disorders (e.g., generalized anxiety disorder vs. sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with onset during withdrawal). The slurred speech, incoordination, and other associated features characteristic of sedative, hypnotic, or anxiolytic intoxication could be the result of another medical condition (e.g., multiple sclerosis) or of a prior head trauma (e.g., a subdural hematoma).

Alcohol use disorder

Sedative, hypnotic, or anxiolytic use disorder must be differentiated from alcohol use disorder.

Clinically appropriate use of sedative, hypnotic, or anxiolytic medications

Individuals may continue to take benzodiazepine medication according to a physician’s direction for a legitimate medical indication over extended periods of time. Even if physiological signs of tolerance or withdrawal are manifested, many of these individuals do not develop symptoms that meet the criteria for sedative, hypnotic, or anxiolytic use disorder because they are not preoccupied with obtaining the substance and its use does not interfere with their performance of usual social or occupational roles(O'Brien 2005).

Comorbidity

Nonmedical use of sedative, hypnotic, or anxiolytic agents is associated with alcohol use disorder, tobacco use disorder, and, generally, illicit drug use(Becker et al. 2007). There may also be an overlap between sedative, hypnotic, or anxiolytic use disorder and antisocial personality disorder(Compton et al. 2005); depressive, bipolar, and anxiety disorders(Becker et al. 2007; Conway et al. 2006); and other substance use disorders, such as alcohol use disorder and illicit drug use disorders(McCabe et al. 2008). Antisocial behavior and antisocial personality disorder are especially associated with sedative, hypnotic, or anxiolytic use disorder when the substances are obtained illegally.

References: Sedative, Hypnotic, or Anxiolytic Use Disorder

· Becker WC , Fiellin DA , Desai RA : Non-medical use, abuse and dependence on sedatives and tranquilizers among U.S. adults: psychiatric and socio-demographic correlates. Drug Alcohol Depend 90(2–3):280–287, 2007

· Compton WM , Conway KP , Stinson FS , et al: Prevalence, correlates, and comorbidity of DSM-IV antisocial personality syndromes and alcohol and specific substance use disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions. J Clin Psychiatry 66(6):677–685, 2005

· Compton WM , Thomas YF , Stinson FS , Grant BF : Prevalence, correlates, disability, and comorbidity of DSM-IV drug abuse and dependence in the United States: results from the national epidemiologic survey on alcohol and related conditions. Arch Gen Psychiatry 64(5):566–576, 2007

· Conway KP , Compton WM , Stinson FS , Grant BF : Lifetime comorbidity of DSM-IV mood and anxiety disorders and specific drug use disorders: results from the National Epidemiologic Survey on Alcohol and Related Conditions. J Clin Psychiatry 67(2):247–257, 2006

· Gillespie NA , Neale MC , Prescott CA , et al: Factor and item-response analysis DSM-IV criteria for abuse of and dependence on cannabis, cocaine, hallucinogens, sedatives, stimulants and opioids. Addiction 102(6):920–930, 2007

· Iguchi MY , Handelsman L , Bickel WK , Griffiths RR : Benzodiazepine and sedative use/abuse by methadone maintenance clients. Drug Alcohol Depend 32(3):257–266, 1993

· Kendler KS , Jacobson KC , Prescott CA , Neale MC : Specificity of genetic and environmental risk factors for use and abuse/dependence of cannabis, cocaine, hallucinogens, sedatives, stimulants, and opiates in male twins. Am J Psychiatry160(4)687–695, 2003

· Licata SC , Rowlett JK : Abuse and dependence liability of benzodiazepine-type drugs: GABA(A) receptor modulation and beyond. Pharmacol Biochem Behav 90(1):74–89, 2008

· McCabe SE , West BT , Morales M , et al: Does early onset of non-medical use of prescription drugs predict subsequent prescription drug abuse and dependence? Results from a national study. Addiction 102(12):1920–1930, 2007

· McCabe SE , Cranford JA , West BT : Trends in prescription drug abuse and dependence: co-occurrence with other substance use disorders, and treatment utilization: results from two national surveys. Addict Behav 33(10):1297–1305, 2008

· O’Brien CP : Benzodiazepine use, abuse, and dependence. J Clin Psychiatry 66(suppl 2):28–33, 2005

· Substance Abuse and Mental Health Services Administration : Results from the 2010 National Survey on Drug Use and Health: Summary of National Findings. NSDUH Series H-41, HHS Publ No (SMA) 11-4658. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2011. Available at:http://www.samhsa.gov/data/nsduh/2k10nsduh/2k10results.htm.

· Tsuang MT , Lyons MJ , Meyer JM , et al: Co-occurrence of abuse of different drugs in men: the role of drug-specific and shared vulnerabilities. Arch Gen Psychiatry 55(11):967–972, 1998

Sedative, Hypnotic, or Anxiolytic Intoxication

Diagnostic Criteria

A. Recent use of a sedative, hypnotic, or anxiolytic.

B. Clinically significant maladaptive behavioral or psychological changes (e.g., inappropriate sexual or aggressive behavior, mood lability, impaired judgment) that developed during, or shortly after, sedative, hypnotic, or anxiolytic use.

C. One (or more) of the following signs or symptoms developing during, or shortly after, sedative, hypnotic, or anxiolytic use:

1. Slurred speech.

2. Incoordination.

3. Unsteady gait.

4. Nystagmus.

5. Impairment in cognition (e.g., attention, 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, including intoxication with another substance.

Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether there is a comorbid sedative, hypnotic, or anxiolytic use disorder. If a mild sedative, hypnotic, or anxiolytic use disorder is comorbid, the ICD-10-CM code is F13.129, and if a moderate or severe sedative, hypnotic, or anxiolytic use disorder is comorbid, the ICD-10-CM code is F13.229. If there is no comorbid sedative, hypnotic, or anxiolytic use disorder, then the ICD-10-CM code is F13.929.

Note: For information on Development and Course; Risk and Prognostic Factors; Culture-Related Diagnostic Issues; Diagnostic Markers; Functional Consequences of Sedative, Hypnotic, or Anxiolytic Intoxication; and Comorbidity, see the corresponding sections in sedative, hypnotic, or anxiolytic use disorder.

Diagnostic Features

The essential feature of sedative, hypnotic, or anxiolytic intoxication (Licata and Rowlett 2008) is the presence of clinically significant maladaptive behavioral or psychological changes (e.g., inappropriate sexual or aggressive behavior, mood lability, impaired judgment, impaired social or occupational functioning) that develop during, or shortly after, use of a sedative, hypnotic, or anxiolytic (Criteria A and B). As with other brain depressants, such as alcohol, these behaviors may be accompanied by slurred speech, incoordination (at levels that can interfere with driving abilities and with performing usual activities to the point of causing falls or automobile accidents), an unsteady gait, nystagmus, impairment in cognition (e.g., attentional or memory problems), and stupor or coma (Criterion C). Memory impairment is a prominent feature of sedative, hypnotic, or anxiolytic intoxication and is most often characterized by an anterograde amnesia that resembles “alcoholic blackouts,” which can be disturbing to the individual. The symptoms must not be attributable to another medical condition and are not better explained by another mental disorder (Criterion D). Intoxication may occur in individuals who are receiving these substances by prescription, are borrowing the medication from friends or relatives, or are deliberately taking the substance to achieve intoxication.

Associated Features Supporting Diagnosis

Associated features include taking more medication than prescribed, taking multiple different medications, or mixing sedative, hypnotic, or anxiolytic agents with alcohol, which can markedly increase the effects of these agents.

Prevalence

The prevalence of sedative, hypnotic, or anxiolytic intoxication in the general population is unclear. However, it is probable that most nonmedical users of sedatives, hypnotics, or anxiolytics would at some time have signs or symptoms that meet criteria for sedative, hypnotic, or anxiolytic intoxication; if so, then the prevalence of nonmedical sedative, hypnotic, or anxiolytic use in the general population may be similar to the prevalence of sedative, hypnotic, or anxiolytic intoxication. For example, tranquilizers are used nonmedically by 2.2% of Americans older than 12 years(Substance Abuse and Mental Health Services Administration 2011).

Differential Diagnosis

Alcohol use disorders

Since the clinical presentations may be identical, distinguishing sedative, hypnotic, or anxiolytic intoxication from alcohol use disorders requires evidence for recent ingestion of sedative, hypnotic, or anxiolytic medications by self-report, informant report, or toxicological testing. Many individuals who misuse sedatives, hypnotics, or anxiolytics may also misuse alcohol and other substances, and so multiple intoxication diagnoses are possible.

Alcohol intoxication

Alcohol intoxication may be distinguished from sedative, hypnotic, or anxiolytic intoxication by the smell of alcohol on the breath. Otherwise, the features of the two disorders may be similar.

Other sedative-, hypnotic-, or anxiolytic-induced disorders

Sedative, hypnotic, or anxiolytic intoxication is distinguished from the other sedative-, hypnotic-, or anxiolytic-induced disorders (e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with onset during withdrawal) because the symptoms in the latter disorders predominate in the clinical presentation and are severe enough to warrant clinical attention.

Neurocognitive disorders

In situations of cognitive impairment, traumatic brain injury, and delirium from other causes, sedatives, hypnotics, or anxiolytics may be intoxicating at quite low dosages. The differential diagnosis in these complex settings is based on the predominant syndrome. An additional diagnosis of sedative, hypnotic, or anxiolytic intoxication may be appropriate even if the substance has been ingested at a low dosage in the setting of these other (or similar) co-occurring conditions.

References: Sedative, Hypnotic, or Anxiolytic Intoxication

· Licata SC , Rowlett JK : Abuse and dependence liability of benzodiazepine-type drugs: GABA(A) receptor modulation and beyond. Pharmacol Biochem Behav 90(1):74–89, 2008

· Substance Abuse and Mental Health Services Administration : Results from the 2010 National Survey on Drug Use and Health: summary of national findings. NSDUH Series H-41, HHS Publ No (SMA) 11-4658. Rockville, MD, Substance Abuse and Mental Health Services Administration, 2011

Sedative, Hypnotic, or Anxiolytic Withdrawal

Diagnostic Criteria

A. Cessation of (or reduction in) sedative, hypnotic, or anxiolytic use that has been prolonged.

B. Two (or more) of the following, developing within several hours to a few days after the cessation of (or reduction in) sedative, hypnotic, or anxiolytic use described in Criterion A:

1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).

2. Hand tremor.

3. Insomnia.

4. Nausea or vomiting.

5. Transient visual, tactile, or auditory hallucinations or illusions.

6. Psychomotor agitation.

7. Anxiety.

8. Grand mal seizures.

C. The signs or symptoms in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication or withdrawal from another substance.

Specify if:

· With perceptual disturbances: This specifier may be noted when hallucinations 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 292.0. The ICD-10-CM code for sedative, hypnotic, or anxiolytic withdrawal depends on whether or not there is a comorbid moderate or severe sedative, hypnotic, or anxiolytic use disorder and whether or not there are perceptual disturbances. For sedative, hypnotic, or anxiolytic withdrawal without perceptual disturbances, the ICD-10-CM code is F13.239. For sedative, hypnotic, or anxiolytic withdrawal with perceptual disturbances, the ICD-10-CM code is F13.232. Note that the ICD-10-CM codes indicate the comorbid presence of a moderate or severe sedative, hypnotic, or anxiolytic use disorder, reflecting the fact that sedative, hypnotic, or anxiolytic withdrawal can only occur in the presence of a moderate or severe sedative, hypnotic, or anxiolytic use disorder. It is not permissible to code a comorbid mild sedative, hypnotic, or anxiolytic use disorder with sedative, hypnotic, or anxiolytic withdrawal.

Note: For information on Development and Course; Risk and Prognostic Factors; Culture-Related Diagnostic Issues; Functional Consequences of Sedative, Hypnotic, or Anxiolytic Withdrawal; and Comorbidity, see the corresponding sections in sedative, hypnotic, or anxiolytic use disorder.

Diagnostic Features

The essential feature of sedative, hypnotic, or anxiolytic withdrawal is the presence of a characteristic syndrome that develops after a marked decrease in or cessation of intake after several weeks or more of regular use (Criteria A and B). This withdrawal syndrome is characterized by two or more symptoms (similar to alcohol withdrawal) that include autonomic hyperactivity (e.g., increases in heart rate, respiratory rate, blood pressure, or body temperature, along with sweating); a tremor of the hands; insomnia; nausea, sometimes accompanied by vomiting; anxiety; and psychomotor agitation. A grand mal seizure may occur in perhaps as many as 20%–30% of individuals undergoing untreated withdrawal from these substances. In severe withdrawal, visual, tactile, or auditory hallucinations or illusions can occur but are usually in the context of a delirium. If the individual’s reality testing is intact (i.e., he or she knows the substance is causing the hallucinations) and the illusions occur in a clear sensorium, the specifier “with perceptual disturbances” can be noted. When hallucinations occur in the absence of intact reality testing, a diagnosis of substance/medication-induced psychotic disorder should be considered. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). The symptoms must not be attributable to another medical condition and are not better explained by another mental disorder (e.g., alcohol withdrawal or generalized anxiety disorder) (Criterion D). Relief of withdrawal symptoms with administration of any sedative-hypnotic agent would support a diagnosis of sedative, hypnotic, or anxiolytic withdrawal.

Associated Features Supporting Diagnosis

The timing and severity of the withdrawal syndrome will differ depending on the specific substance and its pharmacokinetics and pharmacodynamics. For example, withdrawal from shorter-acting substances that are rapidly absorbed and that have no active metabolites (e.g., triazolam) can begin within hours after the substance is stopped; withdrawal from substances with long-acting metabolites (e.g., diazepam) may not begin for 1–2 days or longer. The withdrawal syndrome produced by substances in this class may be characterized by the development of a delirium that can be life-threatening. There may be evidence of tolerance and withdrawal in the absence of a diagnosis of a substance use disorder in an individual who has abruptly discontinued benzodiazepines that were taken for long periods of time at prescribed and therapeutic doses. However, ICD-10-CM codes only allow a diagnosis of sedative, hypnotic, or anxiolytic withdrawal in the presence of comorbid moderate to severe sedative, hypnotic, or anxiolytic use disorder.

The time course of the withdrawal syndrome is generally predicted by the half-life of the substance. Medications whose actions typically last about 10 hours or less (e.g., lorazepam, oxazepam, temazepam) produce withdrawal symptoms within 6–8 hours of decreasing blood levels that peak in intensity on the second day and improve markedly by the fourth or fifth day. For substances with longer half-lives (e.g., diazepam), symptoms may not develop for more than 1 week, peak in intensity during the second week, and decrease markedly during the third or fourth week. There may be additional longer-term symptoms at a much lower level of intensity that persist for several months.

The longer the substance has been taken and the higher the dosages used, the more likely it is that there will be severe withdrawal. However, withdrawal has been reported with as little as 15 mg of diazepam (or its equivalent in other benzodiazepines) when taken daily for several months. Doses of approximately 40 mg of diazepam (or its equivalent) daily are more likely to produce clinically relevant withdrawal symptoms, and even higher doses (e.g., 100 mg of diazepam) are more likely to be followed by withdrawal seizures or delirium. Sedative, hypnotic, or anxiolytic withdrawal delirium is characterized by disturbances in consciousness and cognition, with visual, tactile, or auditory hallucinations. When present, sedative, hypnotic, or anxiolytic withdrawal delirium should be diagnosed instead of withdrawal.

Prevalence

The prevalence of sedative, hypnotic, or anxiolytic withdrawal is unclear.

Diagnostic Markers

Seizures and autonomic instability in the setting of a history of prolonged exposure to sedative, hypnotic, or anxiolytic medications suggest a high likelihood of sedative, hypnotic, or anxiolytic withdrawal.

Differential Diagnosis

Other medical disorders

The symptoms of sedative, hypnotic, or anxiolytic withdrawal may be mimicked by other medical conditions (e.g., hypoglycemia, diabetic ketoacidosis). If seizures are a feature of the sedative, hypnotic, or anxiolytic withdrawal, the differential diagnosis includes the various causes of seizures (e.g., infections, head injury, poisonings).

Essential tremor

Essential tremor, a disorder that frequently runs in families, may erroneously suggest the tremulousness associated withsedative, hypnotic, or anxiolytic withdrawal.

Alcohol withdrawal

Alcohol withdrawal produces a syndrome very similar to that of sedative, hypnotic, or anxiolytic withdrawal.

Other sedative-, hypnotic-, or anxiolytic-induced disorders

Sedative, hypnotic, or anxiolytic withdrawal is distinguished from the other sedative-, hypnotic-, or anxiolytic-induced disorders (e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with onset during withdrawal) because the symptoms in the latter disorders predominate in the clinical presentation and are severe enough to warrant clinical attention.

Anxiety disorders

Recurrence or worsening of an underlying anxiety disorder produces a syndrome similar to sedative, hypnotic, or anxiolytic withdrawal. Withdrawal would be suspected with an abrupt reduction in the dosage of a sedative, hypnotic, or anxiolytic medication. When a taper is under way, distinguishing the withdrawal syndrome from the underlying anxiety disorder can be difficult(Licata and Rowlett 2008; O'Brien 2005). As with alcohol, lingering withdrawal symptoms (e.g., anxiety, moodiness, and trouble sleeping) can be mistaken for non-substance/medication-induced anxiety or depressive disorders (e.g.,generalized anxiety disorder).

References: Sedative, Hypnotic, or Anxiolytic Withdrawal

· Licata SC , Rowlett JK : Abuse and dependence liability of benzodiazepine-type drugs: GABA(A) receptor modulation and beyond. Pharmacol Biochem Behav 90(1):74–89, 2008

· O’Brien CP : Benzodiazepine use, abuse and dependence. J Clin Psychiatry 66(suppl 2):28–33, 2005

Other Sedative-, Hypnotic-, or Anxiolytic-Induced Disorders

The following sedative-, hypnotic-, or anxiolytic-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): sedative-, hypnotic-, or anxiolytic-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); sedative-, hypnotic-, or anxiolytic-induced bipolar disorder (“Bipolar and Related Disorders”); sedative-, hypnotic-, or anxiolytic-induced depressive disorder (“Depressive Disorders”); sedative-, hypnotic-, or anxiolytic-induced anxiety disorder (“Anxiety Disorders”); sedative-, hypnotic-, or anxiolytic-induced sleep disorder (“Sleep-Wake Disorders”); sedative-, hypnotic-, or anxiolytic-induced sexual dysfunction (“Sexual Dysfunctions”); and sedative-, hypnotic-, or anxiolytic-induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For sedative, hypnotic, or anxiolytic intoxication delirium and sedative, hypnotic, or anxiolytic withdrawal delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These sedative-, hypnotic-, or anxiolytic-induced disorders are diagnosed instead of sedative, hypnotic, or anxiolytic intoxication or sedative, hypnotic, or anxiolytic withdrawal only when the symptoms are sufficiently severe to warrant independent clinical attention.

Unspecified Sedative-, Hypnotic-, or Anxiolytic-Related Disorder

292.9 (F13.99)

This category applies to presentations in which symptoms characteristic of a sedative-, hypnotic-, or anxiolytic-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific sedative-, hypnotic-, or anxiolytic-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Stimulant-Related Disorders

1. Stimulant Use Disorder

2. Stimulant Intoxication

3. Stimulant Withdrawal

4. Other Stimulant-Induced Disorders

5. Unspecified Stimulant-Related Disorder

Stimulant Use Disorder

Diagnostic Criteria

A. A pattern of amphetamine-type substance, cocaine, or other stimulant use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. The stimulant 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 stimulant use.

3. A great deal of time is spent in activities necessary to obtain the stimulant, use the stimulant, or recover from its effects.

4. Craving, or a strong desire or urge to use the stimulant.

5. Recurrent stimulant use resulting in a failure to fulfill major role obligations at work, school, or home.

6. Continued stimulant use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the stimulant.

7. Important social, occupational, or recreational activities are given up or reduced because of stimulant use.

8. Recurrent stimulant use in situations in which it is physically hazardous.

9. Stimulant 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 the stimulant.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of the stimulant to achieve intoxication or desired effect.

b. A markedly diminished effect with continued use of the same amount of the stimulant.

10. Note: This criterion is not considered to be met for those taking stimulant medications solely under appropriate medical supervision, such as medications for attention-deficit/hyperactivity disorder or narcolepsy.

. Withdrawal, as manifested by either of the following:

a. The characteristic withdrawal syndrome for the stimulant (refer to Criteria A and B of the criteria set for stimulant withdrawal, p. 569).

b. The stimulant (or a closely related substance) is taken to relieve or avoid withdrawal symptoms.

1. Note: This criterion is not considered to be met for those taking stimulant medications solely under appropriate medical supervision, such as medications for attention-deficit/hyperactivity disorder or narcolepsy.

Specify if:

· In early remission: After full criteria for stimulant use disorder were previously met, none of the criteria for stimulant use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the stimulant,” may be met).

· In sustained remission: After full criteria for stimulant use disorder were previously met, none of the criteria for stimulant use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the stimulant,” may be met).

Specify if:

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to stimulants is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If an amphetamine intoxication, amphetamine withdrawal, or another amphetamine-induced mental disorder is also present, do not use the codes below for amphetamine use disorder. Instead, the comorbid amphetamine use disorder is indicated in the 4th character of the amphetamine-induced disorder code (see the coding note for amphetamine intoxication, amphetamine withdrawal, or a specific amphetamine-induced mental disorder). For example, if there is comorbid amphetamine-type or other stimulant-induced depressive disorder and amphetamine-type or other stimulant use disorder, only the amphetamine-type or other stimulant-induced depressive disorder code is given, with the 4th character indicating whether the comorbid amphetamine-type or other stimulant use disorder is mild, moderate, or severe: F15.14 for mild amphetamine-type or other stimulant use disorder with amphetamine-type or other stimulant-induced depressive disorder or F15.24 for a moderate or severe amphetamine-type or other stimulant use disorder with amphetamine-type or other stimulant-induced depressive disorder. Similarly, if there is comorbid cocaine-induced depressive disorder and cocaine use disorder, only the cocaine-induced depressive disorder code is given, with the 4th character indicating whether the comorbid cocaine use disorder is mild, moderate, or severe: F14.14 for mild cocaine use disorder with cocaine-induced depressive disorder or F14.24 for a moderate or severe cocaine use disorder with cocaine-induced depressive disorder.

Specify current severity /remission :

· Mild: Presence of 2–3 symptoms.

· 305.70 (F15.10) Amphetamine-type substance

· 305.60 (F14.10) Cocaine

· 305.70 (F15.10) Other or unspecified stimulant

· Mild, In early remission

· (F15.11) Amphetamine-type substance

· (F14.11) Cocaine

· (F15.11) Other or unspecified stimulant

· Mild, In sustained remission

· (F15.11) Amphetamine-type substance

· (F14.11) Cocaine

· (F15.11) Other or unspecified stimulant

· Moderate: Presence of 4–5 symptoms.

· 304.40 (F15.20) Amphetamine-type substance

· 304.20 (F14.20) Cocaine

· 304.40 (F15.20) Other or unspecified stimulant

· Moderate, In early remission

· (F15.21) Amphetamine-type substance

· (F14.21) Cocaine

· (F15.21) Other or unspecified stimulant

· Moderate, In sustained remission

· (F15.21) Amphetamine-type substance

· (F14.21) Cocaine

· (F15.21) Other or unspecified stimulant

· Severe: Presence of 6 or more symptoms.

· 304.40 (F15.20) Amphetamine-type substance

· 304.20 (F14.20) Cocaine

· 304.40 (F15.20) Other or unspecified stimulant

· Severe, In early remission

· (F15.21) Amphetamine-type substance

· (F14.21) Cocaine

· (F15.21) Other or unspecified stimulant

· Severe, In sustained remission

· (F15.21) Amphetamine-type substance

· (F14.21) Cocaine

· (F15.21) Other or unspecified stimulant

Specifiers

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Diagnostic Features

The amphetamine and amphetamine-type stimulants include substances with a substituted-phenylethylamine structure, such as amphetamine, dextroamphetamine, and methamphetamine. Also included are those substances that are structurally different but have similar effects, such as methylphenidate. These substances are usually taken orally or intravenously, although methamphetamine is also taken by the nasal route. In addition to the synthetic amphetamine-type compounds, there are naturally occurring, plant-derived stimulants such as khât. Amphetamines and other stimulants may be obtained by prescription for the treatment of obesity, attention-deficit/hyperactivity disorder, and narcolepsy. Consequently, prescribed stimulants may be diverted into the illegal market. The effects of amphetamines and amphetamine-like drugs are similar to those of cocaine, such that the criteria for stimulant use disorder are presented here as a single disorder with the ability to specify the particular stimulant used by the individual. Cocaine may be consumed in several preparations (e.g., coca leaves, coca paste, cocaine hydrochloride, and cocaine alkaloids such as freebase and crack) that differ in potency because of varying levels of purity and speed of onset. However, in all forms of the substance, cocaine is the active ingredient. Cocaine hydrochloride powder is usually “snorted” through the nostrils or dissolved in water and injected intravenously.

Individuals exposed to amphetamine-type stimulants or cocaine can develop stimulant use disorder as rapidly as 1 week, although the onset is not always this rapid. Regardless of the route of administration, tolerance occurs with repeated use. Withdrawal symptoms, particularly hypersomnia, increased appetite, and dysphoria, can occur and can enhance craving. Most individuals with stimulant use disorder have experienced tolerance or withdrawal.

Use patterns and course are similar for disorders involving amphetamine-type stimulants and cocaine, as both substances are potent central nervous system stimulants with similar psychoactive and sympathomimetic effects. Amphetamine-type stimulants are longer acting than cocaine and thus are used fewer times per day(Cruickshank and Dyer 2009). Usage may be chronic or episodic, with binges punctuated by brief non-use periods. Aggressive or violent behavior is common when high doses are smoked, ingested, or administered intravenously. Intense temporary anxiety resembling panic disorder orgeneralized anxiety disorder, as well as paranoid ideation and psychotic episodes that resemble schizophrenia, is seen with high-dose use.

Withdrawal states are associated with temporary but intense depressive symptoms that can resemble a major depressive episode (Mooney et al. 2009); the depressive symptoms usually resolve within 1 week(Newton et al. 2004). Tolerance to amphetamine-type stimulants develops and leads to escalation of the dose. Conversely, some users of amphetamine-type stimulants develop sensitization, characterized by enhanced effects.

Associated Features Supporting Diagnosis

When injected or smoked, stimulants typically produce an instant feeling of well-being, confidence, and euphoria. Dramatic behavioral changes can rapidly develop with stimulant use disorder. Chaotic behavior, social isolation, aggressive behavior, and sexual dysfunction can result from long-term stimulant use disorder.

Individuals with acute intoxication may present with rambling speech, headache, transient ideas of reference, and tinnitus. There may be paranoid ideation, auditory hallucinations in a clear sensorium, and tactile hallucinations, which the individual usually recognizes as drug effects. Threats or acting out of aggressive behavior may occur. Depression, suicidal ideation, irritability, anhedonia, emotional lability, or disturbances in attention and concentration commonly occur during withdrawal. Mental disturbances associated with cocaine use usually resolve hours to days after cessation of use but can persist for 1 month. Physiological changes during stimulant withdrawal are opposite to those of the intoxication phase, sometimes including bradycardia(McGregor et al. 2005). Temporary depressive symptoms may meet symptomatic and duration criteria for major depressive episode. Histories consistent with repeated panic attacks, social anxiety disorder (social phobia)–like behavior, and generalized anxiety–like syndromes are common, as are eating disorders. One extreme instance of stimulant toxicity is stimulant-induced psychotic disorder, a disorder that resembles schizophrenia, with delusions and hallucinations.

Individuals with stimulant use disorder often develop conditioned responses to drug-related stimuli (e.g., craving on seeing any white powderlike substance). These responses contribute to relapse, are difficult to extinguish, and persist after detoxification.

Depressive symptoms with suicidal ideation or behavior can occur and are generally the most serious problems seen duringstimulant withdrawal.

Prevalence

Stimulant use disorder: amphetamine-type stimulants

Estimated 12-month prevalence of amphetamine-type stimulant use disorder in the United States is 0.2% among 12- to 17-year-olds and 0.2% among individuals 18 years and older(Substance Abuse and Mental Health Services Administration 2011). Rates are similar among adult males and females (0.2%), but among 12- to 17-year-olds, the rate for females (0.3%) is greater than that for males (0.1%). Intravenous stimulant use has a male-to-female ratio of 3:1 or 4:1, but rates are more balanced among non-injecting users, with males representing 54% of primary treatment admissions. Twelve-month prevalence is greater among 18- to 29-year-olds (0.4%) compared with 45- to 64-year-olds (0.1%). For 12- to 17-year-olds, rates are highest among whites and African Americans (0.3%) compared with Hispanics (0.1%) and Asian Americans and Pacific Islanders (0.01%), with amphetamine-type stimulant use disorder virtually absent among Native Americans. Among adults, rates are highest among Native Americans and Alaska Natives (0.6%) compared with whites (0.2%) and Hispanics (0.2%), with amphetamine-type stimulant use disorder virtually absent among African Americans and Asian Americans and Pacific Islanders. Past-year nonprescribed use of prescription stimulants occurred among 5%–9% of children through high school, with 5%–35% of college-age persons reporting past-year use(Wilens et al. 2008).

Stimulant use disorder: cocaine

Estimated 12-month prevalence of cocaine use disorder in the United States is 0.2% among 12- to 17-year-olds and 0.3% among individuals 18 years and older(Substance Abuse and Mental Health Services Administration 2011). Rates are higher among males (0.4%) than among females (0.1%). Rates are highest among 18- to 29-year-olds (0.6%) and lowest among 45- to 64-year-olds (0.1%). Among adults, rates are greater among Native Americans (0.8%) compared with African Americans (0.4%), Hispanics (0.3%), whites (0.2%), and Asian Americans and Pacific Islanders (0.1%). In contrast, for 12- to 17-year-olds, rates are similar among Hispanics (0.2%), whites (0.2%), and Asian Americans and Pacific Islanders (0.2%); and lower among African Americans (0.02%); with cocaine use disorder virtually absent among Native Americans and Alaska Natives.

Development and Course

Stimulant use disorders occur throughout all levels of society and are more common among individuals ages 12–25 years compared with individuals 26 years and older(Substance Abuse and Mental Health Services Administration 2008). First regular use among individuals in treatment occurs, on average, at approximately age 23 years(Hser et al. 2008). For primary methamphetamine–primary treatment admissions, the average age is 31 years(Substance Abuse and Mental Health Services Administration 2008).

Some individuals begin stimulant use to control weight or to improve performance in school, work, or athletics. This includes obtaining medications such as methylphenidate or amphetamine salts prescribed to others for the treatment of attention-deficit/hyperactivity disorder. Stimulant use disorder can develop rapidly with intravenous or smoked administration; among primary admissions for amphetamine-type stimulant use, 66% reported smoking, 18% reported injecting, and 10% reported snorting(Substance Abuse and Mental Health Services Administration 2009).

Patterns of stimulant administration include episodic or daily (or almost daily) use. Episodic use tends to be separated by 2 or more days of non-use (e.g., intense use over a weekend or on one or more weekdays). “Binges” involve continuous high-dose use over hours or days and are often associated with physical dependence. Binges usually terminate only when stimulant supplies are depleted or exhaustion ensues. Chronic daily use may involve high or low doses, often with an increase in dose over time.

Stimulant smoking and intravenous use are associated with rapid progression to severe-level stimulant use disorder, often occurring over weeks to months. Intranasal use of cocaine and oral use of amphetamine-type stimulants result in more gradual progression occurring over months to years. With continuing use, there is a diminution of pleasurable effects due to tolerance and an increase in dysphoric effects.

Risk and Prognostic Factors

Temperamental

Comorbid bipolar disorder, schizophrenia, antisocial personality disorder, and other substance use disorders are risk factors for developing stimulant use disorder and for relapse to cocaine use in treatment samples(Poling et al. 2007). Also, impulsivity and similar personality traits may affect treatment outcomes. Childhood conduct disorder and adult antisocial personality disorder are associated with the later development of stimulant-related disorders.

Environmental

Predictors of cocaine use among teenagers include prenatal cocaine exposure, postnatal cocaine use by parents, and exposure to community violence during childhood(Delaney-Black et al. 2011). For youths, especially females, risk factors include living in an unstable home environment, having a psychiatric condition, and associating with dealers and users(Russell et al. 2008).

Culture-Related Diagnostic Issues

Stimulant use–attendant disorders affect all racial/ethnic, socioeconomic, age, and gender groups. Diagnostic issues may be related to societal consequences (e.g., arrest, school suspensions, employment suspension). Despite small variations, cocaine and other stimulant use disorder diagnostic criteria perform equally across gender and race/ethnicity groups(Blanco et al. 2007; Schmidt and Room 1999; Wu et al. 2009; Wu et al. 2010).

Chronic use of cocaine impairs cardiac left ventricular function in African Americans(Ren et al. 2006). Approximately 66% of individuals admitted for primary methamphetamine/amphetamine-related disorders are non-Hispanic white, followed by 21% of Hispanic origin, 3% Asian and Pacific Islander, and 3% non-Hispanic black(Substance Abuse and Mental Health Services Administration 2009).

Diagnostic Markers

Benzoylecgonine, a metabolite of cocaine, typically remains in the urine for 1–3 days after a single dose and may be present for 7–12 days in individuals using repeated high doses. Mildly elevated liver function tests can be present in cocaine injectors or users with concomitant alcohol use. There are no neurobiological markers of diagnostic utility. Discontinuation of chronic cocaine use may be associated with electroencephalographic changes, suggesting persistent abnormalities(Levin et al. 2007); alterations in secretion patterns of prolactin; and downregulation of dopamine receptors.

Short-half-life amphetamine-type stimulants (MDMA [3,4-methylenedioxy-N-methylamphetamine], methamphetamine) can be detected for 1–3 days, and possibly up to 4 days depending on dosage and metabolism. Hair samples can be used to detect presence of amphetamine-type stimulants for up to 90 days. Other laboratory findings, as well as physical findings and other medical conditions (e.g., weight loss, malnutrition; poor hygiene), are similar for both cocaine and amphetamine-type stimulant use disorder.

Functional Consequences of Stimulant Use Disorder

Various medical conditions may occur depending on the route of administration. Intranasal users often develop sinusitis, irritation, bleeding of the nasal mucosa, and a perforated nasal septum. Individuals who smoke the drugs are at increased risk for respiratory problems (e.g., coughing, bronchitis, and pneumonitis). Injectors have puncture marks and “tracks,” most commonly on their forearms. Risk of HIV infection increases with frequent intravenous injections and unsafe sexual activity. Other sexually transmitted diseases, hepatitis, and tuberculosis and other lung infections are also seen. Weight loss and malnutrition are common(Darke et al. 2008).

Chest pain may be a common symptom during stimulant intoxication (Schwartz et al. 2010). Myocardial infarction, palpitations and arrhythmias, sudden death from respiratory or cardiac arrest, and stroke have been associated with stimulant use among young and otherwise healthy individuals. Seizures can occur with stimulant use. Pneumothorax can result from performing Valsalva-like maneuvers done to better absorb inhaled smoke(Khalsa et al. 1992). Traumatic injuries due to violent behavior are common among individuals trafficking drugs. Cocaine use is associated with irregularities in placental blood flow, abruptio placentae, premature labor and delivery, and an increased prevalence of infants with very low birth weights.

Individuals with stimulant use disorder may become involved in theft, prostitution, or drug dealing in order to acquire drugs or money for drugs.

Neurocognitive impairment is common among methamphetamine users(Mooney et al. 2009; Scott et al. 2007; Wang et al. 2004). Oral health problems include “meth mouth” with gum disease, tooth decay, and mouth sores related to the toxic effects of smoking the drug and to bruxism while intoxicated(Shetty et al. 2010). Adverse pulmonary effects appear to be less common for amphetamine-type stimulants because they are smoked fewer times per day. Emergency department visits are common for stimulant-related mental disorder symptoms, injury, skin infections, and dental pathology(Hendrickson et al. 2008).

Differential Diagnosis

Primary mental disorders

Stimulant-induced disorders may resemble primary mental disorders (e.g., major depressive disorder) (for discussion of this differential diagnosis, see “Stimulant Withdrawal”). The mental disturbances resulting from the effects of stimulants should be distinguished from the symptoms of schizophrenia; depressive and bipolar disorders; generalized anxiety disorder; and panic disorder.

Phencyclidine intoxication

Intoxication with phencyclidine (“PCP” or “angel dust”) or synthetic “designer drugs” such as mephedrone (known by different names, including “bath salts”) may cause a similar clinical picture and can only be distinguished from stimulant intoxicationby the presence of cocaine or amphetamine-type substance metabolites in a urine or plasma sample.

Stimulant intoxication and withdrawal

Stimulant intoxication and withdrawal are distinguished from the other stimulant-induced disorders (e.g., anxiety disorder, with onset during intoxication) because the symptoms in the latter disorders predominate the clinical presentation and are severe enough to warrant independent clinical attention.

Comorbidity

Stimulant-related disorders often co-occur with other substance use disorders, especially those involving substances with sedative properties, which are often taken to reduce insomnia, nervousness, and other unpleasant side effects. Cocaine users often use alcohol, while amphetamine-type stimulant users often use cannabis. Stimulant use disorder may be associated with posttraumatic stress disorder, antisocial personality disorder, attention-deficit/hyperactivity disorder, and gambling disorder. Cardiopulmonary problems are often present in individuals seeking treatment for cocaine-related problems, with chest pain being the most common(Lange and Hillis 2001; Schwartz et al. 2010). Medical problems occur in response to adulterants used as “cutting” agents. Cocaine users who ingest cocaine cut with levamisole, an antimicrobial and veterinary medication, may experience agranulocytosis and febrile neutropenia(Chang et al. 2010; Marinetti 2009).

References: Stimulant Use Disorder

· Blanco C , Harford TC , Nunes E , et al: The latent structure of marijuana and cocaine use disorders: results from the National Longitudinal Alcohol Epidemiologic Survey (NLAES). Drug Alcohol Depend 91(1):91–96. 2007

· Chang A , Osterloh J , Thomas J : Levamisole: a dangerous new cocaine adulterant. Clin Pharmacol Ther 88(3):408–411,2010

· Cruickshank CC , Dyer KR : A review of the clinical pharmacology of methamphetamine. Addiction 104(7):1085–1099, 2009

· Darke S , Kaye S , McKetin R , Duflou J : Major physical and psychological harms of methamphetamine use. Drug Alcohol Rev 27(3):253–262, 2008

· Delaney-Black V , Chiodo LM , Hannigan JH , et al: Prenatal and postnatal cocaine exposure predict teen cocaine use. Neurotoxicol Teratol 33(1):110–119, 2011

· Hendrickson RG , Cloutier R , McConnell KJ : Methamphetamine-related emergency department utilization and cost. Acad Emerg Med 15(1):23–31, 2008

· Hser YI , Evans E , Huang D , et al: Comparing the dynamic course of heroin, cocaine, and methamphetamine use over 10 years. Addict Behav 33(12):1581–1589, 2008

· Khalsa ME , Tashkin DP , Perrochet B : Smoked cocaine: patterns of use and pulmonary consequences. J Psychoactive Drugs24(3):265–272, 1992

· Lange RA , Hillis LD : Cardiovascular complications of cocaine use. N Engl J Med 345(5):351–358, 2001

· Levin KH , Herning RI , Better WE , et al: EEG absolute power during extended cocaine abstinence. J Addict Med 1(3):139–144, 2007

· Marinetti LJ : Observations regarding levamisole in the cocaine supply. Ann Intern Med, Jan 29 2009

· McGregor C , Srisurapanont M , Jittiwutikarn J , et al: The nature, time course and severity of methamphetamine withdrawal. Addiction 100(9):1320–1329, 2005

· Mooney LJ , Glasner-Edwards S , Marinelli-Casey P , et al: Health conditions in methamphetamine-dependent adults 3 years after treatment. J Addict Med 3(3):155–163, 2009

· Newton TF , Kalechstein AD , Duran S , et al: Methamphetamine abstinence syndrome: preliminary findings. Am J Addict13(3):248–255, 2004

· Poling J , Kosten TR , Sofuoglu M : Treatment outcome predictors for cocaine dependence. Am J Drug Alcohol Abuse33(2):191–206, 2007

· Ren S , Tong W , Lai A , et al: Effect of long-term cocaine use on regional left ventricular function as determined by magnetic resonance imaging. Am J Cardiol 97(7):1085–1088, 2006

· Russell K , Dryden DM, Liang Y , et al: Risk factors for methamphetamine use in youth: a systematic review. BMC Pediatr8:48, 2008

· Schmidt L , Room R : Cross-cultural applicability in international classifications and research on alcohol dependence. J Stud Alcohol 60(4):448–462, 1999

· Schwartz BG , Rezkalla S , Kloner RA : Cardiovascular effects of cocaine. Circulation 122(24):2558–2569, 2010

· Scott JC , Woods SP , Matt GE , et al: Neurocognitive effects of methamphetamine: a critical review and meta-analysis. Neuropsychol Rev 17(3):275–297, 2007

· Shetty VS , Mooney LJ , Zigler CM , et al: The relationship between methamphetamine use and increased dental disease. J Am Dent Assoc 141(3):307–318, 2010

· Substance Abuse and Mental Health Services Administration, Office of Applied Studies : Primary methamphetamine/amphetamine admissions to substance abuse treatment: 2005. The DASIS Report. Rockville, MD,Substance Abuse and Mental Health Services Administration, February 7, 2008. Available at:http://www.samhsa.gov/data/2k8/methamphetamineTX/meth.htm. Accessed September 2012..

· Substance Abuse and Mental Health Services Administration, Office of Applied Studies : Trends in methamphetamine admissions to treatment: 1997–2007. The TEDS Report.. Rockville, MD, Substance Abuse and Mental Health Services Administration, October 1, 2009. Available at: http://www.samhsa.gov/data/2k9/209/209MethTrends2k9_web.pdf. Accessed September 2012..

· Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality : Results from the 2010 National Survey on Drug Use and Health: summary of national findings. NSDUH Series H-41, HHS Publ No SMA 11-4658. Rockville, MD, Substance Abuse and Mental Health Services Administration, September 2011. Available at:http://www.samhsa.gov/data/nsduh/2k10nsduh/2k10results.htm. Accessed September 2012..

· Wang GJ , Volkow ND , Chang L , et al: :Partial recovery of brain metabolism in methamphetamine abusers after protracted abstinence. Am J Psychiatry 161(2):242–248, 2004

· Wilens TE , Adler LA , Adams J , et al: Misuse and diversion of stimulants prescribed for ADHD: a systematic review of the literature. J Am Acad Child Adolesc Psychiatry 47(1):21–31, 2008

· Wu LT , Pan JJ , Blazer DG , et al: The construct and measurement equivalence of cocaine and opioid dependences: a National Drug Abuse Treatment Clinical Trials Network (CTN) study. Drug Alcohol Depend 103(3):114–123. 2009

· Wu LT , Pan JJ , Blazer DG , et al: Using a latent variable approach to inform gender and racial/ethnic differences in cocaine dependence: a National Drug Abuse Treatment Clinical Trials Network study. J Subst Abuse Treat 38(suppl 1):S70–S79,2010

Stimulant Intoxication

Diagnostic Criteria

A. Recent use of an amphetamine-type substance, cocaine, or other stimulant.

B. Clinically significant problematic behavioral or psychological changes (e.g., euphoria or affective blunting; changes in sociability; hypervigilance; interpersonal sensitivity; anxiety, tension, or anger; stereotyped behaviors; impaired judgment) that developed during, or shortly after, use of a stimulant.

C. Two (or more) of the following signs or symptoms, developing during, or shortly after, stimulant use:

1. Tachycardia or bradycardia.

2. Pupillary dilation.

3. Elevated or lowered blood pressure.

4. Perspiration or chills.

5. Nausea or vomiting.

6. Evidence of weight loss.

7. Psychomotor agitation or retardation.

8. Muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias.

9. Confusion, seizures, dyskinesias, dystonias, or coma.

D. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication with another substance.

Specify the specific intoxicant (i.e., amphetamine-type substance, cocaine, or other stimulant).

Specify if:

· With perceptual disturbances: This specifier may be noted when hallucinations 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 292.89. The ICD-10-CM code depends on whether the stimulant is an amphetamine, cocaine, or other stimulant; whether there is a comorbid amphetamine, cocaine, or other stimulant use disorder; and whether or not there are perceptual disturbances.

· For amphetamine, cocaine, or other stimulant intoxication, without perceptual disturbances: If a mild amphetamine or other stimulant use disorder is comorbid, the ICD-10-CM code is F15.129, and if a moderate or severe amphetamine or other stimulant use disorder is comorbid, the ICD-10-CM code is F15.229. If there is no comorbid amphetamine or other stimulant use disorder, then the ICD-10-CM code is F15.929. Similarly, if a mild cocaine use disorder is comorbid, the ICD-10-CM code is F14.129, and if a moderate or severe cocaine use disorder is comorbid, the ICD-10-CM code is F14.229. If there is no comorbid cocaine use disorder, then the ICD-10-CM code is F14.929.

· For amphetamine, cocaine, or other stimulant intoxication, with perceptual disturbances: If a mild amphetamine or other stimulant use disorder is comorbid, the ICD-10-CM code is F15.122, and if a moderate or severe amphetamine or other stimulant use disorder is comorbid, the ICD-10-CM code is F15.222. If there is no comorbid amphetamine or other stimulant use disorder, then the ICD-10-CM code is F15.922. Similarly, if a mild cocaine use disorder is comorbid, the ICD-10-CM code is F14.122, and if a moderate or severe cocaine use disorder is comorbid, the ICD-10-CM code is F14.222. If there is no comorbid cocaine use disorder, then the ICD-10-CM code is F14.922.

Diagnostic Features

The essential feature of stimulant intoxication, related to amphetamine-type stimulants and cocaine, is the presence of clinically significant behavioral or psychological changes that develop during, or shortly after, use of stimulants (Criteria A and B). Auditory hallucinations may be prominent, as may paranoid ideation, and these symptoms must be distinguished from an independent psychotic disorder such as schizophrenia. Stimulant intoxication usually begins with a “high” feeling and includes one or more of the following: euphoria with enhanced vigor, gregariousness, hyperactivity, restlessness, hypervigilance, interpersonal sensitivity, talkativeness, anxiety, tension, alertness, grandiosity, stereotyped and repetitive behavior, anger, impaired judgment, and, in the case of chronic intoxication, affective blunting with fatigue or sadness and social withdrawal. These behavioral and psychological changes are accompanied by two or more of the following signs and symptoms that develop during or shortly after stimulant use: tachycardia or bradycardia; pupillary dilation; elevated or lowered blood pressure; perspiration or chills; nausea or vomiting; evidence of weight loss; psychomotor agitation or retardation; muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias; and confusion, seizures, dyskinesias, dystonias, or coma (Criterion C). Intoxication, either acute or chronic, is often associated with impaired social or occupational functioning. Severe intoxication can lead to convulsions, cardiac arrhythmias, hyperpyrexia, and death. For the diagnosis of stimulant intoxication to be made, the symptoms must not be attributable to another medical condition and not better explained by another mental disorder (Criterion D). While stimulant intoxication occurs in individuals with stimulant use disorders, intoxication is not a criterion for stimulant use disorder, which is confirmed by the presence of two of the 11 diagnostic criteria for use disorder.

Associated Features Supporting Diagnosis

The magnitude and direction of the behavioral and physiological changes depend on many variables, including the dose used and the characteristics of the individual using the substance or the context (e.g., tolerance, rate of absorption, chronicity of use, context in which it is taken). Stimulant effects such as euphoria, increased pulse and blood pressure, and psychomotor activity are most commonly seen. Depressant effects such as sadness, bradycardia, decreased blood pressure, and decreased psychomotor activity are less common and generally emerge only with chronic high-dose use.

Differential Diagnosis

Stimulant-induced disorders

Stimulant intoxication is distinguished from the other stimulant-induced disorders (e.g., stimulant-induced depressive disorder, bipolar disorder, psychotic disorder, anxiety disorder) because the severity of the intoxication symptoms exceeds that associated with the stimulant-induced disorders, and the symptoms warrant independent clinical attention. Stimulant intoxication delirium would be distinguished by a disturbance in level of awareness and change in cognition.

Other mental disorders

Salient mental disturbances associated with stimulant intoxication should be distinguished from the symptoms ofschizophrenia, paranoid type; bipolar and depressive disorders; generalized anxiety disorder; and panic disorder as described in DSM-5.

Stimulant Withdrawal

Diagnostic Criteria

A. Cessation of (or reduction in) prolonged amphetamine-type substance, cocaine, or other stimulant use.

B. Dysphoric mood and two (or more) of the following physiological changes, developing within a few hours to several days after Criterion A:

1. Fatigue.

2. Vivid, unpleasant dreams.

3. Insomnia or hypersomnia.

4. Increased appetite.

5. Psychomotor retardation or 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 better explained by another mental disorder, including intoxication or withdrawal from another substance.

Specify the specific substance that causes the withdrawal syndrome (i.e., amphetamine-type substance, cocaine, or other stimulant).

· Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code depends on whether the stimulant is an amphetamine, cocaine, or other stimulant. The ICD-10-CM code for amphetamine or an other stimulant withdrawal is F15.23, and the ICD-10-CM for cocaine withdrawal is F14.23. Note that the ICD-10-CM code indicates the comorbid presence of a moderate or severe amphetamine, cocaine, or other stimulant use disorder, reflecting the fact that amphetamine, cocaine, or other stimulant withdrawal can only occur in the presence of a moderate or severe amphetamine, cocaine, or other stimulant use disorder. It is not permissible to code a comorbid mild amphetamine, cocaine, or other stimulant use disorder with amphetamine, cocaine, or other stimulant withdrawal.

Diagnostic Features

The essential feature of stimulant withdrawal is the presence of a characteristic withdrawal syndrome that develops within a few hours to several days after the cessation of (or marked reduction in) stimulant use (generally high dose) that has been prolonged (Criterion A). The withdrawal syndrome is characterized by the development of dysphoric mood accompanied by two or more of the following physiological changes: fatigue, vivid and unpleasant dreams, insomnia or hypersomnia, increased appetite, and psychomotor retardation or agitation (Criterion B). Bradycardia is often present and is a reliable measure of stimulant withdrawal(Ahmadi et al. 2008; Ahmadi et al. 2009; McGregor et al. 2005).

Anhedonia and drug craving can often be present but are not part of the diagnostic criteria. These symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion C). The symptoms must not be attributable to another medical condition and are not better explained by another mental disorder (Criterion D).

Associated Features Supporting Diagnosis

Acute withdrawal symptoms (“a crash”) are often seen after periods of repetitive high-dose use (“runs” or “binges”). These periods are characterized by intense and unpleasant feelings of lassitude and depression and increased appetite, generally requiring several days of rest and recuperation. Depressive symptoms with suicidal ideation or behavior can occur and are generally the most serious problems seen during “crashing” or other forms of stimulant withdrawal. The majority of individuals with stimulant use disorder experience a withdrawal syndrome at some point, and virtually all individuals with the disorder report tolerance.

Differential Diagnosis

Stimulant use disorder and other stimulant-induced disorders

Stimulant withdrawal is distinguished from stimulant use disorder and from the other stimulant-induced disorders (e.g., stimulant-induced intoxication delirium, depressive disorder, bipolar disorder, psychotic disorder, anxiety disorder, sexual dysfunction, sleep disorder) because the symptoms of withdrawal predominate the clinical presentation and are severe enough to warrant independent clinical attention.

References: Stimulant Withdrawal

· Ahmadi J , Kampman K , Dackis C , et al: Cocaine withdrawal symptoms identify “Type B” cocaine-dependent patients. Am J Addict 17(1):60–64, 2008

· Ahmadi J , Kampman KM , Oslin DM , et al: Predictors of treatment outcome in outpatient cocaine and alcohol dependence treatment. Am J Addict 18(1):81–86, 2009

· McGregor C , Srisurapanont M , Jittiwutikarn J , et al: The nature, time course and severity of methamphetamine withdrawal. Addiction 100(9):1320–1329, 2005

Other Stimulant-Induced Disorders

The following stimulant-induced disorders (which include amphetamine-, cocaine-, and other stimulant–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): stimulant-induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); stimulant-induced bipolar disorder (“Bipolar and Related Disorders”); stimulant-induced depressive disorder (“Depressive Disorders”); stimulant-induced anxiety disorder (“Anxiety Disorders”); stimulant-induced obsessive-compulsive disorder (“Obsessive-Compulsive and Related Disorders”); stimulant-induced sleep disorder (“Sleep-Wake Disorders”); and stimulant-induced sexual dysfunction (“Sexual Dysfunctions”). For stimulant intoxication delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These stimulant-induced disorders are diagnosed instead of stimulant intoxication or stimulant withdrawal only when the symptoms are sufficiently severe to warrant independent clinical attention.

Unspecified Stimulant-Related Disorder

This category applies to presentations in which symptoms characteristic of a stimulant-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific stimulant-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Coding note: The ICD-9-CM code is 292.9. The ICD-10-CM code depends on whether the stimulant is an amphetamine, cocaine, or another stimulant. The ICD-10-CM code for an unspecified amphetamine- or other stimulant-related disorder is F15.99. The ICD-10-CM code for an unspecified cocaine-related disorder is F14.99.

Tobacco-Related Disorders

1. Tobacco Use Disorder

2. Tobacco Withdrawal

3. Other Tobacco-Induced Disorders

4. Unspecified Tobacco-Related Disorder

Tobacco Use Disorder

Diagnostic Criteria

A. A problematic pattern of tobacco use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. Tobacco 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 tobacco use.

3. A great deal of time is spent in activities necessary to obtain or use tobacco.

4. Craving, or a strong desire or urge to use tobacco.

5. Recurrent tobacco use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., interference with work).

6. Continued tobacco use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of tobacco (e.g., arguments with others about tobacco use).

7. Important social, occupational, or recreational activities are given up or reduced because of tobacco use.

8. Recurrent tobacco use in situations in which it is physically hazardous (e.g., smoking in bed).

9. Tobacco 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 tobacco.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of tobacco to achieve the desired effect.

b. A markedly diminished effect with continued use of the same amount of tobacco.

11. Withdrawal, as manifested by either of the following:

11. The characteristic withdrawal syndrome for tobacco (refer to Criteria A and B of the criteria set for tobacco withdrawal).

11. Tobacco (or a closely related substance, such as nicotine) is taken to relieve or avoid withdrawal symptoms.

Specify if:

· In early remission: After full criteria for tobacco use disorder were previously met, none of the criteria for tobacco 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 tobacco,” may be met).

· In sustained remission: After full criteria for tobacco use disorder were previously met, none of the criteria for tobacco 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 tobacco,” may be met).

Specify if:

· On maintenance therapy: The individual is taking a long-term maintenance medication, such as nicotine replacement medication, and no criteria for tobacco use disorder have been met for that class of medication (except tolerance to, or withdrawal from, the nicotine replacement medication).

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to tobacco is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If a tobacco withdrawal or tobacco-induced sleep disorder is also present, do not use the codes below for tobacco use disorder. Instead, the comorbid tobacco use disorder is indicated in the 4th character of the tobacco-induced disorder code (see the coding note for tobacco withdrawal or tobacco-induced sleep disorder). For example, if there is comorbid tobacco-induced sleep disorder and tobacco use disorder, only the tobacco-induced sleep disorder code is given, with the 4th character indicating whether the comorbid tobacco use disorder is moderate or severe: F17.208 for moderate or severe tobacco use disorder with tobacco-induced sleep disorder. It is not permissible to code a comorbid mild tobacco use disorder with a tobacco-induced sleep disorder.

Specify current severity /remission :

· 305.1 (Z72.0) Mild: Presence of 2–3 symptoms.

· 305.1 (F17.200) Moderate: Presence of 4–5 symptoms.

· (F17.201) Moderate, In early remission

· (F17.201) Moderate, In sustained remission

· 305.1 (F17.200) Severe: Presence of 6 or more symptoms.

· (F17.201) Severe, In early remission

· (F17.201) Severe, In sustained remission

Specifiers

“On maintenance therapy” applies as a further specifier to individuals being maintained on other tobacco cessation medication (e.g., bupropion, varenicline) and as a further specifier of remission if the individual is both in remission and on maintenance therapy. “In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Diagnostic Features

Tobacco use disorder is common among individuals who use cigarettes and smokeless tobacco daily(Hughes et al. 2006) and is uncommon among individuals who do not use tobacco daily or who use nicotine medications(Shiffman et al. 2003). Tolerance to tobacco is exemplified by the disappearance of nausea and dizziness after repeated intake and with a more intense effect of tobacco the first time it is used during the day. Cessation of tobacco use can produce a well-defined withdrawal syndrome(Hughes 2007). Many individuals with tobacco use disorder use tobacco to relieve or to avoid withdrawal symptoms (e.g., after being in a situation where use is restricted). Many individuals who use tobacco have tobacco-related physical symptoms or diseases and continue to smoke. The large majority report craving when they do not smoke for several hours(Hughes 2007). Spending excessive time using tobacco can be exemplified by chain-smoking (i.e., smoking one cigarette after another with no time between cigarettes). Because tobacco sources are readily and legally available, and because nicotine intoxication is very rare, spending a great deal of time attempting to procure tobacco or recovering from its effects is uncommon. Giving up important social, occupational, or recreational activities can occur when an individual forgoes an activity because it occurs in tobacco use–restricted areas. Use of tobacco rarely results in failure to fulfill major role obligations (e.g., interference with work, interference with home obligations), but persistent social or interpersonal problems (e.g., having arguments with others about tobacco use, avoiding social situations because of others’ disapproval of tobacco use) or use that is physically hazardous (e.g., smoking in bed, smoking around flammable chemicals) occur at an intermediate prevalence. Although these criteria are less often endorsed by tobacco users, if endorsed, they can indicate a more severe disorder(Shmulewitz et al. 2011).

Associated Features Supporting Diagnosis

Smoking within 30 minutes of waking, smoking daily, smoking more cigarettes per day, and waking at night to smoke are associated with tobacco use disorder (Baker et al. 2012; Piper et al. 2006). Environmental cues can evoke craving and withdrawal. Serious medical conditions, such as lung and other cancers, cardiac and pulmonary disease, perinatal problems, cough, shortness of breath, and accelerated skin aging, often occur(National Center for Chronic Disease Prevention and Health Promotion 2004).

Prevalence

Cigarettes are the most commonly used tobacco product(Giovino 2007), representing over 90% of tobacco/nicotine use. In the United States, 57% of adults have never been smokers, 22% are former smokers, and 21% are current smokers(Centers for Disease Control and Prevention 2011). Approximately 20% of current U.S. smokers are nondaily smokers(Centers for Disease Control and Prevention 2011). The prevalence of smokeless tobacco use is less than 5%, and the prevalence of tobacco use in pipes and cigars is less than 1%(Centers for Disease Control and Prevention 2011; Giovino 2007).

DSM-IV nicotine dependence criteria can be used to estimate the prevalence of tobacco use disorder, but since they are a subset of tobacco use disorder criteria, the prevalence of tobacco use disorder will be somewhat greater. The 12-month prevalence of DSM-IV nicotine dependence in the United States is 13% among adults age 18 years and older(Grant et al. 2004). Rates are similar among adult males (14%) and females (12%) and decline in age from 17% among 18- to 29-year-olds to 4% among individuals age 65 years and older(Grant et al. 2004). The prevalence of current nicotine dependence is greater among Native American and Alaska Natives (23%) than among whites (14%) but is less among African Americans (10%), Asian Americans and Pacific Islanders (6%), and Hispanics (6%)(Grant et al. 2004). The prevalence among current daily smokers is approximately 50%(Hughes et al. 2006).

In many developing nations, the prevalence of smoking is much greater in males than in females, but this is not the case in developed nations(Wipfli and Samet 2009). However, there often is a lag in the demographic transition such that smoking increases in females at a later time(Wipfli and Samet 2009).

Development and Course

The majority of U.S. adolescents experiment with tobacco use, and by age 18 years, about 20% smoke at least monthly. Most of these individuals become daily tobacco users(Giovino 2007). Initiation of smoking after age 21 years is rare. In general, some of the tobacco use disorder criteria symptoms occur soon after beginning tobacco use(DiFranza 2008), and many individuals’ pattern of use meets current tobacco use disorder criteria by late adolescence(Giovino 2007). More than 80% of individuals who use tobacco attempt to quit at some time, but 60% relapse within 1 week and less than 5% remain abstinent for life(Hughes et al. 2004). However, most individuals who use tobacco make multiple attempts such that one-half of tobacco users eventually abstain(Giovino 2007). Individuals who use tobacco who do quit usually do not do so until after age 30 years. Although nondaily smoking in the United States was previously rare, it has become more prevalent in the last decade, especially among younger individuals who use tobacco.

Risk and Prognostic Factors

Temperamental

Individuals with externalizing personality traits are more likely to initiate tobacco use(Ziedonis et al. 2008). Children with attention-deficit/hyperactivity disorder or conduct disorder, and adults with depressive, bipolar, anxiety, personality, psychotic, or other substance use disorders, are at higher risk of starting and continuing tobacco use and of tobacco use disorder (Ziedonis et al. 2008).

Environmental

Individuals with low incomes and low educational levels are more likely to initiate tobacco use and are less likely to stop(Giovino 2007).

Genetic and physiological

Genetic factors contribute to the onset of tobacco use, the continuation of tobacco use, and the development of tobacco use disorder, with a degree of heritability equivalent to that observed with other substance use disorders (i.e., about 50%)(Munafò et al. 2004). Some of this risk is specific to tobacco, and some is common with the vulnerability to developing any substance use disorder.

Culture-Related Diagnostic Issues

Cultures and subcultures vary widely in their acceptance of the use of tobacco. The prevalence of tobacco use declined in the United States from the 1960s through the 1990s, but this decrease has been less evident in African American and Hispanic populations(Giovino 2007). Also, smoking in developing countries is more prevalent than in developed nations(Wipfli and Samet 2009). The degree to which these cultural differences are due to income, education, and tobacco control activities in a country is unclear(Giovino 2007; World Health Organization 2008). Non-Hispanic white smokers appear to be more likely to develop tobacco use disorder than are smokers(Giovino 2007). Some ethnic differences may be biologically based(Mickens et al. 2010). African American males tend to have higher nicotine blood levels for a given number of cigarettes, and this might contribute to greater difficulty in quitting. Also, the speed of nicotine metabolism is significantly different for whites compared with African Americans and can vary by genotypes associated with ethnicities.

Diagnostic Markers

Carbon monoxide in the breath, and nicotine and its metabolite cotinine in blood, saliva, or urine, can be used to measure the extent of current tobacco or nicotine use; however, these are only weakly related to tobacco use disorder (SRNT Subcommittee on Biochemical Verification 2002).

Functional Consequences of Tobacco Use Disorder

Medical consequences of tobacco use often begin when tobacco users are in their 40s and usually become progressively more debilitating over time(National Center for Chronic Disease Prevention and Health Promotion 2004). One-half of smokers who do not stop using tobacco will die early from a tobacco-related illness, and smoking-related morbidity occurs in more than one-half of tobacco users. Most medical conditions result from exposure to carbon monoxide, tars, and other non-nicotine components of tobacco. The major predictor of reversibility is duration of smoking. Secondhand smoke increases the risk of heart disease and cancer by 30%. Long-term use of nicotine medications does not appear to cause medical harm(Shields 2011).

Comorbidity

The most common medical diseases from smoking are cardiovascular illnesses, chronic obstructive pulmonary disease, and cancers(National Center for Chronic Disease Prevention and Health Promotion 2004). Smoking also increases perinatal problems, such as low birth weight and miscarriage(National Center for Chronic Disease Prevention and Health Promotion 2004). The most common psychiatric comorbidities are alcohol/substance, depressive, bipolar, anxiety, personality, and attention-deficit/hyperactivity disorders (Ziedonis et al. 2008). In individuals with current tobacco use disorder, the prevalence of current alcohol, drug, anxiety, depressive, bipolar, and personality disorders ranges from 22% to 32%(Grant et al. 2004). Nicotine-dependent smokers are 2.7–8.1 times more likely to have these disorders than nondependent smokers, never-smokers, or ex-smokers.

References: Tobacco Use Disorder

· Baker TB , Breslau N , Covey L , Shiffman S : DSM criteria for tobacco use disorder and tobacco withdrawal: a critique and proposed revisions for DSM-5. Addiction 107(2):263–275, 2012 10.1111/j.1360-0443.2011.03657.x

· Centers for Disease Control and Prevention : Vital signs: current cigarette smoking among adults aged ≥18 years—United States, 2005–2010. MMWR Morb Mortal Wkly Rep 60(35):1207–1211, 2011

· DiFranza JR : Hooked from the first cigarette. Sci Am 298(5):82–87, 2008

· Giovino GA : The tobacco epidemic in the United States. Am J Prev Med 33(6 suppl):S318–S326, 2007

· Grant BF , Hasin DS , Chou SP , et al: Nicotine dependence and psychiatric disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions. Arch Gen Psychiatry 61(11):1107–1115, 2004

· Hughes JR : The effects of abstinence from tobacco: valid symptoms and time course. Nicotine Tob Res 9(3):315–327, 2007

· Hughes JR , Keely J , Naud S : Shape of the relapse curve and long-term abstinence among untreated smokers. Addiction99(1):29–38, 2004

· Hughes JR , Helzer JE , Lindberg SA : Prevalence of DSM/ICD-defined nicotine dependence. Drug Alcohol Depend85(2):91–102, 2006

· Kroon LA : Drug interactions with smoking. Am J Health Syst Pharm 64(18):1917–1921, 2007

· Mickens L , Ameringer K , Brightman M , Leventhal AM : Epidemiology, determinants, and consequences of cigarette smoking in African American women: an integrative review. Addict Behav 35(5):383–391, 2010

· Munafò M , Clark T , Johnstone E , et al: The genetic basis for smoking behavior: a systematic review and meta-analysis.Nicotine Tob Res 6(4):583–597, 2004

· National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health : The Health Consequences of Smoking. A Report of the Surgeon General.. Atlanta, GA, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, May 27, 2004. Available at:http://www.cdc.gov/tobacco/data_statistics/sgr/2004/complete_report/index.htm. Accessed September 2012.

· Piper ME , McCarthy DE , Baker TB : Assessing tobacco dependence: a guide to measure evaluation and selection. Nicotine Tob Res 8(3):339–351,

· Shields P : Long-term nicotine replacement therapy: cancer risk in context. Cancer Prev Res 4(11):1719–1723, 2011

· Shiffman S , Hughes JR , Pillitteri JL , Burton SL : Persistent use of nicotine replacement therapy: an analysis of actual purchase patterns in a population-based sample. Tob Control 12(3):310–316, 2003

· Shmulewitz D , Keyes KM , Wall MM , et al: Nicotine dependence, abuse and craving: dimensionality in an Israeli sample.Addiction 106(9):1675–1686, 2011 10.1111/j.1360-0443.2011.03484.x

· SRNT Subcommittee on Biochemical Verification : Biochemical verification of tobacco use and cessation. Nicotine Tob Res4(2):149–159, 2002

· Wipfli H , Samet J : Global economic and health benefits of tobacco control, part 1. Clin Pharmacol Ther 86(3):263–271,2009

· World Health Organization : WHO Report on the Global Tobacco Epidemic, 2008: The MPOWER Package. Geneva, World Health Organization, 2008

· Ziedonis D , Hitsman B , Beckham JC , et al: Tobacco use and cessation in psychiatric disorders: National Institute of Mental Health report. Nicotine Tob Res 10(12):1691–1715, 2008

Tobacco Withdrawal

Diagnostic Criteria

292.0 (F17.203)

A. Daily use of tobacco for at least several weeks.

B. Abrupt cessation of tobacco use, or reduction in the amount of tobacco used, followed within 24 hours by four (or more) of the following signs or symptoms:

1. Irritability, frustration, or anger.

2. Anxiety.

3. Difficulty concentrating.

4. Increased appetite.

5. Restlessness.

6. Depressed mood.

7. Insomnia.

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 attributed to another medical condition and are not better explained by another mental disorder, including intoxication or withdrawal from another substance.

Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for tobacco withdrawal is F17.203. Note that the ICD-10-CM code indicates the comorbid presence of a moderate or severe tobacco use disorder, reflecting the fact that tobacco withdrawal can only occur in the presence of a moderate or severe tobacco use disorder. It is not permissible to code a comorbid mild tobacco use disorder with tobacco withdrawal.

Diagnostic Features

Withdrawal symptoms impair the ability to stop tobacco use. The symptoms after abstinence from tobacco are in large part due to nicotine deprivation. Symptoms are much more intense among individuals who smoke cigarettes or use smokeless tobacco than among those who use nicotine medications. This difference in symptom intensity is likely due to the more rapid onset and higher levels of nicotine with cigarette smoking. Tobacco withdrawal is common among daily tobacco users who stop or reduce but can also occur among nondaily users. Typically, heart rate decreases by 5–12 beats per minute in the first few days after stopping smoking, and weight increases an average of 4–7 lb (2–3 kg) over the first year after stopping smoking. Tobacco withdrawal can produce clinically significant mood changes and functional impairment.

Associated Features Supporting Diagnosis

Craving for sweet or sugary foods and impaired performance on tasks requiring vigilance are associated with tobacco withdrawal(Hughes 2007). Abstinence can increase constipation, coughing, dizziness, dreaming/nightmares, nausea, and sore throat. Smoking increases the metabolism of many medications used to treat mental disorders; thus, cessation of smoking can increase the blood levels of these medications, and this can produce clinically significant outcomes(Kroon 2007). This effect appears to be due not to nicotine but rather to other compounds in tobacco.

Prevalence

Approximately 50% of tobacco users who quit for 2 or more days will have symptoms that meet criteria for tobacco withdrawal(Hughes 2007). The most commonly endorsed signs and symptoms are anxiety, irritability, and difficulty concentrating. The least commonly endorsed symptoms are depression and insomnia.

Development and Course

Tobacco withdrawal usually begins within 24 hours of stopping or cutting down on tobacco use, peaks at 2–3 days after abstinence, and lasts 2–3 weeks(Hughes 2007). Tobacco withdrawal symptoms can occur among adolescent tobacco users, even prior to daily tobacco use(DiFranza 2008). Prolonged symptoms beyond 1 month are uncommon.

Risk and Prognostic Factors

Temperamental

Smokers with depressive disorders, bipolar disorders, anxiety disorders, attention-deficit/hyperactivity disorder, and other substance use disorders have more severe withdrawal(Ziedonis et al. 2008).

Genetic and physiological

Genotype can influence the probability of withdrawal upon abstinence(Pergadia et al. 2006).

Diagnostic Markers

Carbon monoxide in the breath, and nicotine and its metabolite cotinine in blood, saliva, or urine, can be used to measure the extent of tobacco or nicotine use but are only weakly related to tobacco withdrawal (SRNT Subcommittee on Biochemcial Verification 2002).

Functional Consequences of Tobacco Withdrawal

Abstinence from cigarettes can cause clinically significant distress(Hughes 2007). Withdrawal impairs the ability to stop or control tobacco use. Whether tobacco withdrawal can prompt a new mental disorder or recurrence of a mental disorder is debatable(Prochaska et al. 2004), but if this occurs, it would be in a small minority of tobacco users.

Differential Diagnosis

The symptoms of tobacco withdrawal overlap with those of other substance withdrawal syndromes (e.g., alcohol withdrawal; sedative, hypnotic, or anxiolytic withdrawal; stimulant withdrawal; caffeine withdrawal; opioid withdrawal); caffeine intoxication; anxiety, depressive, bipolar, and sleep disorders; and medication-induced akathisia(Hughes 1993). Admission to smoke-free inpatient units or voluntary smoking cessation can induce withdrawal symptoms that mimic, intensify, or disguise other disorders or adverse effects of medications used to treat mental disorders (e.g., irritability thought to be due to alcohol withdrawal could be due to tobacco withdrawal). Reduction in symptoms with the use of nicotine medications confirms the diagnosis.

References: Tobacco Withdrawal

· DiFranza JR : Hooked from the first cigarette. Sci Am 298(5):82–87, 2008

· Hughes JR : Possible effects of smoke-free inpatient units on psychiatric diagnosis and treatment. J Clin Psychiatry54(3):109–114, 1993

· Hughes JR : Effects of abstinence from tobacco: valid symptoms and time course. Nicotine Tob Res 9(3):315–327, 2007

· Kroon L : Drug interactions with smoking. Am J Health Syst Pharm 64(18):1917–1921, 2007

· Pergadia ML , Heath AC , Martin NG , Madden PA : Genetic analyses of DSM-IV nicotine withdrawal in adult twins. Psychol Med 36(7):963–972, 2006

· Prochaska J , Delucchi K , Hall SM : A meta-analysis of smoking cessation interventions with individuals in substance abuse treatment or recovery. J Consult Clin Psychol 72(6):1144–1156, 2004

· SRNT Subcommittee on Biochemical Verification : Biochemical verification of tobacco use and cessation. Nicotine Tob Res4(2):149–159, 2002

· Ziedonis D , Hitsman B , Beckham JC , et al: Tobacco use and cessation in psychiatric disorders: National Institute of Mental Health report. Nicotine Tob Res 10(12):1691–1715, 2008

Other Tobacco-Induced Disorders

Tobacco-induced sleep disorder is discussed in the chapter “Sleep-Wake Disorders” (see “Substance/Medication-Induced Sleep Disorder”).

Unspecified Tobacco-Related Disorder

292.9 (F17.209)

This category applies to presentations in which symptoms characteristic of a tobacco-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific tobacco-related disorder or any of the disorders in the substance-related and addictive disorders diagnostic class.

Other (or Unknown) Substance–Related Disorders

1. Other (or Unknown) Substance Use Disorder

2. Other (or Unknown) Substance Intoxication

3. Other (or Unknown) Substance Withdrawal

4. Other (or Unknown) Substance–Induced Disorders

5. Unspecified Other (or Unknown) Substance–Related Disorder

Other (or Unknown) Substance Use Disorder

Diagnostic Criteria

A. A problematic pattern of use of an intoxicating substance not able to be classified within the alcohol; caffeine; cannabis; hallucinogen (phencyclidine and others); inhalant; opioid; sedative, hypnotic, or anxiolytic; stimulant; or tobacco categories and leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. The substance 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 use of the substance.

3. A great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from its effects.

4. Craving, or a strong desire or urge to use the substance.

5. Recurrent use of the substance resulting in a failure to fulfill major role obligations at work, school, or home.

6. Continued use of the substance despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of its use.

7. Important social, occupational, or recreational activities are given up or reduced because of use of the substance.

8. Recurrent use of the substance in situations in which it is physically hazardous.

9. Use of the substance is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance.

10. Tolerance, as defined by either of the following:

a. A need for markedly increased amounts of the substance to achieve intoxication or desired effect.

b. A markedly diminished effect with continued use of the same amount of the substance.

11. Withdrawal, as manifested by either of the following:

11. The characteristic withdrawal syndrome for other (or unknown) substance (refer to Criteria A and B of the criteria sets for other [or unknown] substance withdrawal, p. 583).

11. The substance (or a closely related substance) is taken to relieve or avoid withdrawal symptoms.

Specify if:

· In early remission: After full criteria for other (or unknown) substance use disorder were previously met, none of the criteria for other (or unknown) substance use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the substance,” may be met).

· In sustained remission: After full criteria for other (or unknown) substance use disorder were previously met, none of the criteria for other (or unknown) substance use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the substance,” may be met).

Specify if:

· In a controlled environment: This additional specifier is used if the individual is in an environment where access to the substance is restricted.

Coding based on current severity /remission : Note for ICD-10-CM codes: If an other (or unknown) substance intoxication, other (or unknown) substance withdrawal, or another other (or unknown) substance–induced mental disorder is present, do not use the codes below for other (or unknown) substance use disorder. Instead, the comorbid other (or unknown) substance use disorder is indicated in the 4th character of the other (or unknown) substance–induced disorder code (see the coding note for other (or unknown) substance intoxication, other (or unknown) substance withdrawal, or specific other (or unknown) substance–induced mental disorder). For example, if there is comorbid other (or unknown) substance–induced depressive disorder and other (or unknown) substance use disorder, only the other (or unknown) substance–induced depressive disorder code is given, with the 4th character indicating whether the comorbid other (or unknown) substance use disorder is mild, moderate, or severe: F19.14 for other (or unknown) substance use disorder with other (or unknown) substance–induced depressive disorder or F19.24 for a moderate or severe other (or unknown) substance use disorder with other (or unknown) substance–induced depressive disorder.

Specify current severity /remission :

· 305.90 (F19.10) Mild: Presence of 2–3 symptoms.

· (F19.11) Mild, In early remission

· (F19.11) Mild, In sustained remission

· 304.90 (F19.20) Moderate: Presence of 4–5 symptoms.

· (F19.21) Moderate, In early remission

· (F19.21) Moderate, In sustained remission

· 304.90 (F19.20) Severe: Presence of 6 or more symptoms.

· (F19.21) Severe, In early remission

· (F19.21) Severe, In sustained remission

Specifiers

“In a controlled environment” applies as a further specifier of remission if the individual is both in remission and in a controlled environment (i.e., in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.

Diagnostic Features

The diagnostic class other (or unknown) substance use and related disorders comprises substance-related disorders unrelated to alcohol; caffeine; cannabis; hallucinogens (phencyclidine and others); inhalants; opioids; sedative, hypnotics, or anxiolytics; stimulants (including amphetamine and cocaine); or tobacco. Such substances include anabolic steroids(Kanayama et al. 2009); nonsteroidal anti-inflammatory drugs; cortisol; antiparkinsonian medications(Dagher and Robbins 2009); antihistamines; nitrous oxide; amyl-, butyl-, or isobutyl-nitrites(Wu et al. 2005); betel nut(Gupta and Ray 2004), which is chewed in many cultures to produce mild euphoria and a floating sensation; kava (from a South Pacific pepper plant), which produces sedation, incoordination, weight loss, mild hepatitis, and lung abnormalities; or cathinones (including khât plant agents and synthetic chemical derivatives) that produce stimulant effects(Kelly 2011). Unknown substance-related disorders are associated with unidentified substances, such as intoxications in which the individual cannot identify the ingested drug, or substance use disorders involving either new, black market drugs not yet identified or familiar drugs illegally sold under false names.

Other (or unknown) substance use disorder is a mental disorder in which repeated use of an other or unknown substance typically continues, despite the individual’s knowing that the substance is causing serious problems for the individual. Those problems are reflected in the diagnostic criteria. When the substance is known, it should be reflected in the name of the disorder upon coding (e.g., nitrous oxide use disorder).

Associated Features Supporting Diagnosis

A diagnosis of other (or unknown) substance use disorder is supported by the individual’s statement that the substance involved is not among the nine classes listed in this chapter; by recurring episodes of intoxication with negative results in standard drug screens (which may not detect new or rarely used substances); or by the presence of symptoms characteristic of an unidentified substance that has newly appeared in the individual’s community.

Because of increased access to nitrous oxide (“laughing gas”), membership in certain populations is associated with diagnosis of nitrous oxide use disorder. The role of this gas as an anesthetic agent leads to misuse by some medical and dental professionals(Blanton 2006). Its use as a propellant for commercial products (e.g., whipped cream dispensers) contributes to misuse by food service workers. With recent widespread availability of the substance in “whippet” cartridges for use in home whipped cream dispensers, nitrous oxide misuse by adolescents and young adults is significant(Substance Abuse and Mental Health Services 2008), especially among those who also inhale volatile hydrocarbons. Some continuously using individuals, inhaling from as many as 240 whippets per day, may present with serious medical complications and mental conditions, including myeloneuropathy(Alt et al. 2010), spinal cord subacute combined degeneration(Cartner et al. 2007), peripheral neuropathy(Richardson 2010), and psychosis(Sethi et al. 2006). These conditions are also associated with a diagnosis ofnitrous oxide use disorder.

Use of amyl-, butyl-, and isobutyl nitrite gases has been observed among homosexual men(Colfax et al. 2005; Hidaka et al. 2006; Lampinen et al. 2007) and some adolescents, especially those with conduct disorder (Wu et al. 2005). Membership in these populations may be associated with a diagnosis of amyl-, butyl-, or isobutyl-nitrite use disorder. However, it has not been determined that these substances produce a substance use disorder (Ridenour et al. 2007). Despite tolerance(Marsh and Marsh 2000), these gases may not alter behavior through central effects(Balster 1998), and they may be used only for their peripheral effects.

Substance use disorders generally are associated with elevated risks of suicide, but there is no evidence of unique risk factors for suicide with other (or unknown) substance use disorder.

Prevalence

Based on extremely limited data, the prevalence of other (or unknown) substance use disorder is likely lower than that of use disorders involving the nine substance classes in this chapter.

Development and Course

No single pattern of development or course characterizes the pharmacologically varied other (or unknown) substance use disorders. Often unknown substance use disorders will be reclassified when the unknown substance eventually is identified.

Risk and Prognostic Factors

Risk and prognostic factors for other (or unknown) substance use disorders are thought to be similar to those for most substance use disorders and include the presence of any other substance use disorders, conduct disorder, or antisocial personality disorder in the individual or the individual’s family; early onset of substance problems; easy availability of the substance in the individual’s environment; childhood maltreatment or trauma; and evidence of limited early self-control and behavioral disinhibition.

Culture-Related Diagnostic Issues

Certain cultures may be associated with other (or unknown) substance use disorders involving specific indigenous substances within the cultural region, such as betel nut.

Diagnostic Markers

Urine, breath, or saliva tests may correctly identify a commonly used substance falsely sold as a novel product. However, routine clinical tests usually cannot identify truly unusual or new substances, which may require testing in specialized laboratories.

Differential Diagnosis

Use of other or unknown substances without meeting criteria for other (or unknown) substance use disorder

Use of unknown substances is not rare among adolescents, but most use does not meet the diagnostic standard of two or more criteria for other (or unknown) substance use disorder in the past year.

Substance use disorders

Other (or unknown) substance use disorder may co-occur with various substance use disorders, and the symptoms of the disorders may be similar and overlapping. To disentangle symptom patterns, it is helpful to inquire about which symptoms persisted during periods when some of the substances were not being used.

Other (or unknown) substance/medication-induced disorder

This diagnosis should be differentiated from instances when the individual’s symptoms meet full criteria for one of the following disorders, and that disorder is caused by an other or unknown substance: delirium, major or mild neurocognitive disorder, psychotic disorder, depressive disorder, anxiety disorder, sexual dysfunction, or sleep disorder.

Other medical conditions

Individuals with substance use disorders, including other (or unknown) substance use disorder, may present with symptoms of many medical disorders. These disorders also may occur in the absence of other (or unknown) substance use disorder. A history of little or no use of other or unknown substances helps to exclude other (or unknown) substance use disorder as the source of these problems.

Comorbidity

Substance use disorders, including other (or unknown) substance use disorder, are commonly comorbid with one another, with adolescent conduct disorder and adult antisocial personality disorder, and with suicidal ideation and suicide attempts.

References: Other (or Unknown) Substance Use Disorder

· Alt RS , Morrissey RP , Gang MA , et al: Severe myeloneuropathy from acute high-dose nitrous (N2O) abuse. J Emerg Med41(4):378–380, 2010

· Balster RL : Neural basis of inhalant abuse. Drug Alcohol Depend 51(1–2):207–214, 1998

· Blanton A : Nitrous oxide abuse: dentistry's unique addiction. J Tenn Dent Assoc 86(4):30–31, 2006

· Cartner M , Sinnott M , Silburn P : Paralysis caused by “nagging.” Med J Aust 187(6):366–367, 2007

· Colfax G , Coates TJ , Husnik MJ , et al: Longitudinal patterns of methamphetamine, popper (amyl nitrite), and cocaine use and high-risk sexual behavior among a cohort of San Francisco men who have sex with men. J Urban Health 82(1, suppl 1):i62–i70,

· Dagher A , Robbins TW : Personality, addiction, dopamine: insights from Parkinson’s disease. Neuron 61(4):502–510, 2009

· Gupta PC , Ray CS : Epidemiology of betel quid usage. Ann Acad Med Singapore 33(4, suppl):31–36, 2004

· Hidaka Y , Ichikawa S , Koyano J , et al: Substance use and sexual behaviours of Japanese men who have sex with men: a nationwide internet survey conducted in Japan. BMC Public Health 6(239), September 26, 2006 10.1186/1471-2458-6-239

· Kanayama G , Brower KJ , Wood RI , et al: Anabolic-androgenic steroid dependence: an emerging disorder. Addiction104(12):1966–1978, 2009

· Kelly JP : Cathinone derivatives: a review of their chemistry, pharmacology and toxicology. Drug Test Anal 3(7–8):439–453,2011

· Lampinen TM , Mattheis K , Chan K , Hogg RS : Nitrite inhalant use among young gay and bisexual men in Vancouver during a period of increasing HIV incidence. BMC Public Health 7(35), March 15, 2007 10.1186/1471-2458-7-35

· Marsh N , Marsh A : A short history of nitoglycerine and nitric oxide in pharmacology and physiology. Clin Exp Pharmacol Physiol 27(4):313–319, 2000

· Richardson PG : Peripheral neuropathy following nitrous oxide abuse. Emerg Med Australas 22(1):88–90, 2010

· Ridenour TA , Bray BC , Cottler LB : Reliability of use, abuse, and dependence of four types of inhalants in adolescents and young adults. Drug Alcohol Depend 91(1):40–49, 2007

· Sethi NK , Mullin P , Torgovnick J , Capasso G : Nitrous oxide “Whippit” abuse presenting with cobalamin responsive psychosis. J Med Toxicol 2(2):71–74, 2006

· Substance Abuse and Mental Health Services Administration, Office of Applied Studies : Inhalant use across the adolescent years. The NSDUH Report,, March 13, 2008. Available at: http://www.samhsa.gov/data/2k8/inhalants/inhalants.htm. Accessed May 26, 2011.

· Wu LT , Schlenger WE , Ringwalt CL : Use of nitrite inhalants (“poppers”) among American youth. J Adolesc Health37(1):52–60, 2005

Other (or Unknown) Substance Intoxication

Diagnostic Criteria

A. The development of a reversible substance-specific syndrome attributable to recent ingestion of (or exposure to) a substance that is not listed elsewhere or is unknown.

B. Clinically significant problematic behavioral or psychological changes that are attributable to the effect of the substance on the central nervous system (e.g., impaired motor coordination, psychomotor agitation or retardation, euphoria, anxiety, belligerence, mood lability, cognitive impairment, impaired judgment, social withdrawal) and develop during, or shortly after, use of the substance.

C. The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including intoxication with another substance.

Coding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether there is a comorbid other (or unknown) substance use disorder involving the same substance. If a mild other (or unknown) substance use disorder is comorbid, the ICD-10-CM code is F19.129, and if a moderate or severe other (or unknown) substance use disorder is comorbid, the ICD-10-CM code is F19.229. If there is no comorbid other (or unknown) substance use disorder involving the same substance, then the ICD-10-CM code is F19.929.

Note: For information on Risk and Prognostic Factors, Culture-Related Diagnostic Issues, and Diagnostic Markers, see the corresponding sections in other (or unknown) substance use disorder.

Diagnostic Features

Other (or unknown) substance intoxication is a clinically significant mental disorder that develops during, or immediately after, use of either a) a substance not elsewhere addressed in this chapter (i.e., alcohol; caffeine; cannabis; phencyclidine and other hallucinogens; inhalants; opioids; sedatives, hypnotics, or anxiolytics; stimulants; or tobacco) or b) an unknown substance. If the substance is known, it should be reflected in the name of the disorder upon coding.

Application of the diagnostic criteria for other (or unknown) substance intoxication is very challenging. Criterion A requires development of a reversible “substance-specific syndrome,” but if the substance is unknown, that syndrome usually will be unknown. To resolve this conflict, clinicians may ask the individual or obtain collateral history as to whether the individual has experienced a similar episode after using substances with the same “street” name or from the same source. Similarly, hospital emergency departments sometimes recognize over a few days numerous presentations of a severe, unfamiliar intoxication syndrome from a newly available, previously unknown substance. Because of the great variety of intoxicating substances, Criterion B can provide only broad examples of signs and symptoms from some intoxications, with no threshold for the number of symptoms required for a diagnosis; clinical judgment guides those decisions. Criterion C requires ruling out other medical conditions, mental disorders, or intoxications.

Prevalence

The prevalence of other (or unknown) substance intoxication is unknown.

Development and Course

Intoxications usually appear and then peak minutes to hours after use of the substance, but the onset and course vary with the substance and the route of administration. Generally, substances used by pulmonary inhalation and intravenous injection have the most rapid onset of action, while those ingested by mouth and requiring metabolism to an active product are much slower. (For example, after ingestion of certain mushrooms, the first signs of an eventually fatal intoxication may not appear for a few days.) Intoxication effects usually resolve within hours to a very few days. However, the body may completely eliminate an anesthetic gas such as nitrous oxide just minutes after use ends. At the other extreme, some “hit-and-run” intoxicating substances poison systems, leaving permanent impairments. For example, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a contaminating by-product in the synthesis of a certain opioid, kills dopaminergic cells and induces permanent parkinsonism in users who sought opioid intoxication(Langston and Palfreman 1995).

Functional Consequences of Other (or Unknown) Substance Intoxication

Impairment from intoxication with any substance may have serious consequences, including dysfunction at work, social indiscretions, problems in interpersonal relationships, failure to fulfill role obligations, traffic accidents, fighting, high-risk behaviors (i.e., having unprotected sex), and substance or medication overdose. The pattern of consequences will vary with the particular substance.

Differential Diagnosis

Use of other or unknown substance, without meeting criteria for other (or unknown) substance intoxication

The individual used an other or unknown substance(s), but the dose was insufficient to produce symptoms that meet the diagnostic criteria required for the diagnosis.

Substance intoxication or other substance/medication-induced disorders

Familiar substances may be sold in the black market as novel products, and individuals may experience intoxication from those substances. History, toxicology screens, or chemical testing of the substance itself may help to identify it.

Different types of other (or unknown) substance–related disorders

Episodes of other (or unknown) substance intoxication may occur during, but are distinct from, other (or unknown) substance use disorder, unspecified other (or unknown) substance–related disorder, and other (or unknown) substance–induced disorders.

Other toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that impair brain function and cognition

Numerous neurological and other medical conditions may produce rapid onset of signs and symptoms mimicking those of intoxications, including the examples in Criterion B. Paradoxically, drug withdrawals also must be ruled out, because, for example, lethargy may indicate withdrawal from one drug or intoxication with another drug.

Comorbidity

As with all substance-related disorders, adolescent conduct disorder, adult antisocial personality disorder, and other substance use disorders tend to co-occur with other (or unknown) substance intoxication.

References: Other (or Unknown) Substance Intoxication

· Langston JW , Palfreman J : The Case of the Frozen Addicts. New York, Pantheon, 1995

Other (or Unknown) Substance Withdrawal

Diagnostic Criteria

292.0 (F19.239)

A. Cessation of (or reduction in) use of a substance that has been heavy and prolonged.

B. The development of a substance-specific syndrome shortly after the cessation of (or reduction in) substance use.

C. The substance-specific syndrome causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

D. The symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including withdrawal from another substance.

E. The substance involved cannot be classified under any of the other substance categories (alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, or anxiolytics; stimulants; or tobacco) or is unknown.

Coding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for other (or unknown) substance withdrawal is F19.239. Note that the ICD-10-CM code indicates the comorbid presence of a moderate or severe other (or unknown) substance use disorder. It is not permissible to code a comorbid mild other (or unknown) substance use disorder with other (or unknown) substance withdrawal.

Note: For information on Risk and Prognostic Factors and Diagnostic Markers, see the corresponding sections in other (or unknown) substance use disorder.

Diagnostic Features

Other (or unknown) substance withdrawal is a clinically significant mental disorder that develops during, or within a few hours to days after, reducing or terminating dosing with a substance (Criteria A and B). Although recent dose reduction or termination usually is clear in the history, other diagnostic procedures are very challenging if the drug is unknown. Criterion B requires development of a “substance-specific syndrome” (i.e., the individual’s signs and symptoms must correspond with the known withdrawal syndrome for the recently stopped drug)—a requirement that rarely can be met with an unknown substance. Consequently, clinical judgment must guide such decisions when information is this limited. Criterion D requires ruling out other medical conditions, mental disorders, or withdrawals from familiar substances. When the substance is known, it should be reflected in the name of the disorder upon coding (e.g., betel nut withdrawal).

Prevalence

The prevalence of other (or unknown) substance withdrawal is unknown.

Development and Course

Withdrawal signs commonly appear some hours after use of the substance is terminated, but the onset and course vary greatly, depending on the dose typically used by the person and the rate of elimination of the specific substance from the body. At peak severity, withdrawal symptoms from some substances involve only moderate levels of discomfort, whereas withdrawal from other substances may be fatal. Withdrawal-associated dysphoria often motivates relapse to substance use. Withdrawal symptoms slowly abate over days, weeks, or months, depending on the particular drug and doses to which the individual became tolerant.

Culture-Related Diagnostic Issues

Culture-related issues in diagnosis will vary with the particular substance.

Functional Consequences of Other (or Unknown) Substance Withdrawal

Withdrawal from any substance may have serious consequences, including physical signs and symptoms (e.g., malaise, vital sign changes, abdominal distress, headache), intense drug craving, anxiety, depression, agitation, psychotic symptoms, or cognitive impairments. These consequences may lead to problems such as dysfunction at work, problems in interpersonal relationships, failure to fulfill role obligations, traffic accidents, fighting, high-risk behavior (e.g., having unprotected sex), suicide attempts, and substance or medication overdose. The pattern of consequences will vary with the particular substance.

Differential Diagnosis

Dose reduction after extended dosing, but not meeting the criteria for other (or unknown) substance withdrawal

The individual used other (or unknown) substances, but the dose that was used was insufficient to produce symptoms that meet the criteria required for the diagnosis.

Substance withdrawal or other substance/medication-induced disorders

Familiar substances may be sold in the black market as novel products, and individuals may experience withdrawal when discontinuing those substances. History, toxicology screens, or chemical testing of the substance itself may help to identify it.

Different types of other (or unknown) substance–related disorders

Episodes of other (or unknown) substance withdrawal may occur during, but are distinct from, other (or unknown) substance use disorder, unspecified other (or unknown) substance–related disorder, and unspecified other (or unknown) substance–induced disorders.

Other toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that impair brain function and cognition

Numerous neurological and other medical conditions may produce rapid onset of signs and symptoms mimicking those of withdrawals. Paradoxically, drug intoxications also must be ruled out, because, for example, lethargy may indicate withdrawal from one drug or intoxication with another drug.

Comorbidity

As with all substance-related disorders, adolescent conduct disorder, adult antisocial personality disorder, and other substance use disorders likely co-occur with other (or unknown) substance withdrawal.

Other (or Unknown) Substance–Induced Disorders

Because the category of other or unknown substances is inherently ill-defined, the extent and range of induced disorders are uncertain. Nevertheless, other (or unknown) substance–induced disorders are possible and 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): other (or unknown) substance–induced psychotic disorder (“Schizophrenia Spectrum and Other Psychotic Disorders”); other (or unknown substance–induced bipolar disorder (“Bipolar and Related Disorders”); other (or unknown) substance–induced depressive disorder (“Depressive Disorders”); other (or unknown) substance–induced anxiety disorders (“Anxiety Disorders”); other (or unknown) substance–induced obsessive-compulsive disorder (“Obsessive-Compulsive and Related Disorders”); other (or unknown) substance–induced sleep disorder (“Sleep-Wake Disorders”); other (or unknown) substance–induced sexual dysfunction (“Sexual Dysfunctions”); and other (or unknown) substance/medication–induced major or mild neurocognitive disorder (“Neurocognitive Disorders”). For other (or unknown) substance–induced intoxication delirium and other (or unknown) substance–induced withdrawal delirium, see the criteria and discussion of delirium in the chapter “Neurocognitive Disorders.” These other (or unknown) substance–induced disorders are diagnosed instead of other (or unknown) substance intoxication or other (or unknown) substance withdrawal only when the symptoms are sufficiently severe to warrant independent clinical attention.

Unspecified Other (or Unknown) Substance–Related Disorder

292.9 (F19.99)

This category applies to presentations in which symptoms characteristic of an other (or unknown) substance–related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any specific other (or unknown) substance–related disorder or any of the disorders in the substance-related disorders diagnostic class.

Non-Substance-Related Disorders

Gambling Disorder

Diagnostic Criteria

312.31 (F63.0)

A. Persistent and recurrent problematic gambling behavior leading to clinically significant impairment or distress, as indicated by the individual exhibiting four (or more) of the following in a 12-month period:

1. Needs to gamble with increasing amounts of money in order to achieve the desired excitement.

2. Is restless or irritable when attempting to cut down or stop gambling.

3. Has made repeated unsuccessful efforts to control, cut back, or stop gambling.

4. Is often preoccupied with gambling (e.g., having persistent thoughts of reliving past gambling experiences, handicapping or planning the next venture, thinking of ways to get money with which to gamble).

5. Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed).

6. After losing money gambling, often returns another day to get even (“chasing” one’s losses).

7. Lies to conceal the extent of involvement with gambling.

8. Has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling.

9. Relies on others to provide money to relieve desperate financial situations caused by gambling.

B. The gambling behavior is not better explained by a manic episode.

Specify if:

· Episodic: Meeting diagnostic criteria at more than one time point, with symptoms subsiding between periods of gambling disorder for at least several months.

· Persistent: Experiencing continuous symptoms, to meet diagnostic criteria for multiple years.

Specify if:

· In early remission: After full criteria for gambling disorder were previously met, none of the criteria for gambling disorder have been met for at least 3 months but for less than 12 months.

· In sustained remission: After full criteria for gambling disorder were previously met, none of the criteria for gambling disorder have been met during a period of 12 months or longer.

Specify current severity:

· Mild: 4–5 criteria met.

· Moderate: 6–7 criteria met.

· Severe: 8–9 criteria met.

Note: Although some behavioral conditions that do not involve ingestion of substances have similarities to substance-related disorders, only one disorder—gambling disorder—has sufficient data to be included in this section.

Specifiers

Severity is based on the number of criteria endorsed. Individuals with mild gambling disorder may exhibit only 4–5 of the criteria, with the most frequently endorsed criteria usually related to preoccupation with gambling and “chasing” losses(Blanco et al. 2006; Gerstein et al. 1999). Individuals with moderately severe gambling disorder exhibit more of the criteria (i.e., 6–7). Individuals with the most severe form will exhibit all or most of the nine criteria (i.e., 8–9). Jeopardizing relationships or career opportunities due to gambling and relying on others to provide money for gambling losses are typically the least often endorsed criteria and most often occur among those with more severe gambling disorder(Blanco et al. 2006;Gerstein et al. 1999). Furthermore, individuals presenting for treatment of gambling disorder typically have moderate to severe forms of the disorder(Petry et al. 2006; Slutske 2006).

Diagnostic Features

Gambling involves risking something of value in the hopes of obtaining something of greater value. In many cultures, individuals gamble on games and events, and most do so without experiencing problems. However, some individuals develop substantial impairment related to their gambling behaviors. The essential feature of gambling disorder is persistent and recurrent maladaptive gambling behavior that disrupts personal, family, and/or vocational pursuits (Criterion A). Gambling disorder is defined as a cluster of four or more of the symptoms listed in Criterion A occurring at any time in the same 12-month period.

A pattern of “chasing one’s losses” may develop, with an urgent need to keep gambling (often with the placing of larger bets or the taking of greater risks) to undo a loss or series of losses. The individual may abandon his or her gambling strategy and try to win back losses all at once. Although many gamblers may “chase” for short periods of time, it is the frequent, and often long-term, “chase” that is characteristic of gambling disorder (Criterion A6). Individuals may lie to family members, therapists, or others to conceal the extent of involvement with gambling; these instances of deceit may also include, but are not limited to, covering up illegal behaviors such as forgery, fraud, theft, or embezzlement to obtain money with which to gamble (Criterion A7). Individuals may also engage in “bailout” behavior, turning to family or others for help with a desperate financial situation that was caused by gambling (Criterion A9).

Associated Features Supporting Diagnosis

Distortions in thinking (e.g., denial, superstitions, a sense of power and control over the outcome of chance events, overconfidence) may be present in individuals with gambling disorder (Xian et al. 2008). Many individuals with gambling disorder believe that money is both the cause of and the solution to their problems. Some individuals with gambling disorderare impulsive, competitive, energetic, restless, and easily bored; they may be overly concerned with the approval of others and may be generous to the point of extravagance when winning. Other individuals with gambling disorder are depressed and lonely, and they may gamble when feeling helpless, guilty, or depressed(Ledgerwood and Petry 2010). Up to half of individuals in treatment for gambling disorder have suicidal ideation, and about 17% have attempted suicide(Petry and Kiluk 2002).

Prevalence

The past-year prevalence rate of gambling disorder is about 0.2%–0.3% in the general population(Gerstein et al. 1999;Kessler et al. 2008; Petry et al. 2005). In the general population, the lifetime prevalence rate is about 0.4%–1.0%(Gerstein et al. 1999; Kessler et al. 2008; Petry et al. 2005; Welte et al. 2001). For females, the lifetime prevalence rate of gambling disorder is about 0.2%, and for males it is about 0.6%(Blanco et al. 2006). The lifetime prevalence of pathological gambling among African Americans is about 0.9%, among whites about 0.4%, and among Hispanics about 0.3%(Alegria et al. 2009).

Development and Course

The onset of gambling disorder can occur during adolescence or young adulthood, but in other individuals it manifests during middle or even older adulthood. Generally, gambling disorder develops over the course of years, although the progression appears to be more rapid in females than in males(Tavares et al. 2003). Most individuals who develop a gambling disorderevidence a pattern of gambling that gradually increases in both frequency and amount of wagering(Currie et al. 2006; Kessler et al. 2008). Certainly, milder forms can develop into more severe cases. Most individuals with gambling disorder report that one or two types of gambling are most problematic for them(Petry et al. 2006), although some individuals participate in many forms of gambling. Individuals are likely to engage in certain types of gambling (e.g., buying scratch tickets daily) more frequently than others (e.g., playing slot machines or blackjack at the casino weekly). Frequency of gambling can be related more to the type of gambling than to the severity of the overall gambling disorder. For example, purchasing a single scratch ticket each day may not be problematic, while less frequent casino, sports, or card gambling may be part of a gambling disorder (Petry 2003). Similarly, amounts of money spent wagering are not in themselves indicative of gambling disorder. Some individuals can wager thousands of dollars per month and not have a problem with gambling, while others may wager much smaller amounts but experience substantial gambling-related difficulties(Walker et al. 2006).

Gambling patterns may be regular or episodic, and gambling disorder can be persistent or in remission(Hodgins and el-Guebaly 2000; Slutske 2006; Slutske et al. 2010). Gambling can increase during periods of stress or depression and during periods of substance use or abstinence. There may be periods of heavy gambling and severe problems, times of total abstinence, and periods of nonproblematic gambling. Gambling disorder is sometimes associated with spontaneous, long-term remissions. Nevertheless, some individuals underestimate their vulnerability to develop gambling disorder or to return to gambling disorder following remission. When in a period of remission, they may incorrectly assume that they will have no problem regulating gambling and that they may gamble on some forms nonproblematically, only to experience a return to gambling disorder.

Early expression of gambling disorder is more common among males than among females(Barnes et al. 2010; Tavares et al. 2003). Individuals who begin gambling in youth often do so with family members or friends(Langhinrichsen-Rohling et al. 2004). Development of early-life gambling disorder appears to be associated with impulsivity and substance abuse(Slutske et al. 2005). Many high school and college students who develop gambling disorder grow out of the disorder over time, although it remains a lifelong problem for some(Slutske et al. 2003). Mid- and later-life onset of gambling disorder is more common among females than among males(Blanco et al. 2006; Tavares et al. 2003).

There are age and gender variations in the type of gambling activities and the prevalence rates of gambling disorder. Gambling disorder is more common among younger and middle-age persons than among older adults(Gerstein et al. 1999; Kessler et al. 2008). Among adolescents and young adults, the disorder is more prevalent in males than in females(Barnes et al. 2010). Younger individuals prefer different forms of gambling (e.g., sports betting), while older adults are more likely to develop problems with slot machine and bingo gambling(Petry 2003). Although the proportions of individuals who seek treatment forgambling disorder are low across all age groups(Slutske 2006), younger individuals are especially unlikely to present for treatment.

Males are more likely to begin gambling earlier in life and to have a younger age at onset of gambling disorder than females, who are more likely to begin gambling later in life and to develop gambling disorder in a shorter time frame(Tavares et al. 2003). Females with gambling disorder are more likely than males with gambling disorder to have depressive, bipolar, and anxiety disorders(Tavares et al. 2003). Females also have a later age at onset of the disorder and seek treatment sooner(Tavares et al. 2003), although rates of treatment seeking are low (<10%) among individuals with gambling disorderregardless of gender(Blanco et al. 2006; Slutske 2006).

Risk and Prognostic Factors

Temperamental

Gambling that begins in childhood or early adolescence is associated with increased rates of gambling disorder (Burge et al. 2006). Gambling disorder also appears to aggregate with antisocial personality disorder (Slutske et al. 2001), depressive and bipolar disorders(Potenza et al. 2005), and other substance use disorders(Kessler et al. 2008; Petry et al. 2005), particularly with alcohol disorders(Slutske et al. 2000).

Genetic and physiological

Gambling disorder can aggregate in families, and this effect appears to relate to both environmental and genetic factors. Gambling problems are more frequent in monozygotic than in dizygotic twins(Eisen et al. 1998). Gambling disorder is also more prevalent among first-degree relatives of individuals with moderate to severe alcohol use disorder than among the general population(Slutske et al. 2000).

Course modifiers

Many individuals, including adolescents and young adults, are likely to resolve their problems with gambling disorder over time, although a strong predictor of future gambling problems is prior gambling problems(Slutske et al. 2003).

Culture-Related Diagnostic Issues

Individuals from specific cultures and races/ethnicities are more likely to participate in some types of gambling activities than others (e.g., pai gow, cockfights, blackjack, horse racing). Prevalence rates of gambling disorder are higher among African Americans than among European Americans, with rates for Hispanic Americans similar to those of European Americans(Alegria et al. 2009). Indigenous populations have high prevalence rates of gambling disorder (Volberg and Abbott 1997; Wardman et al. 2001).

Gender-Related Diagnostic Issues

Males develop gambling disorder at higher rates than females, although this gender gap may be narrowing. Males tend to wager on different forms of gambling than females, with cards, sports, and horse race gambling more prevalent among males, and slot machine and bingo gambling more common among females(Petry 2003).

Functional Consequences of Gambling Disorder

Areas of psychosocial, health, and mental health functioning may be adversely affected by gambling disorder. Specifically, individuals with gambling disorder may, because of their involvement with gambling, jeopardize or lose important relationships with family members or friends. Such problems may occur from repeatedly lying to others to cover up the extent of gambling or from requesting money that is used for gambling or to pay off gambling debts. Employment or educational activities may likewise be adversely impacted by gambling disorder; absenteeism or poor work or school performance can occur with gambling disorder, as individuals may gamble during work or school hours or be preoccupied with gambling or its adverse consequence when they should be working or studying. Individuals with gambling disorder have poor general health and utilize medical services at high rates(Morasco et al. 2006).

Differential Diagnosis

Nondisordered gambling

Gambling disorder must be distinguished from professional and social gambling. In professional gambling, risks are limited and discipline is central. Social gambling typically occurs with friends or colleagues and lasts for a limited period of time, with acceptable losses. Some individuals can experience problems associated with gambling (e.g., short-term chasing behavior and loss of control) that do not meet the full criteria for gambling disorder.

Manic episode

Loss of judgment and excessive gambling may occur during a manic episode. An additional diagnosis of gambling disordershould be given only if the gambling behavior is not better explained by manic episodes (e.g., a history of maladaptive gambling behavior at times other than during a manic episode). Alternatively, an individual with gambling disorder may, during a period of gambling, exhibit behavior that resembles a manic episode, but once the individual is away from the gambling, these manic-like features dissipate.

Personality disorders

Problems with gambling may occur in individuals with antisocial personality disorder and other personality disorders. If the criteria are met for both disorders, both can be diagnosed.

Other medical conditions

Some patients taking dopaminergic medications (e.g., for Parkinson‘s disease) may experience urges to gamble. If such symptoms dissipate when dopaminergic medications are reduced in dosage or ceased, then a diagnosis of gambling disorderwould not be indicated.

Comorbidity

Gambling disorder is associated with poor general health (Morasco and Petry 2006; Morasco et al. 2006). In addition, some specific medical diagnoses, such as tachycardia and angina, are more common among individuals with gambling disorder than in the general population, even when other substance use disorders, including tobacco use disorder, are controlled for(Morasco et al. 2006). Individuals with gambling disorder have high rates of comorbidity with other mental disorders, such as substance use disorders, depressive disorders, anxiety disorders, and personality disorders(Kessler et al. 2008; Petry et al. 2005). In some individuals, other mental disorders may precede gambling disorder and be either absent or present during the manifestation of gambling disorder. Gambling disorder may also occur prior to the onset of other mental disorders, especially anxiety disorders and substance use disorders(Kessler et al. 2008).

References: Gambling Disorder

· Alegria AA , Petry NM , Hasin DS, et al : Disordered gambling among racial and ethnic groups in the US: results from the national epidemiologic survey on alcohol and related conditions. CNS Spectr 14(3):132–142, 2009

· Barnes GM , Welte JW , Hoffman JH , Tidwell MC : Comparisons of gambling and alcohol use among college students and noncollege young people in the United States. J Am Coll Health 58(5):443–452, 2010

· Blanco C , Hasin DS , Petry N, et al : Sex differences in subclinical and DSM-IV pathological gambling: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Psychol Med 36(7):943–953, 2006

· Burge AN , Pietrzak RH , Petry NM : Pre/early adolescent onset of gambling and psychosocial problems in treatment-seeking pathological gamblers. J Gambl Stud 22(3):263–274, 2006

· Currie SR , Hodgins DC , Wang J, et al : Risk of harm among gamblers in the general population as a function of level of participation in gambling activities. Addiction 101(4):570–580, 2006

· Eisen SA , Lin N , Lyons MJ, et al : Familial influences on gambling behavior: an analysis of 3359 twin pairs. Addiction93(9):1375–1384, 1998

· Gerstein D , Hoffmann J , Larison C, et al : Gambling Impact and Behavior Study: Report to the National Gambling Impact Study Commission. Chicago, IL, National Opinion Research Center, University of Chicago, 1999

· Hodgins DC , el-Guebaly N : Natural and treatment-assisted recovery from gambling problems: a comparison of resolved and active gamblers. Addiction 95(5):777–789, 2000

· Kessler RC , Hwang I , LaBrie R, et al : DSM-IV pathological gambling in the National Comorbidity Survey Replication. Psychol Med 38(9):1351–1360, 2008

· Langhinrichsen-Rohling J , Rohde P , Seeley JR , Rohling ML : Individual, family, and peer correlates of adolescent gambling. J Gambl Stud 20(1):23–46, 2004

· Ledgerwood DM , Petry NM : Subtyping pathological gamblers based on impulsivity, depression, and anxiety. Psychol Addict Behav 24(4):680–688, 2010

· Morasco BJ , Petry NM : Gambling problems and health functioning in individuals receiving disability. Disabil Rehabil28(10):619–623, 2006

· Morasco BJ , Pietrzak RH , Blanco C, et al : Health problems and medical utilization associated with gambling disorders: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Psychosom Med 68(6):976–984, 2006

· Petry NM : A comparison of treatment-seeking pathological gamblers based on preferred gambling activity. Addiction98(5):645–655, 2003

· Petry NM , Kiluk BD : Suicidal ideation and suicide attempts in treatment-seeking pathological gamblers. J Nerv Ment Dis190(7):462–469, 2002

· Petry NM , Stinson FS , Grant BF : Comorbidity of DSM-IV pathological gambling and other psychiatric disorders: results from the National Epidemiologic Survey on Alcohol and Related Conditions. J Clin Psychiatry 66(5):564–574, 2005

· Petry NM , Ammerman Y , Bohl J, et al : Cognitive-behavioral therapy for pathological gamblers. J Consult Clin Psychol74(3):555–567, 2006

· Potenza MN , Xian H , Shah K, et al : Shared genetic contributions to pathological gambling and major depression in men. Arch Gen Psychiatry 62(9):1015–1021, 2005

· Slutske WS : Natural recovery and treatment-seeking in pathological gambling: results of two U.S. national surveys. Am J Psychiatry 163(2):297–302, 2006

· Slutske WS , Eisen S , True WR, et al : Common genetic vulnerability for pathological gambling and alcohol dependence in men. Arch Gen Psychiatry 57(7):666–673, 2000

· Slutske WS , Eisen S , Xian H, et al : A twin study of the association between pathological gambling and antisocial personality disorder. J Abnorm Psychol 110(2):297–308, 2001

· Slutske WS , Jackson KM , Sher KJ : The natural history of problem gambling from age 18 to 29. J Abnorm Psychol112(2):263–274, 2003

· Slutske WS , Caspi A , Moffitt TE , Poulton R : Personality and problem gambling: a prospective study of a birth cohort of young adults. Arch Gen Psychiatry 62(7):769–775, 2005

· Slutske WS , Piasecki TM , Blaszczynski A , Martin NG : Pathological gambling recovery in the absence of abstinence. Addiction 105(12):2169–2175, 2010 10.1111/j.1360-0443.2010.03080.x

· Tavares H , Martins SS , Lobo DS, et al : Factors at play in faster progression for female pathological gamblers: an exploratory analysis. J Clin Psychiatry 64(4):433–438, 2003

· Volberg RA , Abbott MW : Gambling and problem gambling among indigenous peoples. Subst Use Misuse 32(11):1525–1538,1997

· Walker M , Toneatto T , Potenza MN, et al : A framework for reporting outcomes in problem gambling treatment research: the Banff, Alberta Consensus. Addiction 101(4):504–511, 2006

· Wardman D , el-Guebaly N , Hodgins D : Problem and pathological gambling in North American Aboriginal populations: a review of the empirical literature. J Gambl Stud 17(2):81–100, 2001

· Welte J , Barnes G , Wieczorek W, et al : Alcohol and gambling pathology among U.S. adults: prevalence, demographic patterns and comorbidity. J Stud Alcohol 62(5):706–712, 2001

· Xian H , Shah KR , Phillips SM, et al : Association of cognitive distortions with problem and pathological gambling in adult male twins. Psychiatry Res 160(3):300–307, 2008