CHAPTER 22

Disruptive, Impulse-Control, and Conduct Disorders

Bonnie P. Taylor, Ph.D.

Meredith Weiss, M.D.

Casara Jean Ferretti, M.S.

Gregory Berlin, B.S.

Eric Hollander, M.D.

Disruptive, impulse-control, and conduct disorders is a new diagnostic class in DSM-5 (American Psychiatric Association 2013) that combines related disorders that were previously classified within two distinct DSM-IV-TR (American Psychiatric Association 2000) categories. More specifically, and as illustrated in Figure 22-1, DSM-IV (American Psychiatric Association 1994) included 1) oppositional defiant disorder (ODD), conduct disorder (CD), and disruptive behavior disorder not otherwise specified (DBD NOS) among the Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence, and 2) intermittent explosive disorder (IED), pyromania, and kleptomania among the Impulse-Control Disorders Not Elsewhere Classified. The common thread that runs through these disorders is an underlying construct of emotional and/or behavioral dysregulation that results in impulsive behavior, aggressiveness, and pathological rule breaking. Whereas ODD and CD were conceptualized in DSM-IV-TR as developmental disabilities defined by defiant behaviors and features of impulsivity commonly seen in attention-deficit/hyperactivity disorder (ADHD), they are classified within DSM-5 together with disorders of impulse control that typically persist into adulthood.

Utilizing a spectrum approach to characterize related disorders with overlapping symptom presentation due to underlying emotional and/or behavioral dysregulation, one can easily conceptualize many disorders and conditions (Table 22-1). Clinicians should be aware that individuals with impulsive aggressive behaviors might indeed present with one or more of these related conditions or co-morbid disorders, which may contribute to their pattern of impulsive aggressive behavior.

Figure 22-1. DSM-5 disruptive, impulse-control, and conduct disorders: comparison with DSM-IV classification.

ADHD=attention-deficit/hyperactivity disorder; CD=conduct disorder; IED=intermittent explosive disorder; ODD=oppositional defiant disorder.

Oppositional Defiant Disorder

Definition and Diagnostic Criteria

DSM-5 has introduced several changes to the diagnostic criteria of ODD. These include the addition of an organizational symptom structure that differentiates emotional, behavioral, and spiteful/vindictive behaviors; standard definitions of frequency of symptom occurrence; a severity index; and the removal of exclusionary criteria for CD. These modifications are discussed in more detail in the following paragraphs.

The salient characteristic of ODD is a persistent pattern of hostile, angry, argumentative, and defiant behaviors. Although these behaviors are displayed in all children from time to time, they are significantly more persistent and frequent in children with ODD than is within normal limits for their age and developmental level and, importantly, these behaviors cause considerable impairment in social functioning and/or in educational or vocational activities. Qualitatively, children with ODD often have conflicts with authority figures, resist instruction, question rules, and are stubborn and unwilling to compromise. They may persistently test the limits and deliberately ignore and/or annoy others. In addition, they may present as irritable, blame others for their mistakes or misbehaviors, and become spiteful, revenge seeking, and/or verbally aggressive when upset. The child with ODD believes that his or her behaviors are reasonable reactions to irrational demands or unfair circumstances and, as a result, finds his or her behaviors less disturbing and upsetting than do family, teachers, and peers.

As previously mentioned, DSM-5 now categorizes ODD symptoms based on whether they have an emotional component (e.g., angry, irritable, resentful), a behavioral element (e.g., argumentative, defiant), or a spiteful/vindictive aspect to them (see DSM-5 criteria for oppositional defiant disorder in Box 22-1). This classification structure is important because recent research suggests that the emotional symptoms are linked to the development of future mood and anxiety disorders, whereas the spiteful and vindictive behaviors are predictive of CD and delinquent behaviors (Rowe et al. 2010; Stringaris et al. 2009). To meet DSM-5 criteria for ODD, an individual must exhibit at least four symptoms (which may be emotional, behavioral, and/or vindictive) during interaction with at least one individual who is not a sibling. New to DSM-5 are the frequency criteria of symptom occurrence, which require that the symptoms in the emotional and behavioral categories occur on most days for at least 6 months in children under age 5 years, and at least once per week for at least 6 months in children ages 5 years and older. DSM-IV-TR, in contrast, simply stated that the behaviors must occur "more frequently than is typically observed in individuals of comparable age and developmental level" (American Psychiatric Association 2000, p. 102).

NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.

Notably, although the behaviors displayed in ODD typically first manifest in the home, over time they may expand to multiple settings (e.g., in school, with peers) and are then likely to affect relationships with teachers, peers, and others in the community. When symptoms are reported by multiple informants (e.g., at home and by teachers), the severity of the child's impairment is reportedly greater. In fact, a positive correlation exists between the number of informants who report ODD symptoms and the degree of impairment observed in the child (American Psychiatric Association 2012). Guided by the implications of this cross-situational pervasiveness of symptoms, DSM-5 has instituted a severity index that explicitly specifies the number of settings in which the oppositional behaviors are exhibited. A child categorized with mild severity displays at least four symptoms in only one setting, and a child with moderate severity demonstrates some symptoms in at least two settings. A child labeled with a severe level may similarly display only four symptoms, but some of the symptoms must be present in three or more settings.

Epidemiology

According to DSM-5, the rate of ODD ranges from 1% to 11%. The National Comorbidity Survey Replication, a retrospective study of adults that used DSM-IV diagnostic criteria for ODD, reported a lifetime prevalence of 10.2%, with 11.2% for males and 9.2% for females (Nock et al. 2007). Slightly more boys than girls have been reported to have ODD in other studies as well, but this gender difference appears to even out after puberty (Loeber et al. 2000).

Comorbidity

The most common disorder that coexists with ODD is ADHD, with comorbidity rates reportedly reaching up to 39% (Speltz et al. 1999). Other disorders that frequently occur with ODD include anxiety and depressive disorders (Angold et al. 1999). Whether ODD can manifest with CD has been a question of debate. Although both are considered "disruptive disorders," ODD differs from CD in that children with CD fail to recognize societal rules and personal rights, are physically aggressive toward people or animals, may destroy property, and/or may steal. A concurrent diagnosis of GD with ODD was prohibited in DSM-IV-TR because ODD typically encompasses the features present in CD; however, as mentioned earlier in this section, recent research suggests that the presence of ODD is an important predictor of future clinical outcomes such as depression, anxiety, and CD (Rowe et aL 2010; Stringaris et al. 2009), as well as substance use, ADHD, peer rejection, and family impairment (Nock et al. 2007). The implications of knowing that a child with ODD is at risk for developing other conditions propelled DSM-5 to allow for the diagnosis of both ODD and CD concurrently (i.e., an individual can now be diagnosed with ODD even if the criteria for CD are also met). Other important disorders that are associated with ODD include specific learning disorder and communication disorders.

Pathogenesis

ODD is thought to be caused by a combination of risk, protective, biological, environmental, and societal factors. Environmentally, ODD has been linked to low socioeconomic status, marital discord, poor parenting practices including inconsistent limit setting, low family cohesion, and parental mental disorder and/or substance abuse (Burke et al. 2002). Biologically, research has focused on ODD that is comorbid with other disorders such as ADHD and/or CD (see "Pathogenesis" in the "Conduct Disorder" section); therefore, the unique biological underpinnings of ODD remain largely unknown. To elucidate the biological substrates of ODD without coexisting conditions, studies are needed that investigate children with ODD as a single diagnosis.

Course

The age at onset of ODD is typically between 6 and 8 years, when typical earlier normative oppositional behaviors diminish. Symptoms have a gradual onset, developing over the course of months or even years. As previously mentioned, symptoms commonly first materialize in the home setting. The stability of ODD symptoms over time correlates with the severity of the symptoms, and a high number of ODD symptoms is associated with the development of CD. Early-onset ODD is also predictive of a later diagnosis of CD, as well as ADHD. A child with ODD is also more likely to progress to CD if he or she has low socioeconomic status and has parents with substance abuse. It is important to note that although CD is usually preceded by ODD, the majority of children with ODD do not go on to develop CD or antisocial behaviors in adulthood (Loeber et al. 2000).

Treatment

A comprehensive evaluation for a child presenting with symptoms of ODD should be conducted. Because oppositional behavior is normal in certain developmental stages, particularly between the ages of 2 and 4 years and also during adolescence, a clinician should be cautious when contemplating a diagnosis of ODD during these time periods. Also, because oppositional behaviors generally occur during interactions with familiar adults and peers, symptoms may not materialize during the interview, and the interviewer may need to rely on parent, teacher, and other informant reports to make an accurate diagnosis.

During the evaluation, the clinician needs to assess for other disorders to parcel out whether the oppositional behaviors are truly diagnostic of ODD or whether they are a by-product of another condition. For example, a child with ODD may indeed have concurrent ADHD, or the child may have only ADHD but appear to be oppositional and uncooperative due to inattention, impulsivity, and/or forgetfulness. Similarly, tantrums and antagonistic behaviors are common in young children with depressive and anxiety disorders, as well as in children with language disorders who become frustrated due to an impaired ability to communicate effectively. If another disorder does in fact coexist with the ODD, treating the comorbid disorder will increase the likelihood that the child will benefit from therapeutic treatment for ODD.

Psychotherapeutic interventions are generally indicated to treat children with ODD, with effective treatments targeting the unique needs of both the child and the family. Evidence-based individual approaches are cognitively based and aim to build effective anger management skills, improve problem-solving ability, develop techniques to delay impulsive responses, and improve social interactions. Parent management training is used to help parents manage their child's behavior more effectively, learn successful discipline techniques, and promote desired behaviors in their children.

When treating preschool-aged children, parent management training is often recommended. Some evidence also suggests that programs such as Head Start and home visitation to high-risk families may prevent future oppositional behaviors and delinquency in preschool children. When school age is reached, parent management and individual cognitive-based strategies are the most empirically supported programs. Combining parent training and individual problemsolving approaches has been shown to be more effective than utilizing one treatment alone (Kazdin et al. 1992). School-based programs, such as those aimed at resisting negative peer influences and at reducing bullying and antisocial behaviors, may also be effective for this age group. For adolescents, cognitive-based techniques, vocational and skills training, and parent management tools are recommended. Group-based treatments for adolescents can have negative outcomes (Barlow and Stewart-Brown 2000).

Although no medication has been approved to specifically treat the symptoms of ODD, medications used in children with ODD to treat coexisting conditions (e.g., ADHD, depression, anxiety) may also be effective in improving oppositional behaviors. Some medications that have been helpful in this respect include stimulants (e.g., methylphenidate and dextroamphetamine; Pappadopulos et al. 2006), atomoxetine, guanfacine, atypical antipsychotics (e.g., aripiprazole and risperidone; McKinney and Renk 2011), buspirone, lithium, anticonvulsants (e.g., valproate), and antidepressants such as selective serotonin reuptake inhibitors (SSRIs) (for depression and/or anxiety and/or impulsivity).

Intermittent Explosive Disorder

Definition and Diagnostic Criteria

IED is a disorder characterized by recurrent episodes of inability to control aggressive impulses, reflected by verbal and/or physical aggression. Acts of aggression in IED are not premeditated, are greatly disproportionate to precipitating stressors, and are not targeted toward specific ends. Aggressive acts may be dystonic in that they bring distress to the perpetrating individual. The diagnosis of IED must rule out existing psychopathology that better accounts for displays of aggressive behavior and use of substances with psychotropic properties. Diagnosis of IED cannot be made before age 6. DSM-5 contains revisions to the IED criteria pertaining to the frequency, nature, and severity of the impulsive aggressive outbursts (see DSM-5 criteria for intermittent explosive disorder in Box 22-2).

Epidemiology

Lifetime prevalence rates for IED range from 4.0% to 7.3%, while 1-month and 12-month prevalence estimates are 1.6% and 2.7%-3.9%, respectively (Coccaro et al. 2004; Kessler et al. 2006). Lifetime IED is defined broadly as three or more lifetime attacks without ever having as many as three attacks in a single year. IED is prevalent in adolescents; 7.8% of adolescents polled report a lifetime prevalence of IED, and 63.3% report lifetime anger attacks involving property destruction or the threat or act of violence (McLaughlin et al. 2012). Individuals with IED are frequently young males with "other" race/ethnicity who have low education, are married, and have a low family income; however, these are general characteristics, and IED is widely distributed and not condensed in any one part of the population (Kessler et al. 2006).

Comorbidity

Approximately 64% of individuals with IED meet criteria for at least one comorbid DSM-IV disorder (McLauglin et al. 2012). IED is most commonly associated with fear disorders, substance abuse disorders, and distress disorders, and the onset of IED almost always occurs before the onset of a comorbid substance abuse disorder. There are also strong correlations between IED and major depressive disorder, social phobia, anxiety disorders, and other impulse-control disorders (Kessler et al. 2006; McLauglin et al. 2012).

Pathogenesis

Family and Twin Studies

Relatives of probands with IED have an elevated risk of meeting IED criteria. More importantly, family members of children with frequent, low-intensity displays of aggressive outbursts have a greater chance of developing IED (Coccaro 2010). A history of traumatic experiences also correlates with IED and affects development in adulthood. The relationship between trauma and violent outbursts should not be surprising and is currently being studied in relation to IED.

Molecular and Genetic Studies

Chromosome 15ql3.3 has been of interest in disorders that show signs of impulsivity and aggression. In individuals with autism, microdeletions on chromosome 15ql3.3 were found to be associated with aggression and head-banging (Ben-Shachar et al. 2009). Interestingly, a duplication of approximately 430 kilobase pairs within the BP4-BP5 locus encompassing CHRNA7 (the cholinergic receptor, nicotinic, alpha 7 [neuronal] gene) was implicated in one subject diagnosed with IED with a history of depression, alcohol dependence, drug dependence, and oppositional defiant disorder.

The serotonin receptor IB (HTR1B) rs6296 genotype is emerging as a potential link between childhood aggressive behavior and the prediction of adult hostility. Although the presence of the gene may predict adult aggressive outbursts, it is not related to constructs of anger.

Biological Correlates

Serotonin and Dopamine Systems

The serotonin system, and serotonin type 2A (5-HT_2A) receptors, may have a wide, diffuse effect on the display of impulsive behaviors, including aggression associated with IED, by inhibiting impulsive circuits. Psychostimulants such as methylphenidate or amphetamine are readily prescribed for the treatment of ADHD. In terms of impulsive aggression specifically, more research is needed on the mediating effect of dopamine and psychostimulants.

Imaging and Brain Localization

Recent research points to the role of frontostriatal circuits in modulating affective aggression. Specifically, males with borderline personality disorder who meet criteria for IED show reduced relative glucose metabolism in the lower striatum compared with matched control subjects; however, no such data are present for females in the same population (Perez-Rodriguez et al. 2012). The striatum, gender effects, and glucose metabolism may offer a promising road for further research in behavioral aggression.

Emerging data suggest interesting relationships between facial emotion recognition in subjects with IED and amygdala-orbitofrontal cortex (OFC) dysfunction. Specifically, individuals with IED have exaggerated amygdala and diminished OFC reactivity to faces conveying anger and a lack of amygdala-OFC function during facial processing (Coccaro et al. 2007).

Course

Onset of IED is abrupt, with no prodromal period. IED appears as early as prepubertal childhood and peaks in adolescence, with a mean age at onset of 12-21 years. Symptoms can last from 12 to 20 years or chronically through a lifetime. Severe aggressive outbursts associated with IED can have serious effects on a patient's quality of life (divorce, financial stress, unlawful activity) that may, in turn, promote the onset of other pathologies.

Treatment

Pharmacotherapy

Pharmacological treatment for IED and other impulse-control disorders is precarious due to their comorbidity with other volatile disorders. Because IED is highly comorbid with other disorders characterized by impulsivity, such as bipolar disorder and substance abuse disorders, the prescribing doctor must be prudent when trying new medication regimens. An overview of pharmacotherapy for symptoms of IED is found in Table 22-2.

Symptoms of IED may respond to SSRIs, anticonvulsants, antipsychotics, phenytoin, β-blockers, and α₂-adrenergic agonists (Dell'Osso et al. 2006). SSRIs typically fail to produce long-term remission of aggressive symptoms. Temperamental factors, including neuroticism and harm avoidance, may be indicators for SSRI treatment response (Phan et al. 2011).

Divalproex has shown promise as an option for the treatment of aggression, performing better than placebo in treating impulsive aggression in borderline personality disorder. Higher baseline trait impulsivity and state aggression symptoms may be solid candidate markers for divalproex treatment. Divalproex, however, did not have antiaggressive effects in IED patients, although it did have such effects in patients with Cluster B personality disorders. The drug may be preferentially effective in highly aggressive subjects with personality disorders (Hollander et al. 2003, 2005).

Psychotherapy

A large portion of patients with IED seek emotional treatment (37.7%), and 17.1% of those who seek treatment do so specifically for anger (McLaughlin et al. 2012). Data on effective psychotherapeutic treatment for IED are sparse. In part, this is due to the capricious, unpredictable nature of violent outbursts in IED. Multi-component cognitive-behavioral therapy (CBT) programs in group and individual settings produce significant posttreatment effects in measures of trait anger, hostile thoughts, anger expression, anger control, and aggression. In one study (McCloskey et al. 2008), individual CBT did not have as large an effect as group CBT in reducing aggression, but treatment effects were nearly identical after a 3-month follow-up. In group settings, a therapist may have less opportunity to focus on cognitions and anger control strategies in individual participants. Neither group nor individual CBT reduced hostile thoughts when compared with a control group (McCloskey et al. 2008).

Conduct Disorder

Definition and Diagnostic Criteria

The diagnostic criteria for CD in DSM-5 (Box 22-3) remain largely unchanged from those in DSM-IV-TR, except for "minor wording changes" and the addition of a new specifier, "with limited prosocial emotions" (American Psychiatric Association 2012). CD remains perhaps one of the most commonly given diagnoses within child psychiatry in both inpatient and outpatient psychiatric pediatric facilities (American Psychiatric Association 2000). There is much debate on whether this diagnosis is overused and misused. Nevertheless, it is believed that treatment may be inadequate for a large part of the population diagnosed with CD. CD is characterized by a persistent and recurrent style of behavior that violates accepted age-appropriate rules or societal norms as well as the fundamental rights of other individuals. Subtyping of initial-symptom age at onset (onset during childhood vs. adolescence) may help to determine prognosis. Severity subclassifications range from mild to severe, based on both the extent of induced harm and the number of problem symptoms. CD can be diagnosed in individuals older than age 18 years, provided that they do not meet criteria for antisocial personality disorder (see Criterion C in Box 22-5). The pattern of delinquent behavior is generally present in multiple environments, such as the community, school, and home.

The various symptoms of CD are categorized in DSM-5 into four major groups: aggressive behavior that threatens or causes bodily harm to animals or people, nonaggressive behavior that results in property damage or loss, theft or deceitfulness, and significant breaches of rules and regulations (see Box 22-3). Because many individuals with CD may minimize their behavior problems, clinicians must often depend on other sources for information (American Psychiatric Association 2000). The importance of distinguishing CD from other deviant behavior is not entirely appreciated, and identifying subcultural or adaptive delinquency in particular sociocultural settings is valuable for correct diagnosis.

Epidemiology

The prevalence of CD appears to be increasing and may be higher in urban than in rural environments (American Psychiatric Association 1994). Prevalence estimates of CD in the general population range widely, from less than 1% to greater than 10%, depending on the type of population studied and the diagnostic methods and criteria used (Maughan et al. 2004). What consistently emerges, however, is that CD is more common among males than among females (with ratios ranging from 2:1 to 4:1) (Moffitt et al. 2001). It is debatable whether the finding of lower prevalence rates of CD in females reflects a real gender difference in CD or a diagnostic criteria gender bias against females.

The childhood-onset subtype demonstrates a considerable male predominance and may be predictive of more numerous and severe symptoms. The prevalence of CD increases with age and levels off at approximately 15-16 years, with males showing a more linear year-to-year increase than females, who demonstrate a greater increase starting mostly in adolescence (Maughan et al. 2004).

Comorbidity

CD is commonly comorbid with other psychiatric disorders, further contributing to the ambiguity of the epidemiological data for CD. Males demonstrate higher rates of comorbidity than females (Maughan et al. 2004), and comorbidity with ODD and ADHD is extremely common. Comorbid ADHD adds to antisocial behavior and increased violence. Mood and anxiety symptoms, cognitive disabilities, and substance use disorders are also commonly comorbid with CD, with the prevalence rate for each exceeding 50% in individuals with CD.

Pathogenesis

The interaction among biological, psychological, and sociological elements contributes to CD development. Metaanalyses of genetic studies indicate that CD is influenced moderately by genetics. Individuals with the childhood-onset subtype of CD, which tends to be persistent and pervasive, appear to have stronger genetic influences, a more severe and prolonged course, and a greater likelihood of developing antisocial personality disorder in adulthood (Moffitt 2005). Adoption and twin studies show that both environmental and genetic factors influence CD. An increased risk for CD occurs in children who have an adoptive or a biological parent with antisocial personality disorder, psychopathology, or atypical maternal caregiving, or who have a sibling diagnosed with CD. CD may be more frequent in offspring of biological parents diagnosed with mood disorders, schizophrenia, alcohol dependence, ADHD, or CD (American Psychiatric Association 1994; Moffitt 2005).

Studies suggest that the frequent cooccurrence of CD, ODD, and ADHD is caused by shared genetic factors, yet this theory remains controversial because each individual disorder retains unique genetic elements. Genetic studies show that in CD, approximately half of its genetic influences are unique to the disorder and the other half are common to other disorders (Lahey et al. 2011). Traits that may factor into CD and are associated with elements of antisocial personality include inattention, aggressiveness, and novelty seeking, and these may have genetic correlates. Childhood conduct problems have also been correlated with specific genes for the serotonin 5-HT_1B receptor, the serotonin transporter, and adrenergic performance. Specifically, in individuals experiencing challenges in controlling their impulsivity and aggression, aberrations in the components of serotonin function are commonly noted.

The relationship between hormone levels and behavioral changes remains unclear because few studies have been done in this area. Although increased aggression has been correlated with higher levels of testosterone for boys within deviant peer groups, similar increases in testosterone levels have been found among boys who display greater levels of leadership in nondeviant peer groups (Rowe et al. 2004).

Neuropsychological correlates, when controlled for socioeconomic class, include a relatively decreased IQ. Cognitively, children with behavior problems are more immature with regard to their style of social interaction and problem solving (Teichner and Golden 2000). Although the association is unclear, the significance of poor socioeconomic home environments and degree of parental psychopathology is considerable. The level of parental conflict, absent fathers, greater family size, and fewer ethnic or cultural interests are all associated with a higher risk of conduct problems (Bassarath 2001).

Within the existing scant neuroimaging literature, temporal and frontal abnormalities appear to play a role in CD. Event-related potential (ERP) studies indicate changes (reductions) in P300 amplitudes in anterior brain regions (above the anterior cingulate) when children with CD are given monitoring and executive tasks (Bauer and Hesselbrock 2003). Other changes demonstrated in ERP studies include differences in reaction time to a warning stimulus (faster) in longitudinal studies of future criminals compared with controls. Studies using functional magnetic resonance imaging have shown lower anterior cingulate reactivity to emotional stimuli in children diagnosed with CD, which reflects deficient emotional control. Additionally, children with CD demonstrate decreased reactivity in the amygdala when anxiety-inducing emotional stimuli are applied (Sterzer et al. 2005).

Magnetic resonance imaging in children diagnosed with CD demonstrates abnormalities in temporal region gray matter volume and hyperintensities in frontal lobe white matter (Kruesi et al. 2004). Abnormal resting activity in electroencephalographic data in left frontal regions is correlated with CD symptoms in children in retrospective studies (Deckel et al. 1996). These temporal and frontal brain region structural and functional changes correlate with neuropsychological findings that suggest that children with CD have poor affective processing and executive functioning. Further studies focusing on these findings' predictive reliability and validity are necessary.

Course

Symptom onset for CD can begin in the preschool years but rarely occurs after age 16 years. Generally, significant symptoms emerge between middle childhood and middle adolescence, and ODD is commonly seen prior to the childhood-onset subtype of CD (i.e., before age 10 years). CD has an extremely unpredictable course. For most individuals, CD abates by adulthood. Younger age at onset, incidence of aggression, and greater symptom severity are each independently associated with a higher likelihood of chronicity (American Psychiatric Association 2000) and with increased risk for development of antisocial personality disorder and substance-related disorders in adulthood. CD is more strongly correlated with adult psychopathology than is ODD (Lahey et al. 2008).

Estimates suggest that up to 40% of children diagnosed with CD develop antisocial personality disorder as adults, especially children who use substances before age 15 years, children living in severe poverty, and children placed in foster care or other out-of-home placement (Robins and Ratcliff 1979). Those with CD have a greater risk for development of mood, anxiety, somatoform, and substance-related disorders throughout life (American Psychiatric Association 1994). Children categorized as "resilient" generally have high intelligence, are first born, and come from small, low-discord families. Children with CD symptom onset in adolescence also have a greater likelihood for successful treatment.

Assessment of the family history of children with CD is common in clinical settings to enhance calculation of CD prognosis. Family history accounts for genetic influences and parental environmental factors, both of which play significant roles in children's behavioral development. For example, individuals with childhood-onset CD had more relatives who were convicted of crimes than did individuals with adolescent-onset CD (Taylor et al. 2000). Other research has shown that parents with prior diagnoses of CD generally have inadequate parenting and disordered home environments typified by maternal hostility, physical abuse, and domestic violence. When family history is taken into account, it can provide for better prediction of a poor prognosis, in addition to levels of CD symptoms and significant risk factors of childhood, including ADHD. Thus, it is imperative for clinicians to gain as much knowledge of an individual's family history as possible to learn useful information regarding both the family's and the child's potential ability to respond to treatment and work with the treatment team.

Treatment

The differential diagnosis for CD includes ODD, ADHD, IED, depressive and bipolar disorders, and adjustment disorders (with disturbance of conduct or with mixed disturbance of emotions and conduct). Accurate diagnosis of CD requires correct information and may necessitate access to various information sources, commonly from multiple agencies. Although acquiring this information tends to present unique challenges to the individual responsible for the evaluation, the expended effort commonly results in significant effects. However, accurate information is crucial for diagnosis, treatment recommendations, and prognosis prediction.

Treatment for CD varies widely, likely due to the nonspecific nature of the CD diagnosis, and can include therapy, medication, or a combination of the two. With regard to therapy, the broad range of existing interventions likely reflects the ambiguity of the CD diagnosis itself. Appreciation and understanding of the psychosocial components inherent in the disorder and knowledge of the resources available in the community will help direct the clinician in selecting a treatment with a high probability of success.

Recognition and treatment of comorbid psychiatric disorders is extremely important. The most successful interventions for CD require parental participation; however, parents with antisocial traits are most likely to terminate treatment. Three main forms of therapeutic intervention for the disorder are supported by the current evidence: parent management training, problem-solving skills training, and multisystemic therapy (Farmer et al. 2002). Parent management training instructs individuals in appropriate methods of interpersonal interaction that encourages positive and discourages negative or antisocial interpersonal behaviors. This is accomplished by teaching negotiating skills, utilizing negative consequences and positive reinforcement. Parental involvement and effort is necessary in this modality, but can be a treatment-specific liability in this demographic. Problem-solving skills instruction is rooted in cognitive-based methods and utilizes role-playing and modeling to aid individuals in better identification and management of potentially challenging situations. Treating CD symptoms in individuals with deficits in executive function and with comorbid ADHD may be difficult, and emphasizes the necessity for correct assessment, management, and treatment of comorbidities. Not surprisingly, older children demonstrate a greater rate of success. Multisystemic therapy utilizes systems available within the individual's environment and maximizes positive interactions. Families, schools, peers, and other communities are simultaneously involved. The system is then tailored to the needs of the individual. The multiple systems involved render this therapy expensive and hard to replicate. Nevertheless, it is very effective.

Pharmacological interventions are targeted toward troublesome behaviors and symptoms. However, given the dearth of symptom specificity of CD, unambiguous replicable findings are lacking. The most suitable symptom targets for pharmacological intervention are impulsivity, hyperactivity, aggression, and mood symptoms. Pharmacological agents such as antidepressants, mood stabilizers, stimulants, antipsychotics, anticonvulsants, and adrenergic medications all show some efficacy, but further controlled studies are needed. Nevertheless, difficulty remains in differentiating whether the pharmacological benefit is due to amelioration of CD symptoms or of comorbid psychiatric symptoms.

"With Limited Prosocial Emotions" Specifier

In DSM-5, the specifier "with limited prosocial emotions" has been introduced based on findings that individuals with CD and extreme callousness and negativity across multiple settings have more frequent episodes and more severe patterns of aggression that are relatively stable across time and are less responsive to behavioral treatment (Frick and Moffitt 2010). To qualify for this specifier, the individual must meet full criteria for CD and show two or more characteristics of the specifier, persistently over at least 12 months and in more than one relationship or setting. Multiple sources of information (e.g., self-report, as well as reports from family members, teachers, and/or peers who have observed the child's behavior for an extended period of time) should be considered to determine the persistent presence of these traits. This specifier is described in the DSM-5 diagnostic criteria for CD (see Box 22-3).

Antisocial Personality Disorder

Due to its close association with conduct disorder, antisocial personality disorder has a dual listing in DSM-5 and is found in both the Personality Disorders and the Disruptive, Impulse-Control, and Conduct Disorders chapters. The DSM-5 criteria for antisocial personality disorder, and further details about the disorder, are available in the DSM-5 Personality Disorders chapter (see also Chapter 25 in this volume, "Personality Disorders," by Skodol et al.).

Pyromania

Definition and Diagnostic Criteria

Originally coined by French physician Charles Chretian Henry Marc in 1833, the term pyromania has long been used to characterize pathological fire setting. Although pyromania was initially ascribed to pubescent girls with mental retardation, abnormal psychosexual development, and menstrual difficulties, the significant study by Lewis and Yarnell (1951) created the modern definition of pyromania and further characterized the behavior of fire setting. Pyromania was listed in DSM-IV-TR as an impulse-control disorder. In DSM-5, pyromania is included in the disruptive, impulse-control, and conduct disorders diagnostic class with no changes to its criteria (see DSM-5 criteria for pyromania in Box 22-4).

There has been a paucity of research concerning the unique clinical characteristics of pyromania, and the disorder is thought to be very rare (Grant and Kim 2007). Research in this area generally focuses on the behavior of fire setting and on arson, the crime resulting from fire setting, rather than on the psychiatric diagnosis of pyromania. Thus, many studies are skewed because they sample too broadly (i.e., surveys of the general population questioning history of fire setting) or too narrowly (i.e., focus on populations of individuals incarcerated or institutionalized for crimes of arson).

Natural curiosity and experimentation with fire typically begins at age 6 years, with certain risk factors and motivations elevating fire-setting behaviors as children age. Juvenile fire setting is more common in males than in females and is associated with a history of physical and sexual abuse, substance abuse disorders, family dysfunction, and hostile or impulsive personality traits (MacKay et al. 2009). Youths account for a large percentage of arson offenses in the United States, the United Kingdom, and Australia (45%, 40%, and 55.6%, respectively), and many of these offenders have high rates of recidivism (Lambie and Randell 2011; MacKay et al. 2009). Childhood fire setting is one of the strongest predictors of adult arson and is also associated with significant psychopathology. Antisocial behavior and substance abuse are the strongest correlates in both girls and boys; however, male fire setters also demonstrate externalizing problems such as hyperactivity, thrill seeking, and cruelty to animals, whereas females demonstrate internalizing problems such as anxiety and depression. Additionally, child and adolescent smoking has been shown to correlate highly with fire-setting behaviors; presence of and interest in firesetting paraphernalia may increase the risk of inappropriate fire setting (MacKay et al. 2009).

Studies on fire-setting behavior and arson in adults show similar correlates. According to results from a National Epidemiologic Survey on Alcohol and Related Conditions, the prevalence of lifetime fire setting in the United States was 1.7% for men and 0.4% for women, and was associated with a broad range of violent and nonviolent antisocial behaviors. Both men and women fire setters were shown to have higher rates of antisocial personality disorder, in addition to alcohol and drug use disorders, major depressive disorder, nicotine dependence, bipolar disorder, and obsessive-compulsive personality disorder (Hoertel et al. 2011). A similar study reported a 1% prevalence rate, with higher proportions of fire setters being male, ranging in age from 18 to 35 years, living in a western region of the United States, and having comparable psychopathology (Vaughn et al. 2010).

Characteristics of arsonists appear to be similar to the general characteristics of fire setters. From the small amount of information known, most arsonists are raised in broken homes and have a lower education level and a history of psychiatric or mental health treatment. Compared with non-arson offenders, arson offenders are less likely to be diagnosed with a major psychotic disorder and tend to have lower abilities to control their impulses and significantly more alcohol abuse problems. (As defined by Labree et al. (2010), non-arson offenders are individuals who are not convicted of arson as an index offense and who have never had a conviction for arson.) Arson offenders and non-arson offenders have the same rates of non-alcohol-related substance abuse. Motives for arson include delusional thinking, revenge, property damage, and excitement from fire setting. More than one motive may be responsible for a single act of arson. In a study of 25 arsonists, 52% of motives stemmed from delusional thinking, 36% from getting revenge, and 12% from sexual excitement. It is hypothesized that the percentage of arson committed due to sexual excitement could be higher, because arsonists may hide behind claims of delusional thinking rather than admitting to this motive (Labree et al. 2010).

As mentioned earlier in this section, not all individuals with fire-setting behavior or who have committed arson meet the criteria for pyromania, and research on the characteristics of those who do is even scarcer. The essential feature of pyromania is multiple instances of deliberate and purposeful fire setting that is unrelated to the following: another psychiatric state or ideology, vengeance, criminality, impaired judgment (e.g., dementia or mental retardation), or arson to communicate a desire or need (commonly seen in arsonists with mental or personality disorders). Individuals with pyromania have a fascination with fire and are commonly "watchers" at fires, or may be seen seeking employment or volunteering as firefighters. Although the fire setting results from a failure to resist an impulse, significance may also lie in the preparation of the fire. Pyromania, however, is considered an uncontrolled and impulsive behavior (Hollander et al. 2008).

Epidemiology

Most research on epidemiology is focused on fire setting and arson rather than specifically on pyromania. The largest study to date is still Lewis and Yarnell's (1951) Pathological Firesetting (Pyromania), which involved analysis of approximately 2,000 records from the National Board of Fire Underwriters and case studies of the topic. The authors reported a 39% rate of pyromania overall, and a 14.8% rate in females, according to the criteria of the time period. A more recent study of Finnish male criminals with a history of recidivist fire setting (Lindberg et al. 2005) found that out of 90 arson recidivists, 12 fulfilled the DSM-IV-TR criteria for pyromania. Of these 12 individuals, 9 were under acute alcohol intoxication during the index arson, which would, by DSM-IV-TR's standards, exclude them from the definition of pyromania. Therefore, the results suggest a rate of 3.3% for "true" pyromania. Those individuals who met criteria for pyromania expressed tension or affective arousal before the act of fire setting, pleasure and release afterward, and an attraction to or interest in fire. The three men who met the criteria for "true" pyromania all worked as volunteer firefighters. The strong correlation between alcohol and fire setting, and more specifically alcohol abuse and pyromania, suggests that reconsideration may need to be made to the DSM criteria regarding substance intoxication as an exclusion criterion for a diagnosis of pyromania.

A possible reason for the seeming rarity of pyromania could be a fallacy in epidemiological sampling. In focusing on a criminal population, researchers miss individuals who meet criteria of pyromania but who do not commit arson. Large epidemiological studies that take broad samples of the population are not specific enough in questioning (e.g., they might simply ask, "Have you intentionally set a fire in your lifetime?") to elicit answers that would glean a potential diagnosis of pyromania, because they do not target motivation or frequency. Studies of noncriminal clinical samples have demonstrated higher rates of pyromania. For example, a study of patients with depression found that 2.8% of them met criteria for pyromania (Lejoyeux et al. 2002). Similarly, studies of individuals with compulsive buying and kleptomania have found rates of 10% and 15%, respectively, of lifetime pyromania. There have been suggestions that impulse-control disorders might be substituted for one another across an individual's lifetime (Grant and Kim 2007).

Although female prevalence rates were low in studies of fire setting and arson, Grant and Kim (2007) found that 21.4% of adults and 100% of adolescents sampled with lifetime pyromania were female. The mean onset of pyromania was reported to be 18.1 ±5.8 years, with a mean duration of 5.6±4.5 years in this study. An additional study of adolescents admitted to an inpatient psychiatric service also found a higher prevalence of pyromania in adolescent females (12.5%) than in adolescent males (0%) (Grant et al. 2007). As seen in other impulse-control disorders among women, these higher rates in females could represent attempts to alleviate dysphoric states through impulsive and planned thrill seeking.

Comorbidity

In one of the first studies to observe psychiatric comorbidity in individuals with lifetime pyromania, Grant and Kim (2007) sampled adult and adolescent subjects recruited from inpatient and outpatient studies of impulse-control disorders with lifetime DSM-IV pyromania. Ninety-five percent of patients reported at least one lifetime Axis I disorder. As seen in previous studies, pyromania was highly co-morbid with major depressive disorder (47.6% prevalence; Lejoyeux et al. 2002); substance abuse disorders, including alcohol abuse (33.3% prevalence); and other impulse-control disorders (66.7% prevalence). Subjects reported that mood and substance abuse symptoms were in response to distress from fire setting, of which 90.5% of patients reported. Unlike studies on arson and fire setting, strong correlations were not found between pyromania and antisocial behavior (Grant and Kim 2007).

Pathogenesis

The etiology of pyromania has not received a significant amount of research; however, the high comorbidity with kleptomania and pathological gambling supports the hypothesis of a phenomenological link between pyromania and impulse-control disorders that may indicate similarities in etiology. Lower levels of cerebrospinal fluid (CSF) monoamine metabolite levels have been found in patients with impulse-control disorders, including pyromania and kleptomania. Low CSF 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid concentrations are associated with a family history positive for paternal alcohol abuse in alcoholic male fire setters, whereas low CSF 5-HIAA and 3-methoxy-4-hydroxyphenylglycol (MHPG) concentrations and paternal absence are found in recidivists (Virkkunen et al. 1996). Imaging studies of fire setters and individuals with pyromania have shown perfusion deficits in the left inferior frontal area (Grant 2006a) and frontal lobe dysfunction (Tyler and Gannon 2012); in one case, sudden fire-setting behaviors were associated with a lacunar stroke (Bosshart and Capek 2011).

History of child maltreatment is strongly associated with psychopathology and poor prognosis. Maltreated children set more fires, have a stronger curiosity, and have more emotional and behavioral problems. The distinction between normal and excessive curiosity about fire is not always evident, and there is likely a continuum between excessive interest in fire and pure pyromania. The original pyromania study by Lewis and Yarnell (1951) described three main groups of fire setters: the accidental, the occasional, and the habitual, which have been further characterized by motive, including excitement, attention seeking/cry for help, and revenge/vandalism (Tyler and Gannon 2012). Although the sexual dimension of pyromania has been noted since it was first defined (i.e., "fire fetish"), not many individuals with this clinical feature have been described in the literature. Females with pyromania frequently have a history of self-harm and psychosocial traumas, and fibre setting could be a way of displacing their aggression and anger and improving self-esteem. Similarly, juvenile fire setters also often have increased suicidal ideation (Hollander et al. 2008).

Course

Pyromania most often begins in late adolescence or early adulthood. Few studies have examined links between fire setting or impulsive behaviors in childhood and pyromania psychopathology in adolescence and adulthood. It appears that pyromania can be chronic if left untreated, although its longitudinal course is currently unknown. Many patients with pyromania set controlled fires in their homes or yards rather than committing acts of arson but admit that over time their urges increase and the time between fires decreases. There is a possibility that these controlled fibres may lead to arson, but further study is needed (Grant and Kim 2007).

Treatment

There has not yet been a controlled treatment study for individuals with pyromania, as there has been for other impulse-control disorders, and the U.S. Food and Drug Administration (FDA) has not yet approved medications for any impulse-control disorder. Studies of impulse-control disorders that are phenomenologically linked to pyromania, such as kleptomania, have shown success with opioid antagonists including naltrexone. Medications that have been demonstrated to work in individual cases of pyromania include topiramate, escitalopram, sertraline, fluoxetine, and lithium (Grant and Kim 2007). In a case study of an 18-year-old man with an 8-month history of pyromania, including increasing intensity and urges, topiramate and CBT were prescribed concurrently. A reduction in the urge to set fires was observed after 3 weeks and was still observed 12 months later (Grant 2006a). An additional study of CBT in comparison to a fire safety intervention for child fire setters demonstrated increased reduction in the CBT group's match-play activities, fire-setting incidents, and overall interest in fires (Kolko 2001). A follow-up study conducted in 2006 replicated the results and showed fire safety education (FSE) and CBT to have the most influential effects on child behavior (Kolko et al. 2006). There is a wider scope of research on treatment for fire setters, which focuses on fire safety intervention programs and therapy, with the rationale that teaching fire knowledge and safety skills will correlate with minimized interest in fire and alternative fire-safe behaviors (Lambie and Randell 2011). The Arson Prevention Program for Children in Toronto, Canada, is an example of a mental health program for fire setters, but it still needs further evaluation. In summary, a multifaceted treatment, whether with CBT and medication in adults with pyromania or with CBT and FSE in at-risk child fire setters, appears to be the strongest candidate for management of this impulse-control disorder.

Kleptomania

Definition and Diagnostic Criteria

Kleptomania has not received much empirical study and, therefore, remains poorly understood. The DSM-5 criteria for kleptomania (Box 22-5) are unchanged from DSM-IV-TR. Kleptomania may cause considerable impairment, can have severe penalties, and can be a lifelong chronic and debilitating condition if not recognized and treated. DSM-5 Criterion A embodies what is thought to be the defining feature of kleptomania—that is, the inability to resist repetitive urges to steal specific items that are not required for personal function or utility or for their monetary worth (American Psychiatric Association 2000). ' Urges are generally played out via shoplifting. The person almost invariably can afford the stolen item, which is often given away, hoarded, hidden, thrown away, or returned secretly. It is the senselessness of the stolen item, as well as the objective of the theft for symptomatic relief rather than for personal gain, that distinguishes kleptomania from ordinary shoplifting (Goldman 1991). Yet, this understanding of the illness remains controversial. Often, individuals keep this condition secret until they no longer can due to legal consequences, and then they will seek help.

Epidemiology

The lifetime prevalence of kleptomania within the general population is approximately 0.38%-0.6% (Goldman 1991; Odlaug and Grant 2010). Many experts, however, believe that this estimate may be too low, because the embarrassment related to shoplifting may preclude many individuals from reporting these symptoms. Although national epidemiological analyses of kleptomania have not been done, reports of kleptomania from multiple clinical samples imply a greater prevalence. As shown in Table 22-3, kleptomania is not uncommon in individuals with comorbid psychiatric conditions, such as psychotic, anxiety, mood, or substance use disorders.

Women appear to have a greater incidence of kleptomania than men, with a female-to-male ratio estimated at 3:1. The reported female predominance of kleptomania may be biased because the courts are more likely to require female shoplifters to present for a psychiatric evaluation and women may be more likely to independently seek psychiatric evaluation than men. Of note, severity and clinical presentation of kleptomania symptoms do not seem to differ between males and females (Grant and Kim 2002b; McElroy et al. 1991).

Comorbidity

Kleptomania is more often comorbid with affective disorders than with any other psychiatric disorders, with lifetime comorbidity rates varying from 59% to 100%. Some studies suggest that bipolar disorder is the most common co-occurring disorder, whereas other studies demonstrate that unipolar depression has the highest rate of comorbidity. Research has also shown high rates of comorbid impulse-control disorders (20%-46%), anxiety disorders (60%-80%), eating disorders (60%), and substance use disorders (23%-50%) over the lifetime. Individuals with kleptomania also have high rates of comorbid personality disorders, ranging from 43% to 55%, with paranoid (17.9%), schizoid (10.7%), borderline (10.7%), and histrionic (18%) personality disorders identified as the most common (Grant 2004; Grant and Kim 2002b; McElroy et al. 1991).

Pathogenesis.

Biological Theories Serotonin and inhibition

Patients diagnosed with kleptomania describe considerable increases in risktaking behaviors and impulsivity compared to control subjects. Lower levels of inhibitory mechanisms could be the basis for this. Serotonin and the prefrontal cortex are among the most investigated inhibitory pathways. Risk-taking behaviors among adults, including pathological gambling, alcoholism, and fire setting, are associated with lower quantities of serotonin. Diminished serotonergic reactions in the ventromedial prefrontal cortex are observed in individuals who exhibit impulsive aggression (New et al. 2002). Compared with healthy control subjects, patients with kleptomania had a reduced amount of the platelet serotonin transporter (Marazziti et al. 2000). Case studies investigating pharmacological outcomes of serotonin reuptake inhibitors, including the SSRIs and clomipramine, show that these agents may lower kleptomania-associated impulsive behavior.

Dopamine and Reward Deficiency

Dopaminergic systems that affect reinforcing and rewarding behaviors may influence kleptomania pathogenesis. Changes in the dopaminergic pathways have been implicated as the underlying cause of increased reward seeking, such as shoplifting, which may trigger dopamine release and produce pleasurable feelings. Dopamine neurons' function and structure within this region, concurrently with intrinsic γ-aminobutyric acid (GABAergic) and afferent glutamatergic activities, seem to adjust in response to experiences, thereby influencing the nucleus accumbens. Later behavior may therefore be influenced by previously rewarding experiences through neuroplastic alterations within the nucleus accumbens. This phenomenon could possibly explain why many individuals with kleptomania report shoplifting as "a habit," without feeling overt urges or cravings beforehand, over time (Hollander et al. 2008).

Opioid System: Craving and Pleasure

Urges associated with the perceived experience of pleasure and rewards are an intrinsic aspect of kleptomania in many cases. Urge regulation is thought to be modulated by the brain's μ opioid system, at least partially through the modulation of mesolimbic pathway dopamine neurons and GABA interneurons (Potenza and Hollander 2002). Moreover, studies with the opioid antagonist naltrexone have shown that this agent, can reduce urges in individuals with kleptomania as well as other impulse-control disorders (Grant et al. 2009).

Therefore, recurrent kleptomanic behavior could be due to an imbalance between a pathologically lowered inhibition and a pathologically elevated urge. In other words, recurrent shoplifting could be a result of more activity in the mesocorticolimbic dopamine pathway circuit, enhanced indirectly by the opioid system, and lower activity in cortical inhibitory processes, influenced largely by serotonin.

Neuroimaging

In a study of individuals with kleptomania versus controls, neuroimaging using diffusion tensor imaging has shown that those with kleptomania have diminished microstructural coherence of white matter in the inferior frontal brain regions. This likely reflects faulty connectivity among the tracts connecting the limbic area to the prefrontal and thalamus regions (Grant et al. 2006).

Psychological Theories

Some have hypothesized that kleptomania could result from attempts to alleviate depressive feelings via stimulation or risktaking behavior. Several reports suggest that antidepressants improve not only symptoms of depression but also kleptomania symptoms. Behavioral models may also provide insight into kleptomania pathogenesis. In the operant model, kleptomania is positively reinforced by acquiring items at no monetary cost and is intermittently reinforced by the periodic inability to shoplift due to the presence of security in stores, therefore rendering kleptomania especially extinction resistant. Shoplifting may also produce physiological arousal, which in turn may further reinforce and perpetuate kleptomanic behavior.

Course

The age at onset of kleptomania is generally during adolescence (ages 16-20 years), although symptoms could occur in early childhood or late adulthood (Grant and Kim 2002b). The average age for treatment presentation, however, is about 35 years for females and 50 years for males (Goldman 1991). Because prevalence rates among adolescents and adults seem similar, kleptomania may be better characterized as a chronic disorder, if left untreated. Data describing kleptomania's course are sparse, and epidemiological longitudinal studies have not been performed. Therefore, prognosis is not clear. Three characteristic progressions have been reported: intermittent with short episodes and extended intervals of remission, intermittent with prolonged episodes of shoplifting and intervals of remission, and chronic with a range of intensity (American Psychiatric Association 2000).

Treatment

Pharmacotherapy

The FDA has not yet approved any medication for the treatment of kleptomania; therefore, patients must be informed about "off-label" applications of various medications for kleptomania and the evidence for treatment with medication. The literature investigating pharmacotherapy for kleptomania remains limited.

Two controlled pharmacological trials to treat kleptomania have been conducted. In a double-blind placebo-controlled trial comparing naltrexone to placebo, naltrexone showed successful reduction in kleptomania symptoms (Grant et al. 2009). This finding is consistent with that of an open-label trial with naltrexone, which demonstrated a significant reduction in urge-to-steal intensity, as well as in thoughts and behaviors associated with stealing (Grant and Kim 2002a). In an open-label trial of es-citalopram followed by a double-blind discontinuation phase, the response initially found in the open phase was not maintained during discontinuation, suggesting that a true drug response did not occur (Koran et al. 2007). Case reports and case series demonstrate some positive treatment response for nortriptyline, SSRIs (fluoxetine, paroxetine, fluvoxamine), trazodone, clonazepam, lithium, valproate, and topiramate.

If kleptomania is a result of both faulty urge control and impaired behavior inhibition, then both opioid antagonists and antidepressants (SSRIs) could play a significant role in alleviating these symptoms and regulating the behavior. Therefore, naltrexone may help in decreasing both the desire and urges to steal as well as the actual behavior by diminishing the "thrill" related with stealing and thereby averting the positive reinforcement associated with the behavior. SSRIs may also effectively reduce kleptomania symptoms by influencing serotonergic systems thought to be associated with deficient impulse regulation.

A suggested treatment approach for kleptomania is to initiate treatment with an SSRI or a serotonin-norepinephrine reuptake inhibitor (SNRI), titrated to the appropriate dose for the appropriate duration. Lack of or incomplete response to this medication can be followed by a trial of naltrexone or topiramate. The average effective dose of naltrexone for kleptomania was found to be 116 mg/day, ranging from 50 to 150 mg/day (Grant et al. 2009). For younger individuals with kleptomania, naltrexone 50 mg/day may be an effective dose (Grant and Kim 2002a).

Psychotherapy

Various types of psychotherapy to treat kleptomania have been attempted. However, controlled trials of psychotherapy do not exist in the literature. Case studies have reported some success for psychoanalysis, as well as for behavioral therapies including exposure and response prevention, conditioning and covert sensitization, imaginal desensitization, and CBT.

Because empirical studies are scant, further research is required to determine which psychotherapy and which combination of psychotherapy and medication are most efficacious in the treatment of people with kleptomania.

Characterization of Kleptomania

Obsessive-Compulsive Disorder Model

Arguments that kleptomania may belong on the obsessive-compulsive disorder (OCD) spectrum are based on kleptomania's characteristic features of repetitive behaviors and faulty inhibition. However, other features of kleptomania, such as the thrill-seeking aspects of the disorder, generally speak against the OCD model because individuals with OCD are mostly harm avoidant (Hollander 1993). Moreover, studies focusing on rates of comorbid OCD in individuals with kleptomania have been inconsistent, and the co-occurrence of kleptomania in individuals with OCD is low.

Addiction Model

Some research supports the addiction model of kleptomania. Addiction and kleptomania share several distinct features and frequently co-occur over the lifetime. Many individuals with kleptomania have first-degree relatives diagnosed with substance use disorders (Grant and Po-tenza 2004). Behaviorally, an individual can develop tolerance for stealing, and the value of stolen items may increase over time. Pharmacologically, studies of individuals with kleptomania treated with naltrexone, which is used to treat addiction, have demonstrated positive response (Grant and Potenza 2004).

Affective Spectrum Model

Findings that support inclusion of kleptomania within the affective spectrum include studies that show high rates of mood disorders comorbid with kleptomania (McElroy et al. 1991; Presta et al. 2002). Furthermore, kleptomanic symptoms may worsen concurrently with depression, and stealing may represent a form of antidepressant. Additionally, because of the high rates of comorbid bipolar disorder evident in various studies (McElroy et al. 1991), kleptomania is thought by some to be a symptom of mania or subclinical hypomania.

Attention-Deficit/Hyperactivity Model

The ADHD model of kleptomania is only beginning to gain research attention. One study found significant comorbidity of ADHD with kleptomania (Presta et al. 2002). However, confirmatory studies supporting this finding have not yet been published. There have been a few case reports of successful use of ADHD medications in the treatment of a subset of individuals with kleptomania who appear to have inattentive and impulsive traits. This may be indicative of a category of kleptomania that is functionally related to ADHD (Grant 2006b).

Other Specified or Unspecified Disruptive, Impulse-Control, and Conduct Disorder

Other specified (Box 22-6) or unspecified (Box 22-7) disruptive, impulse-control, and conduct disorder is a diagnosis given when an individual displays significant disruptive behavior and clinical impairment but does not meet criteria for a diagnosis of one of the specifically named disorders in this diagnostic class (American Psychiatric Association 2013). DSM-5 differentiates between specified and unspecified disruptive, impulse-control, and conduct disorder. For an "other specified" diagnosis, the clinician cites the reason why criteria are not fully met, whereas for an "unspecified" diagnosis, the clinician does not indicate why criteria are not met for a specific disruptive, impulse-control, or conduct disorder.

Conclusion

This chapter has focused on disorders found in the DSM-5 disruptive, impulse-control, and conduct disorders diagnostic class. Pathological impulsivity, rule breaking, and aggressive behaviors may be a crucial construct in understanding a broad range of psychiatric disorders, including common psychotic disorders (e.g., bipolar disorder), personality disorders (e.g., antisocial personality disorder), and ADHD. The development of reliable diagnostic criteria for disruptive, impulse-control, and conduct disorders has been extremely useful in promoting research on these disorders and has provided a basis for epidemiological work demonstrating the prevalence of these disorders, their high comorbidity and morbidity, and their significant social costs. At the same time, advances in basic research on impulsivity and aggression, together with new methods in clinical research, have led to increased understanding of the overlapping neurocircuitry and neurochemistry that may be involved in a range of these conditions, and this in turn may ultimately lead to a revised nosology of these conditions. Developments in psychometrics and psychobiology have in turn encouraged researchers to conduct rigorous randomized clinical trials of a range of medications and psychotherapies for use in patients with disruptive, impulse-control, and conduct disorders, and a number of effective strategies are now available. Nevertheless, the range of clinical trials in this area remains comparatively limited, and for now clinicians are required to adopt a flexible approach that includes multiple modalities of intervention in the management of these disorders. Although many patients can be helped by such an approach, much further work is needed to delineate fully the psychobiology of these disorders and to develop effective treatments.

Key Clinical Points

• Emotional and/or behavioral dysregulation, resulting in pathological impulsivity, aggression, and rule-breaking behavior, is a useful construct in understanding a broad range of psychiatric symptoms and disorders.
• Although disruptive, impulse-control, and conduct disorders are highly prevalent and associated with significant disability and costs, they receive disproportionately little attention from clinicians and researchers.
• Significant advances have been made to further understanding of the neuronal circuitry that mediates impulsivity and aggression, as well as the contributing genes and proteins in this circuitry.
• Ultimately, a better understanding of the psychobiological underpinnings of emotional and behavioral dysregulation, impulsivity, aggression, and rulebreaking behavior, as well as other related constructs, may lead to changes in the classification of these disorders.
• Although no medication is registered for the treatment of disruptive, impulse-control, and conduct disorders, a number of randomized controlled trials have demonstrated the potential value of pharmacotherapy.
• Current clinical practice also emphasizes the need for a comprehensive approach to management that includes psychotherapy and family intervention. Additional work is needed to improve efficacy.

References

American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC, American Psychiatric Association, 1994

American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000

American Psychiatric Association: DSM-5 Development: Recent Updates to Proposed Revisions for DSM-5. Available at: www.dsm5.org/Pages/RecentUpdates.aspx. Accessed September 27, 2012.

American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Arlington, VA, American Psychiatric Association, 2013

Angold A, Costello EJ, Erkanli A: Comorbidity. J Child Psychol Psychiatry 40:57-87, 1999

Barlow J, Stewart-Brown S: Behavior problems and group-based parent education programs. J Dev Behav Pediatr 21:356-370.2000

Bassarath L: Conduct disorder: a biopsychosocial review. Can J Psychiatry 46:609-616.2001

Bauer LO, Hesselbrock VM: Brain maturation and subtypes of conduct disorder: interactive effects on P300 amplitude and topography in male adolescents. J Am Acad Child Adolesc Psychiatry 42:106-115, 2003

Ben-Shachar S, Lanpher B, German JR, et al: Microdeletion 15ql3.3: a locus with incomplete penetrance for autism, mental retardation, and psychiatric disorders. J Med Genet 46:382-388, 2009

Bosshart H, Capek S: An unusual case of random fire-setting behavior associated with lacunar stroke. Forensic Sci Int 209:e8-el0, 2011

Buitelaar JK, van der Gaag RJ, Cohen-Kettenis P, et al: A randomized controlled trial of risperidone in the treatment of aggression in hospitalized adolescents with subaverage cognitive abilities. J Clin Psychiatry 62:239-248, 2001

Burke JD, Loeber R, Birmaher B: Oppositional defiant disorder and conduct disorder: a review of the past 10 years, part II. J Am Acad Child Adolesc 41:1275-1293, 2002

Coccaro EF: A family history study of intermittent explosive disorder. J Psychiatr Res 44:1101-1105, 2010

Coccaro EF, Schmidt CA, Samuels JF, et al: Lifetime and 1-month prevalence rates of intermittent explosive disorder in a community sample. J Clin Psychiatry 65:820-824, 2004

Coccaro EF, McCloskey MS, Fitzgerald DA, et al: Amygdala and orbitofrontal reactivity to social threat in individuals with impulsive aggression. Biol Psychiatry 62:168-178, 2007

Coccaro EF, Lee RJ, Kavoussi RJ: A doubleblind, randomized, placebo-controlled trial of fluoxetine in patients with intermittent explosive disorder. J Clin Psychiatry 70:653-662, 2009

Deckel AW, Hesselbrock V, Bauer L: Antisocial personality disorder, childhood delinquency, and frontal brain functioning: EEG and neuropsychological findings. J Clin Psychol 52:639-650, 1996

Dell'Osso B, Altamura AC, Allen A, et al: Epidemiologic and clinical updates on impulse control disorders: a critical review. Eur Arch Psychiatry Clin Neuro-sci 256:464-475, 2006

Farmer EMZ, Compton SN, Burns JB, et al: Review of the evidence base for treatment of childhood psychopathology: externalizing disorders. J Consult Clin Psychol 70:1267-1302, 2002

Frick PJ, Moffitt TE: A proposal to the DSM-5 childhood disorders and the ADHD and Disruptive Behavior Disorders Work Groups to include a specifier to the diagnosis of conduct disorder based on the presence of callous-unemotional traits. Washington, DC, American Psychiatric Association, 2010. Available at: www.dsm5.org/Proposed%20Revision%20Attachments/Proposal%20for%20Callous%20and%20Unemotional%20Specifier%20of%20Con-duct%20Disorder.pdf. Accessed March 9, 2013.

Goldman MJ: Kleptomania: making sense of the nonsensical. Am J Psychiatry 148:986-996, 1991

Grant JE: Co-occurrence of personality disorders in persons with kleptomania: a preliminary investigation. J Am Acad Psychiatry Law 32:395-398, 2004

Grant JE: SPECT imaging and treatment of pyromania. J Clin Psychiatry 67:998, 2006a

Grant JE: Understanding and treating kleptomania: new models and new treatments. Isr J Psychiatry Relat Sci 43:81-87, 2006b

Grant JE, Kim SW: An open-label study of naltrexone in the treatment of kleptomania. J Clin Psychiatry 63:349-356, 2002a

Grant JE, Kim SW: Clinical characteristics and associated psychopathology of 22 patients with kleptomania. Compr Psychiatry 43:378-384, 2002b

Grant JE, Kim SW: Comorbidity of impulse control disorders in pathological gamblers. Acta Psychiatr Scand 108:203-207, 2003

Grant JE, Kim SW: Clinical characteristics and psychiatric comorbidity of pyromania. J Clin Psychiatry 68:1717-1722, 2007

Grant JE, Potenza MN: Impulse control disorders: clinical characteristics and pharmacological management. Ann Clin Psychiatry 16:27-34, 2004

Grant JE, Levine L, Kim SW: Impulse control disorders in adult psychiatric inpatients. Am J Psychiatry 162:2184-2188, 2005

Grant JE, Correia S, Brennan-Krohn T: White matter integrity in kleptomania: a pilot study. Psychiatry Res 147:233-237, 2006

Grant JE, Williams KA, Potenza MN: Impulse-control disorders in adolescent psychiatric inpatients: co-occurring disorders and sex differences. J Clin Psychiatry 68:1584-1592, 2007

Grant JE, Kim SW, Odlaug BL: A double-blind, placebo-controlled study of the opiate antagonist, naltrexone, in the treatment of kleptomania. Biol Psychiatry 65:600-606, 2009

Hoertel N, Le Strat Y, Schuster JP, et al: Gender differences in firesetting: results from the national epidemiologic survey on alcohol and related conditions (NESARC). Psychiatry Res 190:352-358, 2011

Hollander E (ed): Obsessive-Compulsive Related Disorders. Washington, DC, American Psychiatric Press, 1993

Hollander E, Tracy KA, Swann AC, et al: Divalproex in the treatment of impulsive aggression: efficacy in Cluster B personality disorders. Neuropsychopharmacology 28:1186-1197, 2003

Hollander E, Swann AC, Coccaro EF, et al: Impact of trait impulsivity and state aggression on divalproex versus placebo response in borderline personality disorder. Am J Psychiatry 162:621-624, 2005

Hollander E, Berlin HA, Stein DJ: Impulse-control disorders not elsewhere classified, in The American Psychiatric Publishing Textbook of Psychiatry, 5th Edition. Edited by Hales RE, Yudofsky SC, Gabbard GO. Washington, DC, American Psychiatric Publishing, 2008, pp 777-820

Hudson JI, Pope HG, Jonas JM, et al: Phenomenologic relationship of eating disorders to major affective disorder. Psychiatry Res 9:345-354, 1983

Kazdin AE, Bass D, Siegel T: Cognitive problem-solving skills training and parent management training in the treatment of antisocial behavior in children. J Consult Clin Psychol 60:733-747, 1992

Kessler RC, Coccaro EF, Fava M, et al: The prevalence and correlates of DSM-IV intermittent explosive disorder in the National Comorbidity Survey Replication. Arch Gen Psychiatry 63:669-678, 2006

Kolko DJ: Efficacy of cognitive-behavioral treatment and fire safety education for children who set fires: initial and followup outcomes. J Child Psychol Psychiatry 42:359-369, 2001

Kolko DJ, Herschell AD, Scharf DM: Education and treatment for boys who set fires: specificity, moderators, and predictors of recidivism. Journal of Emotional and Behavioral Disorders 14:227-239, 2006

Koran LM, Aboujaoude E, Gamel N: Escitalopram treatment of kleptomania: an open-label trial followed by doubleblind discontinuation. J Clin Psychiatry 68:422-427, 2007

Kruesi MJP, Casanova MF, Mannheim G, et al: Reduced temporal lobe volume in early onset conduct disorder. Psychiatry Res 132:1-11, 2004

Labree W, Nijman H, van Marie H, et al: Backgrounds and characteristics of arsonists. Int J Law Psychiatry 33:149-153, 2010

Lahey BB, Van Hulle CA, Keenan K, et al: Temperament and parenting during the first year of life predict future child conduct problems. J Abnorm Child Psychol 36:1139-1158, 2008

Lahey BB, Van Hulle CA, Singh AL, et al: Higher-order genetic and environmental structure of prevalent forms of child and adolescent psychopathology. Arch Gen Psychiatry 68:181-189, 2011

Lambie I, Randell I: Creating a firestorm: a review of children who deliberately light fires. Clin Psychol Rev 31:307-327, 2011

Lejoyeux M, Feuche N, Loi S, et al: Study of impulse-control disorders among alcohol-dependent patients. J Clin Psychiatry 60:302-305, 1999

Lejoyeux M, Arbaretaz M, McLoughlin M, et al: Impulse control disorders and depression. J Nerv Ment Dis 190:310-314, 2002

Lewis NDC, Yarnell H: Pathological Firesetting (Pyromania): Nervous and Mental Disease (Monograph No 82). New York, Coolidge Foundation, 1951

Lindberg N, Holi MM, Tani P, et al: Looking for pyromania: characteristics of a consecutive sample of Finnish male criminals with histories of recidivist fire-set-ting between 1973 and 1993. BMC Psychiatry 5:1-5, 2005

Loeber R, Green SM, Lahey BB, et al: Findings on disruptive behavior disorders from the first decade of the developmental trends study. Clin Child Fam Psychol Rev 3:37-60, 2000

MacKay S, Paglia-Boak A, Henderson J, et al: Epidemiology of firesetting in adolescents: mental health and substance use correlates. J Child Psychol Psychiatry 50: 1282-1290, 2009

Marazziti D, Presta S, Pfanner C, et al: The biological basis of kleptomania and compulsive buying. Paper presented at the American College of Neuropsychopharmacology 39th Annual Meeting. San Juan, Puerto Rico, December 2000

Maughan B, Rowe R, Messer J, et al: Conduct disorder and oppositional defiant disorder in a national sample: developmental epidemiology. J Child Psychol Psychiatry 45:609-621, 2004

McCloskey MS, Noblett KL, Deffenbacher JL, et al: Cognitive-behavioral therapy for intermittent explosive disorder: a pilot randomized clinical trial. J Consult Clin Psychol 76:876-886, 2008

McElroy SL, Pope HG Jr, Hudson JI, et al: Kleptomania: a report of 20 cases. Am J Psychiatry 148:652-657, 1991

McKinney C, Renk K: Atypical antipsychotic medications in the management of disruptive behaviors in children: safety guidelines and recommendations. Clin Psychol Rev 31:465-471, 2011

McLaughlin KA, Green JG, Hwang I, et al: Intermittent explosive disorder in the National Comorbidity Survey Replication Adolescent Supplement. Arch Gen Psychiatry 69:1131-1139, 2012

Moffitt TE: Genetic and environmental influences on antisocial behaviors: evidence from behavioral-genetic research. Adv Genet 55:41-104, 2005

Moffitt TE, Caspi A, Rutter M, et al: Sex Differences in Antisocial Behaviour: Conduct Disorder, Delinquency and Violence in the Dunedin Longitudinal Study. Cambridge, UK, Cambridge University Press, 2001

New AS, Hazlett EA, Buchsbaum MS, et al: Blunted prefrontal cortical 18fluorodeoxyglucose positron emission tomography response to meta-chlorophenylpiperazine in impulsive aggression. Arch Gen Psychiatry 59:621-629, 2002

Nock MK, Kazdin AE, Hiripi E, et al: Lifetime prevalence, correlates, and persistence of oppositional defiant disorder: results from the national comorbidity survey replication. J Child Psychol Psychiatry 48:703-713, 2007

Odlaug BL, Grant JE: Impulse-control disorders in a college sample: results from the self-administered Minnesota Impulse Disorders Interview (MIDI). Prim Care Companion J Clin Psychiatry 12, 2010

Pappadopulos E, Woolston S, Chait B, et al: Pharmacotherapy of aggression in children and adolescents: efficacy and effect size. J Am Acad Child Adolesc Psychiatry 15:27-39, 2006

Perez-Rodriguez MM, Hazlett EA, Rich EL, et al: Striatal activity in borderline personality disorder with comorbid intermittent explosive disorder: sex differences. J Psychiatr Res 46:797-804, 2012

Phan KL, Lee R, Coccaro EF: Personality predictors of antiaggressive response to fluoxetine: inverse association with neuroticism and harm avoidance. Int Clin Psychopharmacol 26:278-283, 2011

Potenza MN, Hollander E: Pathological gambling and impulse-control disorders, in Neuropsychopharmacology: The 5th Generation of Progress. Edited by Coyle JT, Nemeroff C, Chamey D. Baltimore, MD, Lippincott Williams & Wilkins, 2002, pp 1725-1741

Presta S, Marazziti D, Dell'Osso L, et al: Kleptomania: clinical features and comorbidity in an Italian sample. Compr Psychiatry 43:7-12, 2002

Robins LN, Ratcliff KS: Risk factors in the continuation of childhood antisocial behavior into adulthood. Int J Ment Health 7:96-111, 1979

Rowe R, Maughan B, Worthman CM, et al: Testosterone, antisocial behavior, and social dominance in boys: pubertal development and biosocial interaction. Biol Psychiatry 55:546-552, 2004

Rowe R, Costello EJ, Angold A, et al: Developmental pathways in oppositional defiant disorder and conduct disorder. J Abnorm Psychol 119:726-773, 2010

Specker SM, Carison GA, Christenson GA, et al: Impulse control disorders and attention deficit disorder in pathological gamblers. Ann Clin Psychiatry 7:175-179, 1995

Speltz ML, McClellan J, Deklyen M, et al: Preschool boys with oppositional defiant disorder: clinical presentation and diagnostic change. J Am Acad Child Adolesc Psychiatry 38:838-845, 1999

Stanford MS, Helfritz LE, Conklin SM, et al: A comparison of anticonvulsants in the treatment of impulsive aggression. Exp Clin Psychopharmacol 13:72-77, 2005

Sterzer P, Stadler C, Krebs A, et al: Abnormal neural responses to emotional visual stimuli in adolescents with conduct disorder. Biol Psychiatry 57:7-15, 2005

Stringaris A, Goodman R: Longitudinal outcome of youth oppositionality: irritable, headstrong, and hurtful behaviors have distinctive predictions. J Am Acad Child Adolesc Psychiatry 48:404-412, 2009

Taylor J, Iacono WG, McGue M: Evidence for a genetic etiology of early onset delinquency. J Abnorm Psychol 109:634-643, 2000

Teichner G, Golden CJ: The relationship of neuropsychological impairment to conduct disorder in adolescence: a conceptual review. Aggression and Violent Behavior 5:509-528, 2000

Tyler N, Gannon TA: Explanations of firesetting in mentally disordered offenders: a review of the literature. Psychiatry 75:150-166, 2012

Vaughn MG, Fu Q, DeLisi M, et al: Prevalence and correlates of fire-setting in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Compr Psychiatry 51:217-233, 2010

Virkkunen M, Eggert M, Rawlings R, et al: A prospective follow-up study of alcoholic violent offenders and fire setters. Arch Gen Psychiatry 53:523-529, 1996

Suggested Readings

Coccaro E (ed): Aggression: Psychiatric Assessment and Treatment. New York, Informa Healthcare, 2003

Coccaro E: Intermittent explosive disorder. Curr Psychiatry Rep 2:67-71, 2005

Dell'Osso B, Altamura AC, Allen A, et al: Epidemiologic and clinical updates on impulse control disorders: a critical review. Eur Arch Psychiatry Clin Neuro-sci 256: 464-475, 2006

Grant JE, Potenza MN: Impulse-control disorders: clinical characteristics and pharmacological management. Ann Clin Psychiatry 16:27-34, 2004

Hollander E, Evers M: New developments in impulsivity. Lancet 358:949-950, 2001

Hollander E, Stein DJ (eds): Impulsivity and Aggression. Chichester, West Sussex, UK, Wiley, 1995

Hollander E, Stein DJ (eds): Clinical Manual of Impulse-Control Disorders. Washington, DC, American Psychiatric Publishing, 2006

Sholevar G (ed): Conduct Disorders in Children and Adolescents. Washington, DC, American Psychiatric Press, 1995