CHAPTER 23 Impulse-Control Disorders
OVERVIEW
Six impulse-control disorders are defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR)1: intermittent explosive disorder, kleptomania, pyromania, pathological gambling, trichotillomania, and impulse-control disorders not otherwise specified (NOS). Impulsivity is the symptom common to each of these disorders. The pathological aspect of impulsivity is the inability to resist an action that could be harmful to oneself or to others. Hallmarks of this disorder include a building of tension around the desire to carry out any impulsive act that is relieved or gratified by engaging in the activity. There may be guilt, remorse, or self-reproach after the act. Other Axis I and II disorders are related to the impulse-control disorders in a complex manner, in that they are part of the differential diagnosis of impulsivity, as well as co-morbid conditions. Patients with impulse-control disorders are likely to also suffer from affective disorders, anxiety, substance abuse, personality disorders, and eating disorders, as well as paraphilias and attention-deficit disorder.2–5 Our understanding of these disorders from neurobiological studies and evidence-based treatment studies varies from disorder to disorder; nonetheless they share many common features.6–9 This chapter will focus on impulse-control disorders (Table 23-1).
Table 23-1 Impulse-Control Disorders: Diagnostic Criteria and Treatment Strategies
| Condition | DSM-IV-TR Diagnostic Criteria | Treatment |
|---|---|---|
| Intermittent explosive disorder |
• Several discrete episodes of a failure to resist aggressive impulses that result in serious assaultive acts or the destruction of property.
|
ECT, Electroconvulsive therapy; NOS, not otherwise specified.
INTERMITTENT EXPLOSIVE DISORDER
Intermittent explosive disorder is a diagnosis that characterizes individuals with episodes of dyscontrol, assaultive acts, and extreme aggression that is out of proportion to the precipitating event and is not due to another Axis I, II, or III diagnosis.1,10–13
Epidemiology and Risk Factors
Although episodic violence is common in our society, when applying strict diagnostic criteria, intermittent explosive disorder is considered rare. Men account for approximately 80% of the cases. Intermittent explosive disorder and personality change due to a general medical condition, aggressive type, are the diagnoses most often given to a patient with episodic violent behavior.14 Risk factors include physical abuse in childhood, a chaotic family environment, substance abuse, and psychiatric disorders in the patient or his or her relatives.8,9,12
Pathophysiology
This disorder results from a complex convergence of psychosocial and neurobiological factors.15,16 Some studies show that serotonin neurotransmission is disordered, as evidenced by lower cerebrospinal fluid (CSF) levels and by platelet serotonin reuptake.6 An elevated testosterone level may play a role in episodic violence.15 Soft neurological signs may be present and reflect either trauma from earlier life experiences or genetic underpinnings to the violent behavior.7,17 Family members frequently have similar violent outbursts, as well as a host of psychiatric diagnoses, supporting both an environmental and a genetic etiology.18
Clinical Features and Diagnosis
The age of onset for intermittent explosive disorder is in early adolescence through the twenties. An episode of violence may arise in the setting of increased anger and emotional arousal before the loss of control that is out of proportion to the precipitating stressor. Generally, these patients may be seen as having a baseline of anger and irritability. Their lifestyle can be marginal; the disorder may make it difficult to maintain a job and stable relationships. The presence of substance abuse further complicates both the diagnosis and the course of the illness. The most important feature of this disorder is that numerous other diagnoses must be ruled out before intermittent explosive disorder can be diagnosed. See Table 23-1 for the condition’s DSM-IV-TR diagnostic criteria.
Most violent behavior can be accounted for by a variety of psychiatric and medical conditions. The most common diagnosis linked with violence is personality change due to a general medical condition (aggressive or disinhibited type). Causes for this condition include seizures, head trauma, a neurological abnormality, dementia, and delirium. Personality disorders of the borderline or antisocial type must also be considered. Anger attacks associated with major depression must also be ruled out.19 Further, psychosis from schizophrenia or a manic episode may cause episodic violence. Aggressive outbursts while intoxicated or while withdrawing from a substance of abuse would prevent making the diagnosis of intermittent explosive disorder (Table 23-2).
Table 23-2 Differential Diagnosis of Intermittent Explosive Disorder
| General Medical Condition |
| Dementia (multiple cognitive deficits, including memory loss) Delirium (fluctuating course with disturbed consciousness and cognitive deficits) Personality change due to a medical condition |
| Direct Effects of a Substance |
| Substance intoxication Substance withdrawal |
| Delusion-Driven Behavior |
| Schizophrenia Schizoaffective disorder Depression with psychotic features Delusional disorder |
| Elevated Mood |
| Mania Mixed state, bipolar disorder Schizoaffective disorder |
| Depressed Mood |
| Depression Bipolar, depressed Schizoaffective disorder |
| Pattern of Antisocial Behavior |
| Antisocial personality disorder Conduct disorder |
| Pattern of Impulsivity by Early Adulthood |
| Borderline personality disorder |
| Inattention |
| Attention-deficit/hyperactivity disorder |
| Other Conditions |
| Paraphilias Eating disorders Adjustment disorders Other impulse-control disorders |
Treatment
Psychopharmacology (e.g., anticonvulsants, lithium, beta-blockers, anxiolytics, neuroleptics, antidepressants [both serotonergic and polycyclic types], and psychostimulants) can effectively control the chronic manifestations of this disorder.13,20 The acute management of aggressive and violent behavior may also require use of physical restraints and rapid use of parenterally administered neuroleptics and benzodiazepines (see Chapter 65).21,22
KLEPTOMANIA
More than 150 years ago, kleptomania was first recognized as behavior of “nonsensical pilfering,” in which worthless items were stolen; such behavior was deemed outside the person’s usual character.23 Afflicted individuals were not known to have a pattern of stealing or of premeditated thievery. This disorder is characterized by an increased sense of tension before the act of stealing that is relieved by the act of stealing. It is a complex disorder with significant co-morbidity, family history, and similarity with other affective and addictive spectrum disorders.24–26 Since the initial documentation in the 1800s, few systematic or scientifically rigorous studies have been conducted.
Epidemiology and Risk Factors
Although little is known about kleptomania, the prevalence within the general population has been estimated at 6 per 1,000.27 Less than 5% of shoplifters meet criteria for kleptomania.23 Women are more likely than are men to be diagnosed with kleptomania. Typically, there is a lag of many years (often several decades) between the onset of the behavior and the presentation for treatment. On average, women with the disorder seek treatment in their thirties and men seek treatment in their fifties.23 This may or may not be associated with disclosure when seeking treatment for another mental illness or other factors involving legal problems linked with stealing behavior. Co-morbidity with other psychiatric illnesses, substance abuse, and personality disorders is high, ranging from 50% to 100% depending on the study.23,24,26–29
Pathophysiology
A complex interplay of neurotransmitters (including serotonin, dopamine, and the opiates), hormones, and genetic expression are implicated in impulse-control disorders, especially when the behavior is part of the motivation and reward cycle. Serotonin deficiencies in the brain facilitate impulsive behavior. Dopamine release has been associated with a “go” signal in the modulation of risk-taking behaviors. The opioid system has been associated with craving and reward, and may be implicated in the release of tension that surrounds the completion of impulsive acts. Brain regions that play important roles in the processing of motivation and reward include all the structures within the limbic system (e.g., the hypothalamus, amygdala, hippocampus, and cingulum), the prefrontal and frontal cortex, and the association cortices. From a developmental perspective, impulsive stealing may act to lift a depression by an overriding stimulation and distraction. While numerous psychodynamic theories have been offered as an explanation for kleptomania, none of them has been confirmed or refuted. The exact delineation of these biological and psychological factors for the development of kleptomania has not been well established.6,8,27,30,31
Clinical Features and Diagnosis
Kleptomania typically has an onset in late adolescence and a chronic course of intermittent episodes of stealing over many years. Patients generally come to professional attention via court referrals or through disclosure during treatment for a related psychiatric disorder. Ego-dystonic reactions to the behavior and the unpremeditated nature of the stealing episodes should prompt further review. Additionally, co-morbid psychiatric conditions (including affective disorders, anxiety disorders, other impulse-control disorders, substance use disorders, eating disorders, and personality disorders) are common.24,26–29 Diagnostic criteria are shown in Table 23-1.
Treatment
Much of the literature about the pharmacotherapy of kleptomania is based on case series and anecdotal reports; findings vary.27 Based on co-morbidity studies, as well as the diagnostic characteristics of any particular patient, anxiolytics, mood stabilizers, and opiate antagonists should be tried.32 Monotherapy with tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), mood stabilizers, and anxiolytics, alone or in combination with other agents, may be useful (e.g., an antidepressant and a mood stabilizer or anxiolytic).33 Recent studies show that opioid antagonists are effective treatments along with mood stabilizers and anxiolytics in treating the debilitating symptoms of kleptomania.34,35 Psychotherapy (including insight-oriented psychotherapy and CBT that uses covert and aversive sensitization) may be helpful, and somatic therapies (including electroconvulsive therapy) may be useful.36 The current emphasis on combining psychotherapy with psychopharmacotherapy is promising yet needs more systematic and controlled study.
PYROMANIA
Pyromania is the irresistible impulse to set fires, without any motive beyond creating the fire itself; it occurs in the absence of any other condition that would impair judgment. Pyromania is rare, but fire-setting comes to the attention of the psychiatrist more commonly. Much of the research in this area focuses on individuals who set fires, not on pyromania per se. Children under age 18 account for half of all arrests for arson37; much of the research on effective treatment concentrates on this age-group.
Epidemiology and Risk Factors
Epidemiological research in pyromania examines cases of repeat arson, usually in forensic settings. By definition these are individuals who have been arrested, and may not represent the full population of persons who repeatedly set fires. A classic study by Lewis and Yarnell in 1951 reviewed roughly 2,000 case files from the National Board of Fire Underwriters and found that 39% of these cases did not have a profit motive; instead they were due to pyromania.38 More recent studies have shown that 1% to 3% of repeat arsonists meet criteria for pyromania.39,40 The condition is more prevalent in men than in women.
Although the diagnosis of pyromania excludes fire-setting due to a delusion, hallucination, or another psychiatric condition that impairs judgment, fire-related behaviors are not uncommon in psychiatric patients. Two reviews of nongeriatric inpatient records for history of setting fires, or history of fire-related behaviors (such as hospital admission for threatening to set a fire, setting off a fire alarm, calling in a false report of a fire, or setting fire to oneself or to others), found that roughly 26% of patients exhibited one of these behaviors; 16% actually set a fire.41,42 Patients who had fire-related behaviors were also more likely to have self-injurious behaviors and multiple admissions.
Psychiatric disorders that are highly co-morbid with fire-setting behavior include a high incidence of conditions that exclude the diagnosis of pyromania, that is, mental retardation, conduct disorder, alcohol and other substance abuse, schizophrenia, mania, and antisocial personality disorder.43,44 One-third to two-thirds of cases report intoxication with alcohol or drugs (or both) at the time of the fire.
Pathophysiology
Freud’s assertion that unconscious drives produce behavioral symptoms gave credibility to the idea that the impulse to set fires is on some level irresistible. He claimed a “close connection between the ideas of ambition, fire, and urethral eroticism.”45 He understood fire-setting behavior as representative of psychosexual conflict and as an equivalent of masturbation.
Adolescents who set fires are more likely to have experienced sexual or physical abuse and to come from dysfunctional families. They are more likely to have suicidal thoughts, suicide attempts, and self-injurious behavior, and to express depression and hopelessness.46
Studies of arsonists show lower than normal CSF concentrations of 5-hydroxyindoleacetic acid (5-HIAA), a primary metabolite of serotonin,47–49 and 3-methoxy-4-hydroxyphenylglycol (MHPG), a norepinephrine metabolite.47 Arsonists also show a higher incidence of reactive hypoglycemia.48,49 Fire-setting has also been associated with Klinefelter’s syndrome,50 epilepsy,51,52 XYY syndrome, acquired immunodeficiency syndrome (AIDS), and late luteal phase dysphoric disorder.53
Differential Diagnosis
Exclusionary criteria include fire-setting “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,”1 and the firesetting cannot be “better accounted for by conduct disorder, a manic episode, or antisocial personality disorder.”1
Treatment
Serotonergic medications are widely used for impulse-control disorders because of the link between serotonin dysfunction and impulsivity. However, no randomized controlled trials of the pharmacotherapy for pyromania or for fire-setting have been conducted. One brief account by a female patient described being helped by clomipramine, but co-morbid depression and borderline personality disorder were present, as well as pyromania.54 Another case report described treatment with CBT and topiramate; a left frontal perfusion defect seen on a single-photon emission computed tomography (SPECT) scan resolved with treatment.55 Any co-morbid condition (such as bipolar disorder, schizophrenia, alcohol or substance abuse, or seizure disorder) should be treated with appropriate medications.
Behavioral treatments are widely used, although much of the research is being done in child and adolescent populations.56,57 One behavioral treatment is chain analysis or graphing: this requires that the patient chart the time, place, and circumstances of the fire-setting event, and the thoughts and feelings that led up to the behavior. Working with a therapist, the patient can learn to identify the antecedents of the behavior, to understand the emotions that preceded the behavior, and to learn how to substitute alternative expressions or outlets for those emotions. Alternative solutions to problems are generated with the therapist. Relaxation training is also used to give the patient a means of coping with emotions. Social skills training can also be used to help patients manage interpersonal situations more successfully. Fire-safety instruction is also used. Another prevention program to reduce recidivism is aimed at children and adolescents; it involves education on the consequences to the community, including the medical and financial consequences.58 It also teaches about the legal consequences to the offender.
Prognosis
Cognitive and behavioral treatment programs directed at children and adolescents have been very successful, with recidivism rates as low as 0.8%.58 One 20-year follow-up of adult offenders found a repeat conviction rate of 4%.59 The prognosis is worse for offenders who have a history of alcohol dependence or antisocial personality disorder. There is also a high rate of repeat offense for individuals who had prolonged bedwetting as a child. Patients who were psychotic at the time that they set a fire are less likely to repeat the behavior.
PATHOLOGICAL GAMBLING
Epidemiology and Risk Factors
A meta-analysis of epidemiological studies of gambling in the United States and Canada estimated a 1.1% prevalence of pathological gambling, with a 1.6% lifetime prevalence.60 This analysis showed a higher prevalence in adolescents, and an even higher rate in those who are incarcerated or receiving psychiatric treatment.
The Gambling Impact and Behavior Study interviewed a total of 2,947 adults and 534 adolescents in the United States, and reviewed a database of statistics of 100 communities and 10 case studies of the effects of casino openings. The study estimated that 2.5 million Americans were pathological gamblers at the time of the survey, and that another 3 million should be considered “problem gamblers.” The prevalence of pathological gambling is doubled in the area within 50 miles of a casino. The population segment with the highest and growing rate of pathological gambling consists of those over age 65.61
The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) interviewed 43,093 adults in the United States and found an overall lifetime prevalence of pathological gambling of 0.42%; women had a rate of 0.23% and men a rate of 0.64%. Increased prevalence was associated with being male, African American, 45 to 64 years of age, and single.62
Pathological gambling is more likely if there is a family history of alcohol or other substance dependence, mood disorders, pathological gambling, or antisocial personality disorder.63,64 Twin studies have shown an increased incidence of pathological gambling in the twins of affected individuals.65 There is also an increased incidence of alcohol dependence and major depressive disorder in co-twins, suggesting a common genetic vulnerability for both disorders.66,67 Pathological gambling is highly co-morbid with alcohol dependence or abuse, other substance dependence or abuse, and mood, anxiety, or personality disorders; in women, it is also highly co-morbid with nicotine dependence.68,69
Pathophysiology
Abnormalities in serotonin, norepinephrine, and dopamine have been found in individuals with pathological gambling.69,70 Studies of CSF levels of serotonin metabolites have had mixed results, but there is other evidence of low serotonin availability, including decreased platelet monoamine oxidase B (MAO-B) activity.71 Other studies have found a blunted prolactin response after intravenous administration of clomipramine,72 and a higher than normal prolactin release after administration of a serotonin agonist, suggesting decreased activity or availability of serotonin.73
Norepinephrine function is associated with arousal and sensation seeking. CSF levels of norepinephrine and its metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) are higher in pathological gamblers.74 Growth hormone is released in greater amounts after administration of clonidine in pathological gamblers compared to normal controls; this response suggests abnormal reactivity of the alpha-2 postsynaptic norepinephrine receptors.70
Dopamine function is associated with the reward pathways in the brain. Although one study of dopamine levels in CSF, urine, and plasma found no difference between pathological gamblers and controls,74 another study found lower levels of dopamine, and higher levels of dopamine metabolites, in the CSF of pathological gamblers.75 These results suggest higher turnover of dopamine in pathological gamblers. Moreover, patients with Parkinson’s disease treated with dopamine agonists sometimes develop pathological gambling.76
Some specific gene polymorphisms are more frequent in pathological gamblers. The Taq-A1 allele of the D2 dopamine receptor, associated with other impulsive and addictive disorders, is more frequent is pathological gamblers. A less functional seven-repeat allele of the D4 dopamine receptor has a higher incidence in female pathological gamblers. A three-repeat allele of an MAO-A promoter with lower transcriptional activity has higher incidence in male pathological gamblers; this gene has lower transcriptional activity. Male pathological gamblers also have a higher incidence of a short variant of a serotonin transporter with reduced promoter activity.69,70
Pathological gamblers show deficits in a variety of tasks designed to demonstrate executive function. The delay discounting task tests preference for a smaller immediate reward or a larger delayed reward; preference can shift depending on how long the subject will have to wait for the delayed reward.77 Pathological gamblers are more likely to select the immediate reward. In the Iowa Gambling Tasks, subjects have to learn to choose the card decks that offer long-term advantage; pathological gamblers are more likely to continue to prefer the high-reward, high-loss decks with long-term net loss.
Persistently making decisions that lead to negative consequences is also found in patients with damage to the ventromedial prefrontal cortex. This has led to the somatic marker hypothesis of decision-making, a hypothesis that has been proposed for impaired decision-making in pathological gambling and in addictive disorders. Somatic markers are the physiological changes that occur in response to primary inducers (which are stimuli associated with high-emotion states present in the environment), or to secondary inducers (which are thoughts or memories that have attached emotions and also produce change in the physiological state). The ventromedial cortex activates somatic states from thoughts or memories. Decision-making involves summation of all of the inducers, from the lights and sounds of the slot machine to the memory of the losses associated with one’s last trip to the casino. Failure to include the negative states associated with thoughts and memories of losses in one’s decision-making calculus biases the behavior choice toward continuing disadvantageous behavior.78
The persistence of the gambling behavior in the face of monetary, vocational, and relationship losses inspires the psychoanalytic interpretations that in some way the gambler wants to lose. Freud suggested that the gambler is punishing himself for ambivalent feelings toward his father.79 Edmund Bergler elaborated further, suggesting that the gambler is acting out his aggression toward the authority figures who forced him to renounce his infantile omnipotence. Because there can be “no neurotic aggression without guilt,” “the unconscious wish to lose becomes, therefore, an integral part of the gambler’s inner motivations.”80
Clinical Features and Diagnosis
The DSM-IV-TR describes the pathological gambler as having persistent and recurrent maladaptive gambling behavior (see Table 23-1 for details).
Differential Diagnosis
Differential diagnoses for pathological gambling are listed in Table 23-3.
| Conditions | Characteristics |
|---|---|
| Social gambling | Gambles on designated occasions |
| Decides in advance how much loss is tolerable, and stops at this amount | |
| Enjoys the social companionship of the activity | |
| Professional gambling | Considers gambling a business |
| Disciplined | |
| Able to endure periods of loss without changing gambling behavior | |
| (Note: The National Opinion Research Center [NORC]61 study found that 20% of those who considered themselves professional gamblers met criteria for pathological gambling.) | |
| Psychosis | Bets and gambles in response to delusions, or to command auditory hallucinations |
| Bipolar disorder | The patient has to meet criteria for pathological gambling while euthymic |
| Antisocial personality disorder | Engages in criminal behavior not related to desperation about gambling |
Treatment
As with the other impulse-control disorders, patients do better with a combination of psychotherapeutic and psychopharmacological treatment. Participation in Gamblers Anonymous is frequently recommended, and the combination of Gamblers Anonymous and professional treatment improves outcomes.81
Use of clomipramine and SSRIs has reduced or eliminated gambling behaviors in the short-term. As with obsessive-compulsive disorder (OCD), patients may require higher doses of these medications than are typically required to treat depression. Although co-morbidity (with depression and pathological gambling) is high, these medications are of benefit even if there were no significant depressive symptoms at the time the medication was started. Naltrexone moderates activity of the mesolimbic dopamine pathway, which is thought to mediate reward and reinforcement. Naltrexone is approved for use in opiate and alcohol dependence and has been shown in case reports, an open-label study, and a placebo-controlled study to reduce urges and thoughts of gambling, as well as gambling behavior. The mood stabilizers (lithium, valproate, and carbamazepine) have helped reduce the symptoms of pathological gambling, especially in gamblers with co-morbid bipolar disorder.69,82,83
CBTs are also effective in the treatment of pathological gambling.69,84,85 Imaginal desensitization, electric aversion therapy, and imaginal relaxation have been studied. Exposure and response prevention, in which participants are exposed to gambling situations without engaging in the behavior, have also been used. Cognitive restructuring involves the intervention in false beliefs about gambling, including an illusion of control, and of memory biases, in which the gambler only remembers winnings. Training in problem solving and social skills is used to reduce the dysphoric states and stress that may trigger gambling behaviors. Self-help approaches include the use of a workbook for self-monitoring and for functional analysis. A meta-analysis of 21 studies that used these behavioral treatments showed an effect size of 2.01; therefore, patients who receive CBT had outcome measures averaging 2 standard deviations above controls.86
Prognosis
Although the DSM-IV describes pathological gambling as a chronic and persistent disorder, Slutske’s 2006 analysis87 of the Gambling Impact and Behavior Study (GIBS)61 and NESARC62 epidemiological data suggests that pathological gamblers may be able to recover naturally from the disease, just as some persons with substance dependence recover without treatment. In the GIBS, 21 individuals had a history of pathological gambling, and only two of them reported seeking treatment. Eighteen of these no longer met full criteria at the time of the survey, and half of those surveyed had no symptoms of pathological gambling in the year before the survey. In the NESARC, 185 respondents had a history of pathological gambling; of those, 22 had treatment or had participated in Gamblers Anonymous, 111 did not meet full criteria at the time of the survey, and 70 had had no symptoms in the past year. Slutske’s87 conclusion that pathological gamblers may have the possibility of natural recovery is controversial.88
TRICHOTILLOMANIA
Trichotillomania is a condition of repeated urges to pull out hair, with tension before the behavior and pleasure or relief after the behavior. Patients are unable to stop pulling out their own hair even after developing visibly thinned areas of hair, shame about the behavior or their appearance, or significant impact on their daily lives. Individuals with trichotillomania report interference with function at work or at school, avoidance of intimate relationships and social activities, and low self-esteem and emotional distress.89,90
Epidemiology and Risk Factors
Prevalence of this condition may be underestimated due to patient shame and denial of the behavior. A survey of college students showed that 0.6% of men and women had met full DSM-III-R criteria for trichotillomania at some point in their lives. In this same study, 1.5% of men and 3.4% of women reported hair-pulling with visible hair loss, but without the tension and relief needed to meet diagnostic criteria.91 Approximately 10% to 13% of college freshmen reported regular hair-pulling in another study, with 1% to 2% having bald patches sometime in their lifetime, and 1% to 2% reporting distress or tension related to the behavior.92
The average age of onset is between 11 and 13 years, with female patients far outnumbering male patients in adult treatment settings.93,94 In a pediatric case series of all clinic patients diagnosed with trichotillomania, 10 children between 9 and 13 years of age were identified; half were male and half female.95 It is not known if the female-to-male ratio changes in adult patients, or if adult men are less likely to seek treatment.
Trichotillomania is highly co-morbid with other Axis I disorders, including mood disorders, anxiety disorders, substance abuse disorders, and eating disorders.94 Evaluated according to the DSM-III-R, two-thirds of patients in one study met criteria for anxiety or a mood disorder; one-half met criteria for Axis II disorder.96 Three-quarters of first-degree relatives of the participants had an Axis I disorder, and 5% of them were hair-pullers.
Pathophysiology
Serotonin has been studied in trichotillomania because of the association between impulsivity and serotonergic dysfunction. A study of CSF concentrations of 5-HIAA showed no significant difference between patients with trichotillomania and normal controls. However, the study demonstrated that the lower the concentration of 5-HIAA at baseline, the higher the degree of improvement after treatment with a serotonergic drug.97
Patients with trichotillomania have also shown smaller left putamen volumes, implicating the striatum in this disease. Symptoms involving repetitive behaviors or thoughts may involve dysfunction in corticostriatal pathways.98 Positron emission tomography (PET) studies have shown increased metabolic activity in the right and left cerebellum and in the right superior parietal area.99 Morphometric magnetic resonance imaging (MRI) analysis has demonstrated lower total, right, and left cerebellar cortex volumes. There is a significant inverse relationship between the severity of trichotillomania and the volume of the left primary sensorimotor cluster of the cerebellum.100
Morphometric studies may demonstrate the cause or the effect of the illness; however, the cerebellum is central to the complex and coordinated motor sequences. The cerebellum also contributes to planning and executive functions, visual-spatial memory, and attention modulation and attention shifting. Studies of cognitive differences between patients with trichotillomania and normal controls have shown conflicting results. Some studies show impaired nonverbal memory and executive function.101 Another study shows no deficits in visual-spatial or executive function, but does show impairment in the Object Alternation Task, which shows an ability to establish and to maintain an alternating set,102 and another showed deficits in tasks of divided attention.103 One interpretation of this deficit is a problem in response flexibility; the trichotillomania patient may have difficulty switching to another behavior once the behavior has started.103
Psychodynamic interpretations of trichotillomania include the idea of a “hair-pulling symbiosis.” In this relationship the symptom of hair-pulling becomes the arena for acting out ambivalence and hostility about separation and individuation.104 Hair-pulling has also been suggested to be a response to a real or a feared object loss.105,106 Other interpretations suggest that hair-pulling is an autoerotic substitution or symbolic castration.107
Several primate species, mice, parrots, cats, dogs, and rabbits develop excessive grooming behaviors when stressed. Excessive grooming has been induced experimentally in some rat pups by injection of an adrenocorticotropic hormone or hypothalamic stimulation, suggesting that grooming is an innate response.108,109
Clinical Features and Diagnosis
Not all patients will admit to pulling out their own hair, and some may have sought treatment for alopecia before referral to a psychiatrist. Patients may have an itching or burning sensation before the behavior. Patients may start hair-pulling in response to having negative thoughts or feelings about themselves, or in response to negatively experienced interactions with others. On the other hand, patients may pull hair when they are relaxed and inattentive to their own behavior, such as when they are reading, watching television, or talking on the phone. Hairs are pulled out one by one, but some patients will pull quickly and others will select hairs carefully by differences in texture. Some patients report particular satisfaction if the root is retrieved. Some patients inspect the hair, others just discard it. Some may separate the root from the hair, and eat the root or the entire hair. Patients are ashamed of the behavior and of the resulting bald areas. They will typically camouflage the affected areas with scarves, hats, wigs, clothing, or makeup. Patients may avoid friendships, social events, athletic activity, sexual intimacy, or even work that involves opportunities for time alone to pull hair.110–112
Differential Diagnosis
Differential diagnoses for trichotillomania can be reviewed in Table 23-4.
| Hair twirling or twisting | Trichotillomania involves extraction of the hair. |
| Psychosis | Hair-pulling is a result of command auditory hallucinations or a response to a bizarre delusion. |
| Obsessive-compulsive disorder | Hair-pulling is undertaken to prevent distress or to ward off a specific feared event. |
| Tourette’s disorder | Hair-pulling behavior may be an involuntary tic. |
| Temporary childhood behavior | In children the behavior may resolve on its own within a few months; the diagnosis should not be made until the behavior has persisted. |
| Dermatological conditions | Alopecia areata, discoid lupus erythematosus, male pattern baldness, and other dermatological illness; punch biopsy can distinguish trichotillomania from dermatological conditions. |
| Non–rapid eye movement (non-REM) parasomnia | There is one case report of repeated hair extraction occurring during non-REM sleep. The prevalence of this phenomenon is unknown; diagnosis requires polysomnography.112 |
Treatment
The Massachusetts General Hospital (MGH) Hair-pulling Scale can be used to measure the clinical severity and response to treatment. Patients report the frequency of urges, the intensity of urges, and the ability to control the urges; the frequency of hair-pulling; attempts to resist hair-pulling; control over hair-pulling; and distress associated with the behavior.113,114 Both pharmacological and behavioral treatments are used in trichotillomania. Combination treatment has been shown to be superior to either modality used alone.115,116
Serotonergic medications (such as fluoxetine, sertraline, clomipramine, and venlafaxine) have reduced hair-pulling behavior in controlled studies,117–119 although other studies have found no significant difference in symptoms between use of fluoxetine and placebo.120,121 Olanzapine, studied in open-label trials, has been helpful122; case reports have shown the benefits of risperidone123 and quetiapine124 and of augmentation of serotonergic drugs with atypical antipsychotics. Topiramate has also been helpful in open-label trials.125
Habit-reversal therapy for trichotillomania involves developing an awareness of the habit using self-monitoring sheets, training in muscle relaxation and diaphragmatic breathing, and then using a competing response. This technique has reduced trichotillomania symptoms.126 Stimulus-control approaches can also be used. Acceptance and commitment therapy, in which patients are helped to reduce their avoidance of unpleasant internal states, has been successfully combined with habit-reversal therapy.127
Prognosis
Patients can significantly improve hair-pulling, depression, anxiety, self-esteem, and psychosocial function with treatment.128 Measures of self-esteem have worsened in patients who have been followed over time even though other measures of improvement have been stable, possibly because treatment gains tended to plateau.129 Over the longer term, patients may develop irreversible damage to the hair follicles with permanent areas of baldness or thinned hair.130 Patients who eat the hair (e.g., with trichophagia) may develop trichobezoars, which are deposits of the hair within the stomach that do not pass through to the rest of the digestive system. Complications of trichobezoars include malabsorption, anemia, pancreatitis, peritonitis, small or large bowel perforation, and acute appendicitis.131
IMPULSE-CONTROL DISORDER NOT OTHERWISE SPECIFIED
This category of disorders (such as pathological spending, pathological shopping, repetitive self-mutilation, compulsive sexual behavior, compulsive use of the Internet, and compulsive face-picking)132–135 does not meet diagnostic criteria for any of the previously discussed impulse-control disorders or for another mental disorder. Compulsive buying and self-mutilation is the most common of these disorders.8 Both are more common in women than in men. Recent research in nonpathological populations shows equal incidence for men and women.136 However, self-mutilation is considered endemic in male prisons.22
Clinical Features and Diagnosis
Pathological spending, pathological shopping, repetitive self-mutilation, and compulsive face-picking are more common in women than in men. However, in male prisons, self-mutilation and face-picking are endemic. Two-thirds of self-mutilators have a history of sexual and physical abuse in childhood.132 These disorders start in adolescence and are characterized by severe psychosocial morbidity, particularly personality disorder.8,132,136 The theories about the causes of self-mutilation range from psychodynamic to psychobiological. Self-mutilation gives a quick sense of relief to stress and is often likened to an addiction. Shopping and spending may distract the patient from feelings of helplessness and futility or even boredom and anger.133,137 These symptoms are frequently associated with other Axis I disorders (including affective illnesses). Because of the heterogeneity of this diagnostic classification, a detailed description and review will not be given. Rather, awareness of these behaviors as independent symptoms or as ones embedded within other psychiatric diagnoses will be useful in the clinical evaluation of any given individual. The key to making a diagnosis of any of these impulse-control disorders is the absence of other significant psychopathology that could explain their manifestation. When patients talk about spending, using the Internet, physically harming themselves in any manner (e.g., cutting, picking, or scratching), and having compulsive sex and there are no other psychiatric or medical diagnoses involved, this category allows for a specific diagnosis of the compulsive or impulsive behaviors. The engagement in these activities must result in dysfunction in the patient’s life and relationships and have negative consequences.
Treatment
Multimodal treatment is currently recommended. Psychopharmacology includes use of serotonergic-enhancing drugs, mood stabilizers, antianxiety agents, neuroleptics, and the narcotic antagonist naltrexone. Other modalities include psychodynamic psychotherapy, behavioral therapy, and involvement in self-help and 12-step programs.36,138 Dialectical behavior therapy (DBT) is gaining acceptance as a successful treatment in those with borderline personality disorder.
Supportive Care and Long-term Management
The approach to the patient with impaired impulse control requires that the clinician evaluate the patient for the presence of organic mental conditions and major psychiatric disorders. Often, impulsivity due to a medical condition, psychoses, and affective disorders can be managed with the treatments best used for those disorders. To the extent that characterological factors, sociocultural issues, and substance abuse plays a role in any particular patient’s impulsivity, treatment includes behavioral therapy, DBT, and 12-step programs.138
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