Prolonged daily use of caffeine

Prolonged daily use of caffeine

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. 2005Hasin et al. 2002Schuckit 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. 2011Fu et al. 2002Nunes et al. 2006Nurnberger 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. 2005Hasin et al. 2006Regier et al. 1990Schuckit 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. 1995Gilder et al. 2004Nunes and Rounsaville 2006Schuckit 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 2009aTrim 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. 2006Schuckit 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 2008Schuckit 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 2007Schuckit 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. 2007Tan et al. 2010).

Despite small variations regarding individual criterion items, the diagnostic criteria perform equally well across most race/ethnicity groups(Borges et al. 2010Harford et al. 2009Saha 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. 2002Niemelä 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 2009Reissig 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. 2008Walsh 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.

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