Chapter 28. Impulse-Control Disorders

Although impulse-control disorders are often thought to be rare conditions, a recent replication of the National Comorbidity Study demonstrated a 12-month prevalence rate of 8.9%. This percentage however also included disorders such as oppositional defiant disorder (1%), conduct disorder (1%), and attention-deficit/hyperactivity disorder (ADHD) (4.1%). Intermittent explosive disorder was reported at 2.6% of the surveyed population. Intermittent explosive disorder and pathological gambling (0.2–3.3% of populations surveyed) are much more common than the other disorders in this group.

Essentials of Diagnosis

DSM-IV-TR Diagnostic Criteria

1. Several discrete episodes of failure to resist aggressive impulses that result in serious assaultive acts or destruction of property.

2. The degree of aggressiveness expressed during the episodes is grossly out of proportion to any precipitating psychosocial stressors.

3. The aggressive episodes are not better accounted for by another mental disorder (e.g., antisocial personality disorder, borderline personality disorder, a psychotic disorder, a manic episode, conduct disorder, or ADHD) and are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., head trauma, Alzheimer's disease).

(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Text Revision. Washington DC: American Psychiatric Association, 2000.)

General Considerations

Epidemiology

The National Comorbidity Study replication reported a 12-month prevalence rate of 2.6%. This is more common than previously realized.

Etiology

The outbursts associated with intermittent explosive disorder (sometimes referred to as episodic dyscontrol) were initially viewed as the result of limbic system discharge or dysfunction or even as interictal phenomena. The Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) does now exclude those patients in whom an aggressive episode was thought to be related to a general medical condition (e.g., temporal lobe seizures, delirium) or to the direct psychological effects of a substance, whether a drug of abuse or a prescribed medication. Disorders that can be identified as resulting from neurological insult or a seizure disorder are now classified elsewhere. Nevertheless, neurological soft signs, nonspecific electroencephalogram anomalies, or mild abnormalities on neuropsychological testing have been noted in patients given this diagnosis.

Psychodynamic explanations have also been proposed. Childhood abuse is thought to be a risk factor for the development of this disorder. Others postulate narcissistic vulnerability as a possible mechanism that triggers these attacks. Thus, one can conceptualize the “explosive” episodes as resulting from a real or perceived insult to one's self-esteem or as a reaction to a perceived threat of rejection, abandonment, or attack.

Genetics

Little is known about the genetics of intermittent explosive disorder. Family studies of individuals with this disorder have shown high rates of mood and substance-use disorders in first-degree relatives.

Clinical Findings

Signs & Symptoms

Aggressive outbursts occur in discrete episodes and are grossly out of proportion to any precipitating event. Furthermore, there is often a lack of rational motivation or clear-cut gain to be realized from the aggressive act itself. The patient expresses embarrassment, guilt, and remorse after the act and is often genuinely perplexed as to why he or she behaved in such a manner. Some patients have described periods of exhaustion and sleepiness immediately after these acts of violence.

Psychological Testing

Neuropsychological testing may reveal minor cognitive difficulties such as letter reversals. A careful history may reveal developmental difficulties such as delayed speech or poor coordination. A history of febrile seizures in childhood, episodes of unconsciousness, or head injury may be reported.

Laboratory Findings

Laboratory findings are nonspecific. Nonspecific EEG findings may be noted. Several research projects have found signs of altered serotonin metabolism in cerebrospinal fluid or platelet models.

Differential Diagnosis

If the behavior can be better explained by an underlying neurological insult, then the correct diagnosis would be personality change due to general medical condition, aggressive type. The clinician must decide whether the aggressive or erratic behavior would be better explained as a result of a personality conduct disorder. Purposeful behavior with subsequent attempts to malinger must be distinguished from intermittent explosive disorder. Recent studies suggest a high rate of combined lifetime mood and substance-use disorders in patients with this disorder.

Treatment

Both psychotherapy and pharmacotherapy have been described as treatments for intermittent explosive disorder; however, no double-blind, randomized, controlled trials have been conducted. There are case reports or open trials of the use of anticonvulsants, antipsychotics, antidepressants, benzodiazepines, β-blockers, lithium carbonate, stimulants, and opioid antagonists. Novel anxiolytics such as buspirone have been efficacious in individual cases. Current scientific data are insufficient and inconclusive regarding treatment of the disorder; therefore, clinicians must proceed with individualized treatment plans based on their best clinical judgment.

Complications/Adverse Outcomes of Treatment

Intermittent explosive disorder can be complicated by legal difficulties, job loss, difficulties with interpersonal relationships, and divorce. Although patients may have been prone to lose their temper repeatedly over a long period of time, they may not seek medical attention until a major life disruption has resulted from one of these outbursts.

Adverse outcomes of treatment are related to the side effects of particular medications used to treat this disorder.

Prognosis

Intermittent explosive disorder is thought to have its onset in adolescence or young adulthood and to run its course by the end of the third decade of life. Here again, the data for such conclusions are quite limited.

Essentials of Diagnosis

DSM-IV-TR Diagnostic Criteria

1. Recurrent failure to resist impulses to steal objects that are not needed for personal use or for their monetary value.

2. Increasing sense of tension immediately before committing the theft.

3. Pleasure, gratification, or relief at the time of committing the theft.

4. The stealing is not committed to express anger or vengeance and is not in response to a delusion or a hallucination.

5. The stealing is not better accounted for by conduct disorder, a manic episode, or antisocial personality disorder.

(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Text Revision. Washington DC: American Psychiatric Association, 2000.)

General Considerations

Although kleptomania has been recognized since the early nineteenth century as an egodystonic impulse to steal, little systematic study has been undertaken to understand this disorder. The individual with kleptomania often feels guilty and fears apprehension and prosecution. Several psychiatric disorders have been linked to kleptomania; the most recent studies point to eating disorders and compulsive spending.

Epidemiology

Because most shoplifters steal for profit, fewer than 5% of shoplifters meet criteria for kleptomania. It is a rare disorder of unknown prevalence, although the disorder may be more common than thought. Kleptomania is more common in women than in men.

Etiology

The etiology of kleptomania is unknown. It may be a symptom rather than a disorder.

Genetics

Little is known about the genetics of kleptomania. Family studies have demonstrated high rates of mood, substance-use, and anxiety disorders in first-degree relatives.

Clinical Findings

Signs & Symptoms

The hallmark of kleptomania is the failure to resist the impulse to steal useless objects that have little monetary value. This behavior is not usually purposeful but is performed to relieve a sense of inner tension. There is often a sense of relief upon completion of the theft. The theft usually occurs in retail stores or work locations or from family members. Some patients report feeling high or euphoric while stealing. Most feel guilty after the act and may donate stolen items to charity, return items to the location from which they were stolen, or pay for the stolen items.

A comprehensive history may reveal other compulsive behavior that does not meet full criteria for obsessive–compulsive disorder (OCD). Symptoms of mood disorders, substance-use disorders, anxiety disorders, and eating disorders may also be common in this population.

Psychological Testing & Laboratory Findings

Neuropsychological testing and laboratory data are nonspecific.

Differential Diagnosis

The diagnosis of kleptomania should not be given if the patient's behavior is better accounted for by antisocial personality disorder, bipolar disorder, or conduct disorder or if stealing occurs as a result of anger or vengeance or as the result of a hallucination or delusional belief. Other important diagnoses to consider include major depression, anxiety disorder, and substance-use disorders.

Treatment

Psychotherapy and pharmacotherapy have been found useful in single reports. Selective serotonin reuptake inhibitors (SSRIs) and lithium are the agents used most frequently to treat kleptomania. Response rates are confounded by the high rates of comorbid mood and eating disorders.

Complications/Adverse Outcomes of Treatment

The majority of patients with kleptomania have a lifetime diagnosis of major mood disorder. Anxiety disorder is also common, as are substance-use and eating disorders. Complications include apprehension, arrest, and conviction for stealing with shame and embarrassment to the patient, friends, and family members. Other risks might include self-destructive behavior associated with major mood disorders and substance use. Adverse outcomes of treatment are related to the side effects of medication and failure to recognize comorbid conditions that may be treated easily.

Prognosis

Kleptomania is thought to begin in adolescence and can continue into the third or fourth decades of life. The course is not well studied and includes a spectrum from brief and episodic to chronic.

Essentials of Diagnosis

DSM-IV-TR Diagnostic Criteria

1. Deliberate and purposeful fire setting on more than one occasion.

2. Tension or affective arousal before the act.

3. Fascination with, interest in, curiosity about, or attraction to fire and its situational contexts (e.g., paraphernalia, uses, consequences).

4. Pleasure, gratification, or relief when setting fires, or when witnessing or participating in their aftermath.

5. The fire setting is not done for monetary gain, as an expression of sociopolitical ideology, to conceal criminal activity, to express anger or vengeance, to improve one's living circumstances, in response to a delusion or hallucination, or as a result of impaired judgment (e.g., in dementia, mental retardation, substance intoxication).

6. The fire setting is not better accounted for by conduct disorder, a manic episode, or antisocial personality disorder.

(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Text Revision. Washington DC: American Psychiatric Association, 2000.)

General Considerations

Pyromania strikes fear in the hearts of mental health professionals, because there is a serious potential for harm to the patient and to society. The therapist must balance carefully the issues surrounding confidentiality and the duty to protect third parties from the danger presented by these patients.

Epidemiology

The epidemiology of pyromania is unclear. After other causes of fire setting are ruled out, only a small population of pyromaniac individuals remains. Pyromania is thought to be rare. In clinical populations, however, fire-setters are not uncommon. Between 2% and 15% of psychiatric inpatients are fire-setters. The peak age of fire-setters is 13 years, and 90% of fire-setters are male. Many are from emotionally and economically deprived families.

Etiology

The etiology of pyromania is not well understood. There is little research to support any hypotheses.

Genetics

Little is known about the genetics of pyromania.

Clinical Findings

Signs & Symptoms

The signs and symptoms of true pyromania may be indistinguishable from other forms of fire setting. Diagnosis is by exclusion. Most fire setting cannot be classified as an impulse-control disorder, but impairment in the ability to control impulses is recognized in most cases of arson. Patients are usually identified after legal charges have been filed.

Psychological Testing

Psychological testing of fire-setters reveals a significant amount of psychiatric comorbidity; however, studies on pure populations of pyromaniacs are not available. Among fire-setters, suicidal behavior has been reported. Screening for suicide is warranted for this population.

Laboratory Findings

Lower cerebrospinal fluid concentrations of 3-methoxy-4-hydroxyphenylglycol and 5-hydroxyindoleacetic acid have been reported in fire-setters as compared to control subjects.

Differential Diagnosis

The diagnosis of pyromania should not be given if fire setting can be accounted for more appropriately by motives of profit, crime concealment, revenge, or as a symptom of another psychiatric disorder. Fire setting has been found in over half of children with conduct disorder. It may be a harbinger of adult antisocial personality disorder.

Treatment

Early intervention programs with adolescent fire-setters have reported success in deterring fire setting. Other comorbid psychiatric disorders such as schizophrenia and bipolar disorder should be treated aggressively.

Complications/Adverse Outcomes of Treatment

A significant number of fire-setters will repeat this behavior. While they are working with such patients, therapists must be constantly aware of the potential for harm to third parties. Little is known about the comorbidity of pyromania with other psychiatric disorders Fire setting is quite common among psychiatric inpatients: The most common associations are psychotic disorders, mood disorders, and severe personality disorder. Two thirds of fire-setters are intoxicated at the time of the index offense. Female fire-setters have a high degree of psychiatric comorbidity, as high as 92% in one study.

Prognosis

The prognosis and course of illness are unclear. Early detection and the treatment of comorbid psychiatric disorders are recommended.

Essentials of Diagnosis

DSM-IV-TR Diagnostic Criteria

1. Persistent and recurrent maladaptive gambling behavior as indicated by five (or more) of the following:

   1. is preoccupied with gambling (e.g., preoccupied with reliving past gambling experiences, handicapping or planning the next venture, or thinking of ways to get money with which to gamble)

   2. needs to gamble with increasing amounts of money in order to achieve the desired excitement

   3. has repeated unsuccessful efforts to control, cut back, or stop gambling

   4. is restless or irritable when attempting to cut down or stop gambling

   5. gambles as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of helplessness, guilt, anxiety, depression)

   6. after losing money gambling, often returns another day to get even (“chasing” one's losses)

   7. lies to family members, therapist, or others to conceal the extent of involvement with gambling

   8. has committed illegal acts such as forgery, fraud, theft, or embezzlement to finance gambling

   9. has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling

   10. relies on others to provide money to relieve a desperate financial situation caused by gambling

2. The gambling behavior is not better accounted for by a manic episode.

(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Text Revision. Washington DC: American Psychiatric Association, 2000.)

General Considerations

Epidemiology

The prevalence of pathological gambling has been estimated at 0.2–3.3%, increasing with the number of gaming venues available. Roughly two thirds of gamblers are male. Pathologic gambling is a growing problem in adolescent and elderly populations.

Etiology

The etiology of pathologic gambling is unknown. Biochemical, behavioral, psychodynamic, and addiction-based theories have been proposed.

Genetics

Family studies of pathologic gamblers reveal higher rates of pathologic gambling in first-degree relatives than in the general population. The rates of mood disorder and substance-use disorder in first-degree relatives are many times that of the general population.

Clinical Findings

Signs & Symptoms

Pathologic gamblers spend excessive amounts of time at gaming establishments or obtaining money to gamble. They deplete family bank accounts, borrow money from family members, lie about their gambling, and attempt to recoup their losses with large bets. They repeatedly promise to cut back on their gambling and make unsuccessful attempts to do so. Pathologic gamblers usually present to mental health professionals after they have been forced into treatment because of illegal activity to obtain funds. For example, they write bad checks, embezzle money, or engage in insurance fraud. Up to 75% of the members of Gamblers Anonymous admit to engaging in illegal activity.

The gambler's spouse is likely to be depressed. Some studies have reported higher rates of child abuse by the gambler and particularly by the spouse. This is more likely to occur when the spouse confronts the gambler about depletion of family resources. The clinician should interview the extended family to understand the full extent of the patient's borrowing. The clinician also should take a careful history of mood symptoms and suicidal ideation, because 20% of individuals in treatment for pathologic gambling have reported attempting suicide.

Differential Diagnosis

Pathologic gambling must be separated from social gambling. Social gambling usually occurs with friends, and the amount of money to be spent is determined before gambling starts. Social gambling is time-limited and does not cause significant financial constraints on the family. Professional gambling, in contrast to pathologic gambling, involves calculated bets without significant attempts to recoup losses (called “chasing losses”). Other differential diagnoses include manic episodes and antisocial personality disorder. Many gamblers appear to be hypomanic while gambling and depressed when on a losing streak, thus making bipolar II disorder particularly difficult to differentiate.

Prognosis

The typical pathologic gambler goes through several phases before coming to the attention of mental health professionals. Onset is usually in adolescence or early adulthood. The winning phase begins after the patient has a large windfall that equals half of a normal year's salary. The gambler then starts betting regularly, feeling euphoric as he or she does so, seeking more and more “action.” At first, many gamblers are adept at winning money.

The losing phase usually begins as a streak of bad luck (referred to by Gamblers Anonymous populations as the “bad beat”). Losing begins a cycle of chasing losses with foolish bets that plunge the gambler further and further into debt. As the bets become more and more risky, the gambler enters a phase of desperation when illegal sources of money are considered. Desperation usually occurs after the family bank account and retirement savings are depleted. The gambler may contemplate or attempt suicide at this point.

Another clinical presentation of gambling has been described as “the escape artist” who gambles to pass time and avoid boredom. Women and the elderly are overrepresented in this group.

Treatment

Several treatment approaches are available, from Gamblers Anonymous to inpatient psychiatric treatment. Some programs involve a multidisciplinary 12-step addiction-based model designed specifically for the pathologic gambler. The gambler must take responsibility for his or her debt, cut up credit cards, and allow someone else to handle his or her money. Medication management can be helpful if comorbid psychiatric disorders are present. SSRIs and opiate antagonists have been studied in controlled trials with some efficacy.

Complications/Adverse Outcomes of Treatment

Complications of treatment include continued gambling, side effects of medication, and suicide. Comorbid conditions include substance-use disorder, depression, bipolar disorder, and attention-deficit/hyperactivity disorder. Antisocial and narcissistic personality disorders may be present. Outcomes vary depending on the population studied and the method used. Some surveys report a 55%-response rate 1 year after inpatient treatment. Surveys of Gamblers Anonymous groups show lower and possibly more accurate response rates, in the 10% range at 1-year follow-up.

Essentials of Diagnosis

DSM-IV-TR Diagnostic Criteria

1. Recurrent pulling out of one's hair resulting in noticeable hair loss.

2. An increasing sense of tension immediately before pulling out the hair or when attempting to resist the behavior.

3. Pleasure, gratification, or relief when puling out the hair.

4. The disturbance is not better accounted for by another mental disorder and is not due to a general medical condition (e.g., a dermatological condition).

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

(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Text Revision. Washington DC: American Psychiatric Association, 2000.)

General Considerations

Epidemiology

The incidence of trichotillomania in the general population is unknown, but estimates have placed its prevalence in the United States as high as 8 million people. A recent survey of 2579 college freshmen indicated that 0.6% would have met criteria for trichotillomania at some point in their lifetimes. Trichotillomania appears to be more prevalent in females (although males may predominate in patients under age 6 years).

Etiology

The etiology of trichotillomania is unknown; however, different theories have been proposed about the pathogenesis of this complex disorder. Psychoanalytic theory views pathologic hair pulling as a manifestation of disrupted psychosexual development, often due to pathologic family constellations. In contrast, behavioral theory conceptualizes hair pulling as a learned habit similar to nail biting or thumb sucking. Recently, a biological theory has been postulated as several researchers have proposed a serotonergic abnormality in trichotillomania and have suggested that the disorder may be a pathologic variant of species-typical grooming behaviors. Neuropsychological abnormalities, treatment response to some antidepressants, and frequent comorbidity with OCD have led to speculation regarding a neurobiological etiology, perhaps involving frontal lobe or basal ganglia dysfunction.

Genetics

Family studies are suggestive of a genetic predisposition for trichotillomania but may reflect environmental learning and are inconclusive.

Clinical Findings

Signs & Symptoms

Patients, particularly young ones, frequently deny that they pull their hair intentionally. Others typically describe pulling their hair when alone, but they may pull it openly in front of immediate family members. These episodes tend to occur during sedentary activities such as watching television, reading, studying, lying in bed, or talking on the telephone, and they may be more frequent during periods of stress. Patients may be unaware that they are pulling their hair until they are in the middle of an episode. Some patients report being in a trance-like state when they pull their hair. These episodes may last a few minutes or a few hours. Patients may pull a few hairs or many hairs per episode. Many patients do not feel pain when the hair is pulled; some patients report that it feels good.

Patients frequently engage in oral manipulation of the hair once it is pulled including nibbling on the roots or swallowing the hair. The later behavior can lead to a rare but serious complication, a trichobezoar (hair ball) in the gastrointestinal tract. The consequences of a trichobezoar can be life-threatening: obstruction, bleeding, perforation, pancreatitis, and obstructive jaundice.

Patients typically pull hair from their scalp, causing diffuse hair thinning or virtual baldness. The typical patient demonstrates patchy areas of alopecia without inflammation that spare the periphery. Many patients are adapt at hiding areas of hair loss by judicious hair styling, but may ultimately resort to hairpieces and wigs when the areas become too large or too numerous to hide. Patients may also pull hair from other parts of their body, including eyelashes, eyebrows, pubic region, or from face, trunk, extremities, or underarms.

Psychological Testing & Laboratory Findings

Although psychological testing may not be useful in confirming a diagnosis of trichotillomania, a punch biopsy may be of some help in this regard. The biopsy results typically reveal increased catagen hairs along with melanin pigment casts and granules in the upper follicles and infundibulum.

Differential Diagnosis

According to DSM-IV-TR diagnostic criteria, a diagnosis of trichotillomania is not warranted if the condition can be better accounted for by another mental disorder or is due to a general medical condition. For example, if a patient has another significant Axis I psychiatric disorder (e.g., a condition with delusions or hallucinations) that might account for the hair pulling, then the diagnosis of trichotillomania would not be warranted. When patients deny that they pull their hair intentionally, dermatologic consultation may be required to rule out other causes of hair loss. Most notable among these conditions is alopecia areata, but tinea capitis, traction alopecia, androgenic alopecia, monilethrix, and other dermatologic conditions should also be considered. A punch biopsy may be indicated particularly when one of these disorders is suspected.

Treatment

An initial double-blind cross-over trial compared clomipramine to desipramine in 13 patients with trichotillomania screened to rule out neurologic disorder, mental retardation, primary affective disorder, psychosis, and OCD. Clomipramine produced improvement in clinical symptoms (33–53% reduction in severity scores) on each of three rating scales designed to assess trichotillomania symptomatology and clinical improvement; scores on two of the three scales were statistically significant. Two subsequent placebo-controlled, double-blind cross-over studies failed to show efficacy for fluoxetine.

Little rigorous research has been conducted concerning the differential effectiveness of treatments for trichotillomania. Clomipramine and behavior therapy probably constitute the current treatments of choice, but this conclusion is tempered by the paucity of treatment outcome studies. Habit renewal training is the most effective form of behavioral therapy. Trichotillomania occurs with variable levels of severity in terms of hair pulling and comorbid psychopathology. As a result, response to treatment is highly variable and rather unpredictable.

Complications/Adverse Outcomes of Treatment

Although hair loss is self-induced, patients are often particularly sensitive to comments about their appearance and go to great lengths to hide their disfigurement. These patients are often fearful that their shameful “secret” will be discovered and that they will be ridiculed in public. If the disorder is protracted, the patient's self-esteem can suffer drastically. Some individuals develop avoidant behavior and become socially withdrawn in order to avoid exposure. Trichobezoar is a rare complication. Little is known about the comorbidity of trichotillomania. Aside from the possibility that the disorder may be related to anxiety or mood disorder, there has been much speculation that it is a variant of OCD. Some research lends support to this hypothesis; however, the studies that failed to show efficacy for fluoxetine would argue against such a relationship.

Trichotillomania in preadolescents (particularly in those younger than 6 years of age) is thought to be associated with little psychopathology. In adolescent and adult patients, however, an association with other mental disorders has been demonstrated. In a study of 60 adult chronic hair-pullers (50 of whom met strict criteria for trichotillomania), only 18% did not demonstrate a current or past diagnosis of an Axis I psychiatric disorder other than trichotillomania. The lifetime prevalence of mood disorders was 65%, and 23% met criteria for current major depressive episode. Lifetime prevalence of anxiety disorders was 57%, and 10% demonstrated a current diagnosis of OCD and 5% a history of OCD. Another 18% endorsed present or past obsessions and compulsions not meeting the full criteria for OCD. Lifetime prevalence of panic disorder with or without agoraphobia was 18%, generalized anxiety disorder 27%, simple phobia 32%, eating disorder 20%, and substance abuse disorder 22%.

A smaller study that used standardized assessment techniques found that 45% of the trichotillomania patients studied met criteria for current or past major depression, 45% had generalized anxiety disorder, 10% had panic disorder, and 35% had alcohol or substance abuse. Unfortunately, patients with OCD were excluded from the study.

Adverse outcomes of treatment are limited to the usual side effects experienced with clomipramine or other antidepressants.

Although there might be adverse consequences of psychodynamic psychotherapy or a behavioral treatment approach, such adverse outcomes are generally thought to be rare and unpredictable.

Prognosis

The prognosis and course of illness generally can be predicted from the age at onset. Trichotillomania begins most often in childhood or young adolescence. Hair pulling in very young children is frequently mild and remits spontaneously. Patients with a later age at onset tend to have more severe symptoms that run a chronic course. These patients are thought to have a higher incidence of comorbid anxiety and depressive disorders.

This category is for disorders of impulse control (e.g., skin picking) that do not meet the criteria for any specific impulse control disorder or for another mental disorder having features involving impulse control described elsewhere in the DSM-IV-TR (e.g., substance dependence, a paraphilia).