PSYC631 Adolescent Psychology

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http://dx.doi.org/10.1037/0000065-018 APA Handbook of Psychopathology: Vol. 2. Child and Adolescent Psychopathology, J. N. Butcher (Editor-in-Chief) Copyright © 2018 by the American Psychological Association. All rights reserved.

C h a P t e r 1 8

Understanding the development and management

of antisocial disorders in adolescents

Michael S. McCloskey and Deborah A. G. Drabick

Adolescence is characterized by numerous neu- robiological, cognitive, and social changes. Peers gain in importance among adolescents, and they experience concurrent changes in their cognitive control, reward-seeking behaviors, and autonomy seeking. It is critical to consider typical develop- ment in determining whether adolescents’ behaviors are problematic. Although research indicates that children exhibit appropriate information processing and determination of consequences for risk-taking behavior (Steinberg, 2008), adolescents are more willing to engage in risk-taking behavior among peers (Weigard, Chein, Albert, Smith, & Steinberg, 2014). Oppositional behavior is expected among adolescents, and it is crucial to identify whether this behavior exceeds what is expected on the basis of normative development. Similarly, engaging in what might be labeled conduct disorder (CD) and/ or substance use behaviors may be expected given the increases in risk-taking and sensation-seeking that are normative among adolescents (Drabick & Kendall,2010; Drabick & Steinberg, 2011). This chapter considers several externalizing disorders that are associated with adolescence within the context of this developmental framework. For example, taking a dimensional (rather than categorical) approach to understanding symptoms, many externalizing behav- iors are relatively common among adolescents. Given that the categorical approach is dominant within the mental health field, we also consider the categorical approach in examining oppositional defiant disorder (ODD), CD, antisocial personality disorder (ASPD),

and intermittent explosive disorder (IED). For each, we provide information regarding the diagnoses, risk factors and correlates, assessment, and intervention strategies with a focus on adolescents.

Psychological DisorDers

In the following section, we consider four externaliz- ing disorders that are often identified in adolescence: ODD, CD, ASPD, and IED. We provide prevalence rates, and discuss current and past diagnostic criteria and specifiers associated with each of these disorders.

oppositional Defiant Disorder ODD is characterized by a recurrent pattern of angry and irritable mood, argumentative and defiant behavior toward authority figures, and vindictive- ness that persists for at least 6 months. Prevalence rates of ODD range from 1% to 11% in the gen- eral population, with an average of 3.3%. Prior to puberty, boys are more likely to evidence ODD than girls; however, rates are similar among boys and girls after that point (American Psychiatric Associa- tion, 2013). Lifetime prevalence of ODD is 10.2%, with boys reporting 11.2% and girls reporting 9.2% (Nock, Kazdin, Hiripi, & Kessler, 2007).

ODD was first included in the Diagnostic and Statistical Manual of Mental Disorders, Third Edi- tion (DSM–III; American Psychiatric Association, 1980). To meet DSM–III criteria for ODD, two of five behaviors (i.e., violations of minor rules, temper tantrums, argumentativeness, provocative behavior,

The authors contributed equally to this chapter.

APA Handbook of Psychopathology: Child and Adolescent Psychopathology, edited by J. N. Butcher and P. C. Kendall Copyright © 2018 American Psychological Association. All rights reserved.

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and stubbornness) had to be present for at least 6 months, with onset after the age of 3. A hierarchi- cal exclusion rule involving CD was also included that indicated ODD could not be diagnosed if diagnostic criteria for CD were met. This criterion was based on the facts that ODD is often a develop- mental precursor to CD, that ODD and CD share numerous risk factors, and the disorders are closely related in taxonomic and developmental terms (Burke, Waldman, & Lahey, 2010). The revised ver- sion of DSM–III (DSM–III–R; American Psychiatric Association, 1987) expanded criteria to include nine behaviors, five of which had to be present for at least 6 months. The word often was added to criteria, along with the statement that the behaviors had to occur more frequently than is typical for adolescents of comparable mental age and developmental level. Finally, the DSM–III requirement of onset after age 3 was removed.

The number of symptoms required was reduced from five to four in the DSM–IV (American Psychi- atric Association, 1994), and the symptom related to swearing was eliminated, leaving a list of eight symptoms with an impairment criterion added. Although these symptoms and criteria were main- tained in the subsequent text revision (DSM–IV–TR; American Psychiatric Association, 2000), several substantive changes have been made in the current edition (DSM–5; American Psychiatric Association, 2013). First, the hierarchical exclusion criterion with CD was removed, given that it obfuscated the high rates of overlap between ODD and CD. Second, ODD symptoms were organized into three categories: angry or irritable mood, argumentative or defiant behavior, and vindictiveness. This deci- sion stemmed from evidence that the “behavioral” symptoms of ODD (e.g., argues, defies, annoys) are differentially associated with attention-deficit/ hyperactivity disorder (ADHD) and CD, whereas “emotional” symptoms of ODD (i.e., loses temper, is touchy or easily annoyed, is angry or resentful) are predictive of mood and anxiety disorders. Third, the DSM–5 provides further guidance regarding how to operationalize often for each of the symptoms. Specifically, the symptom of spitefulness and vindictiveness should occur at least twice in the past 6 months. All other ODD symptoms must occur on

most days among children under age 5, and at least once per week among individuals age 5 and older. Although the disorder is defined in a categorical manner, the DSM–5 includes a continuous severity specifier related to the pervasiveness of ODD symp- toms (mild: one setting; moderate: two settings; and severe: three or more settings).

conduct Disorder To meet criteria for CD based on the DSM–5 (American Psychiatric Association, 2013), three of 15 symptoms have to be met in the past 12 months, with at least one in the past 6 months. Criteria include aggression toward people and animals, destruction of property, deceitfulness or theft, and serious violations of rules. The estimated lifetime prevalence of CD is 9.5%, with boys reporting 12% and girls reporting 7.1% (Nock, Kazdin, Hiripi, & Kessler, 2006).

CD, like ODD, was first listed as a separate con- dition with operationalized criteria in the DSM–III. The CD category included subtypes that differed in terms of whether behaviors were socialized/ undersocialized and aggressive/nonaggressive. The undersocialized component had to do with failure to establish a normal degree of affection, empathy, or bond with others (e.g., experiencing guilt and concern for the welfare of friends). The nonaggressive component involved a repetitive and persistent pattern in which either basic rights of others or major developmentally appropriate societal norms or rules were violated (e.g., truancy, running away), whereas the aggressive component involved aggres- sion toward people and/or animals.

The DSM–III–R (American Psychiatric Associa- tion, 1987) omitted symptoms related to disobedi- ence, substance abuse, and blaming others from the CD category, reducing the total number of symp- toms to 13, and maintained the duration criterion of 6 months. In addition, the required number of symptoms was increased from one to three, and the subtyping approach was modified to include three subtypes: group type, solitary aggressive type, and undifferentiated type. The DSM–IV (American Psy- chiatric Association, 1994) added two symptoms to CD (i.e., bullying, staying out late), modified the lying criterion, and changed the duration criteria.

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Specifically, the requirement of three criteria was maintained, though the duration criteria were modi- fied to indicate that at least three criteria should be met within the past 12 months, with at least one in the past 6 months.

The DSM–IV introduced an age-of-onset speci- fier, differentiating a childhood-onset type (at least one symptom prior to age 10), an adolescent-onset type (absence of any symptom prior to age 10), and an unspecified onset. The addition of these specifiers stemmed from multiple lines of inquiry. Specifically, research examining childhood- and adolescent-onset CD indicates that compared with individuals with adolescent-onset CD, individuals with childhood- onset CD exhibit (a) higher levels of aggressive and antisocial behavior; (b) a more persistent course of CD; (c) more cognitive, verbal, and neuropsycho- logical deficits; (d) higher levels of familial risk fac- tors; (e) different patterns of comorbid conditions; (f) greater impairment in occupational and interper- sonal functioning across developmental periods; and (g) higher levels of antisocial and substance-abusing behaviors in adulthood (Connor, Ford, Albert, & Doerfler, 2007; Frick & Viding, 2009; Loeber, Burke, & Pardini, 2009; Moffitt, 1993; Moffitt & Caspi, 2001; Odgers et al., 2007).

The DSM–5 maintained the symptoms, criteria, and the age-of-onset specifier for CD; however, the additional specifier “with limited prosocial emo- tions” was included. This specifier stemmed from research indicating that adolescents with CD with and without callous-unemotional (CU) traits differ in terms of CD symptom severity, course, genetic, neurobiological, cognitive, emotional, and psycho- social risk factors and correlates, and in response to contextual factors and interventions (Frick, Ray, Thornton, & Kahn, 2014a, 2014b; Frick & White, 2008). This specifier requires at least two characteristics over at least 12 months across relationships and settings, including lack of remorse or guilt, lack of empathy or callous behaviors, lack of concern about performance, and shallow or deficient affect.

antisocial Personality Disorder Though not diagnosed until age 18, ASPD is the development of antisocial behaviors, which began

in childhood or early adolescence, that was (by definition) identified as CD (American Psychiatric Association, 2013). As such, CD and ASPD share the core feature of disregard for and/or violation of the rights of others. Symptoms of ASPD include a failure to conform to societal norms, impulsivity and poor planning, aggressiveness, a disregard for safety, lack of responsibility and a lack of remorse, though only three of the preceding symptoms (plus CD prior to age 18) are needed to meet criteria for ASPD (American Psychiatric Association, 2013). ASPD is differentiated from the older, related construct of psychopathy (which is not included in the DSM–5) in that individuals with ASPD are not required to display the interpersonal and affective symptoms of psychopathy, including shallow affect, lack of empa- thy, or grandiose sense of worth (Cleckley, 1976; Hare, 1991); these affective components are similar to CU traits that served as the foundation for the addition of the specifier of limited prosocial emo- tions to the DSM–5 CD category (Frick et al., 2014a, 2014b). Because of this, most individuals identified as psychopaths meet criteria for ASPD, but only a minority of individuals with ASPD would be consid- ered as evidencing psychopathy. It has been argued that the almost exclusive focus on antisocial behav- ior, rather than potential underlying personality characteristics and interpersonal traits, may not best capture a personality disorder and may overpatholo- gize criminal behavior and fail to distinguish more and less severe subtypes of ASPD (Ogloff, 2006). Reflecting this, proposed alternate criteria for ASPD that focuses more on the affective and interpersonal traits typically associated with psychopathy (e.g., egocentrism, lack of empathy) is included “for fur- ther review” in the DSM–5 (American Psychiatric Association, 2013).

ASPD has a lifetime prevalence of 2% to 4% of the general population, occurring several times more often in men than women (American Psy- chiatric Association, 2013; National Institute for Health and Clinical Excellence, 2010; Rob- ins, Tipp, & Przybeck, 1991). The prevalence of ASPD is much higher in prison samples with estimates of approximately 50% (Fazel & Danesh, 2002). Among those with ASPD, some individu- als show an adolescent time-limited pattern in

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which antisocial symptoms remit in early adult- hood; however, most individuals with ASPD show a more severe and chronic course that lasts well into adulthood (Moffitt, 1993). Not surprisingly, ASPD is associated with high levels of violent and nonviolent crime (Fazel & Danesh, 2002), and is associated with considerable costs to public service agencies (T. Kendall et al., 2009). ASPD is also associated with early death, with one study finding that individuals with ASPD under age 40 were 33 times more likely to die than similar-age men without ASPD (Black, Baumgard, Bell, & Kao, 1996).

intermittent explosive Disorder Of the different disorders associated with antisocial behavior in adolescence, IED is the only disorder that requires excessive levels of aggressive behavior. In fact, excessive aggression is pathognomonic of an IED diagnosis, with the excessive aggression being evidenced as frequent minor aggressive acts (i.e., ver- bal aggression and/ or minor physical aggression that causes no harm or damage occurring twice a week or more on average and/ for 3 or more months) and/or less frequent acts (three or more in a year) of major aggression (i.e., damaging objects and/or injuring people; American Psychiatric Association, 2013). This aggression must be disproportionate to the provocation and must be anger-based. Frequent acts of non–anger-based instrumental aggression, such as attacking an individual to rob him or her would not be considered as meeting IED criteria. Though it is grouped with other disruptive behavioral dis- orders within the Disruptive, Impulse-Control, and Conduct Disorders section of the DSM–5, IED can be considered a disorder of affective aggression.

IED was initially thought to be rare. However, as diagnostic criteria and assessment measures have improved, estimates of IED have increased, and it is currently believed that the lifetime preva- lence rate is closer to 5%, with the 1-month to 1-year prevalence rate at approximately 2% to 3% (Kessler et al., 2006). Adolescence is a critical time in the development of IED, with the typical age of onset for individuals with IED between 13 and 21 (Coccaro, 2012). This age of onset reflects the developmental tendency for aggression to increase throughout adolescence, though in

IED the aggression is more pronounced and longer lasting as IED tends to run a chronic, waxing and waning course lasting on average from 12 to over 20 years. Gender differences are small with some studies suggesting IED may occur more commonly in men (Coccaro, 2012). There does seem to be a gender × age of onset interaction with men tending to have an earlier age of onset than women.

Most individuals with IED display minor and major aggression in sufficient frequency to meet criteria for the disorder (Kulper, Kleiman, McCloskey, Berman, & Coccaro, 2015). This aggression is often an overresponse to minor prov- ocation and can include acts as varied as yelling, threatening, throwing or hitting objects, or physi- cally attacking a person or animal. In general, these aggressive outbursts involve close friends and fam- ily (or their property), but it is not uncommon for those with IED to lash out at acquaintances (e.g., co-workers) or even strangers (e.g., road rage). When aggressive outbursts occur, those with IED report feeling more overwhelmed and less in con- trol of their anger during the outburst, and more disappointed, embarrassed, and remorseful after the outbursts as compared with those without IED (Kulper et al., 2015). These aggressive outbursts cause considerable distress for the individual with IED and often lead to problems in interper- sonal relationships, sleep disruption, and lowered job satisfaction. There is also a financial cost, as individuals with IED will on average cause about $1600 worth of property damage and have 2–3 aggressive outbursts that require medical atten- tion over their lifetime (Kessler et al., 2006). Fur- thermore, IED is associated with several negative health outcomes including heart disease, hyperten- sion, and stroke (McCloskey, Kleabir, Berman, Chen, & Coccaro, 2010). Therefore, IED is a prevalent, chronic, and severe disorder.

Despite the severity of IED and the adolescent age of onset, there are surprisingly few studies focusing on the expression of IED in ado- lescence. One epidemiological study found that adolescents with IED reported an average age of onset and levels of chronicity (measured as 1-year persistence) and comorbidity that was con- sistent with that found for adults with

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IED (McLaughlin, et al., 2012). The field needs studies that directly compare the frequency of aggression and related symptoms among adoles- cents and adults with IED concurrently.

shareD risk Factors

There are a variety of factors that are associated with increased risk for externalizing behaviors, as well as ODD, CD, ASPD, and IED. These risk factors involve numerous domains (e.g., neurobiological, psychological, social) and are often shared by or common to these disorders. These predictors carry valuable information for prevention and treatment.

oppositional Defiant Disorder and conduct Disorder A wide range of risk factors is associated with ODD and CD, which differ based on the developmental period and consequent tasks considered. Children are exposed to different factors that could confer added risk or buffer and reduce risk for ODD and CD as they enter distinct developmental periods, and there is the possibility that risk factors from ear- lier developmental periods can be carried forward to inform risk for continued ODD and/or CD behaviors (Drabick & Kendall, 2010; Drabick & Steinberg, 2011). Note that many of these factors are not spe- cific to ODD or CD and may serve as shared risk fac- tors for comorbid conditions.

In terms of earlier developmental processes, pre- natal exposure to substances is associated with ODD and CD. Children who exhibit temperamental dif- ficulties (e.g., difficult temperament more broadly, as well as specific features of negative emotionality, inflexibility, and poor effortful control) are also at risk for developing ODD, particularly if paren- tal behaviors are not a good fit for children with these temperamental features (Burke, Loeber, & Birmaher, 2002; Lavigne, Gouze, Hopkins, & Bry- ant, 2016; Loeber, Burke, & Pardini, 2009). Given that ODD confers risk for CD, it is not surprising that CD is associated with similar temperamental features. However, it is likely that there are differ- ent developmental trajectories associated with an individual’s temperament that might lead to differ- ent CD presentations. A common pathway for ODD

and CD can be found among children who exhibit strong reactions to anger and frustration. A pathway more specific to CD involves low levels of fear-based inhibitions that might be associated with higher levels of CU traits, and these children exhibit higher levels of approach and are less responsive to con- textual demands including parenting behaviors that might shape behavior (Frick et al., 2014b; Krieger & Stringaris, 2016). Therefore, this presentation is more likely to be associated with CD than ODD.

Parents of adolescents with ODD and CD report elevated levels of their own psychopathology (e.g., depression, substance use), which could interfere with provision of consistent discipline, optimal parent–child communication, and parental posi- tive interactions with their children (Burke et al., 2002; Drabick, Gadow, & Loney, 2007; Lavigne et al., 2016; Loeber et al., 2009). Parental behaviors associated with ODD and CD in adolescents include low warmth, low support, high harsh parental behaviors, and high intrusiveness. In addition, CD is associated with inconsistent discipline, low paren- tal monitoring, and coercive interchanges among parents and their children (Burke et al., 2002; Dish- ion, Bullock, & Granic, 2002; Dodge et al., 2008). Nevertheless, because parents and children engage in transactional relations, parental behaviors likely shape and exacerbate symptoms, particularly among children with difficult temperament. For example, if a child reacts to an adult command or request by becoming irritable or oppositional and the adult subsequently withdraws the request, the child may learn that these behaviors lead to desirable out- comes. These coercive interchanges among adults and children contribute to additional difficulties across domains and developmental periods (Patter- son, 1982). Indeed, prospective research indicates that parenting behaviors worsen over time among adolescents with ODD (Burke, Pardini, & Loeber, 2008). Difficulties managing adolescent behavior lead to decreased monitoring and poor parent–child interactions that ultimately confer risk for associat- ing with deviant peers, lack of investment in school, and CD (Dodge et al., 2008; Fosco, Stormshak, Dishion, & Winter, 2012). Given these challenges among parents and their children with ODD and/ or CD, it is not surprising that families of children

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with these behavior problems report higher levels of conflict and maltreatment, as well as lower levels of cohesion and expressiveness (Burke et al., 2002; Drabick et al., 2007; Lavigne et al., 2016). There- fore, these families may model aggressive and hostile behaviors, and consequently socialize children to engage in similar behaviors.

Several neurobiological correlates of ODD and CD have been identified, though these factors are more associated with externalizing behaviors in general. These correlates include behavioral and molecular genetic factors, low salivary cortisol level, decreased autonomic nervous system activity, atypi- cal frontal lobe activation patterns, and reduced functional connectivity between the amygdala and the medial prefrontal cortex (Beauchaine & Hin- shaw, 2016; Blair, 2010; Burke et al., 2002; Loeber et al., 2009; Lorber, 2004). In terms of cognitive cor- relates, adolescents with ODD and CD exhibit defi- cits in executive functioning, processing of rewards and punishments, cognitive flexibility, and decision making (Beauchaine & Hinshaw, 2016; Blair, 2010; Crowe & Blair, 2008; Loeber et al., 2009). These correlates may underpin other adolescent-specific risk factors, such as difficult temperament and emo- tional lability, and provide convergent evidence that biological factors confer risk for ODD and CD. How- ever, some adolescents with CD exhibit age-appro- priate executive functioning and verbal abilities (Fontaine, Barker, Salekin, & Viding, 2008), which could allow these adolescents to recruit others in engaging in CD behaviors and potentially escape detection (Drabick, Bubier, Chen, Price, & Lanza, 2011). Adolescents with CD also exhibit deficits in social information processing, including increased likelihood of attributing hostile intent to others in ambiguous situations (i.e., hostile attribution bias), selecting aggressive responses to conflict, and expecting that aggressive responses are likely to lead to desired outcomes (Crick & Dodge, 1996).

Regarding peer relationships, adolescents with ODD demonstrate hostile attribution biases and are likely to experience victimization and rejection (Burke et al., 2002; Drabick et al., 2011). Ado- lescents with ODD and CD are also more likely to engage in proactive and reactive aggression than adolescents without these disorders (Blair,

2010; Drabick et al., 2011; Loeber et al., 2009). Parent–child and family factors associated with ODD and CD may lead adolescents to develop these hostile attribution biases, as well as exhibit difficul- ties with emotion regulation and conflict resolu- tion. In childhood, these individuals are potentially ill-prepared to problem solve and manage interper- sonal relationships. Demonstrating oppositional behavior toward teachers, who are sanctioned authority figures, might further contribute to peer rejection among these children. As they become adolescents and the peer group increases in impor- tance, adolescents with ODD may be more likely to select similar children as friends (e.g., adolescents who exhibit ODD symptoms or emotion regula- tion difficulties) and then to be socialized by these adolescents (Dishion & Tipsord, 2011). Earlier problematic interpersonal processes may contribute to the selection of aggressive and dysregulated peers as adolescents with ODD age, and these factors may contribute to further impairment, CD symptoms, and associated negative outcomes across domains (Dodge et al., 2008). Aggressive children are likely to experience peer rejection, which attenuates chil- dren’s ability to develop prosocial relationships and appropriate means of resolving conflict in peer relationships. Given limited experiences with typi- cally developing peers, these children may select deviant or antisocial peers in adolescence, which is one of the most proximal predictors of CD dur- ing this developmental period (Chen, Drabick, & Burgers, 2015; Dishion, Bullock, & Granic, 2002). Challenges with parenting a child with behavior problems might lead to lower levels of monitoring, further enabling adolescents with CD to associate with and be socialized by deviant peers (Dishion & Tipsord, 2011; Fosco et al., 2012). Indeed, adoles- cents with CD often engage in deviancy training, characterized by peer support and encouragement of antisocial behaviors, which is related to increases in antisocial behavior (Dishion & Tipsord, 2011).

Communities characterized by violence, crime, drug use, and poverty have been linked to ODD and CD symptoms (Leventhal & Brooks-Gunn, 2004). Although some studies suggest that the relation between neighborhood characteristics and ODD and CD is mediated by other factors (e.g., parental

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psychopathology, parenting practices, family con- flict, heightened stress responses), such neighbor- hood environments may model aggressive behavior and increase the likelihood that adolescents will engage in ODD and CD behaviors (Burke et al., 2002; Crowe & Blair, 2008; Drabick et al., 2011; Loeber et al., 2009). CD behaviors may be viewed as adaptive or even protective in truly dangerous contexts (Drabick et al., 2011; Leventhal & Brooks-Gunn, 2004).

More recent research has considered correlates among adolescents with CD with and without CU traits. This work indicates that adolescents with CU traits exhibit difficulty labeling sad and fearful expressions, though they can recognize other emo- tions (Blair, 2010; Crowe & Blair, 2008; Dolan & Fullam, 2010; Jones, Laurens, Herba, Barker, & Vid- ing, 2009). In addition, adolescents with CU traits have difficulty with stimulus-reinforcement and reversal learning (i.e., responding to changes in con- tingencies), and this pattern is evidenced with posi- tive and negative stimuli, as well as punishing and rewarding contingencies (Blair, 2010; Budhani & Blair, 2005; Finger et al., 2008; Marini & Stickle, 2010). Finally, adolescents with CU traits perform similarly to comparison children on tasks involv- ing cognitive perspective-taking, but have difficulty with affective perspective-taking (Anastassiou- Hadjicharalambous & Warden, 2008) and tasks requiring recall of emotional information (Dolan & Fullam, 2010).

Given these developmental pathways and poten- tial impairment across domains in which we would like children to be successful (e.g., school, home, peers), adolescents may develop additional psy- chological conditions secondary to ODD or CD. Although oppositional behavior can be considered normative during some developmental periods, it has become clear that ODD confers risk for a variety of subsequent conditions, including CD, anxiety and mood disorders, and substance use disorders, even after controlling for other co-occurring condi- tions and initial levels of co-occurring symptoms (Drabick, Ollendick, & Bubier, 2010; Loeber et al., 2009; Nock et al., 2007). Because of the early age of onset, it is not surprising that ODD developmentally precedes most co-occurring conditions; however,

ODD is typically secondary to ADHD, phobias, and separation anxiety disorder.

In general, co-occurring conditions are associ- ated with greater persistence of ODD and increased ODD symptom severity as is typically the case with comorbidity (Nock et al., 2007). Nevertheless, anxiety may have a differential effect on ODD and CD based on the developmental period consid- ered. Specifically, anxiety may attenuate behavior problems in childhood and adulthood; however, during adolescence, anxiety may exacerbate ODD and CD behaviors and lead to other co-occurring conditions and negative sequelae (Drabick et al., 2010). As CD is more likely to develop in later childhood or adolescence, CD typically follows the development of conditions with earlier onset (e.g., ADHD, ODD). ODD and CD confer risk for depres- sion, which might stem from “failures” related to developmental expectations (Capaldi, 1991). Co- occurring CD and depression are associated with increased rates of substance use, delinquency, and school drop-out compared with either condition alone, though depression is more likely to follow CD than the reverse (Angold, Costello, & Erkanli, 1999; Maughan et al., 2004). The change to the DSM–5 with regard to considering emotional vs. behavioral symptoms of ODD can inform these developmental pathways, as the irritability associ- ated with ODD might be a precursor for adoles- cent depression among adolescents with behavior problems, whereas the behavioral symptoms of ODD might be more likely to lead to CD character- ized by CU traits (Stringaris & Goodman, 2009). Patterns of comorbid conditions differ depending on the presence of CU traits as well. Adolescents with CD without CU traits exhibit elevated levels of impulsivity (including ADHD) and anxiety, whereas CU traits are generally associated with lower levels of anxiety and internalizing problems over time (Frick et al., 2014a, 2014b; Frick & White, 2008).

antisocial Personality Disorder The literature suggests genetic, biological, and psychosocial/environmental influences associated with the development and maintenance of ASPD. For example, twin, family, and adoption studies

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have suggested that antisocial behavior in general and ASPD specifically is roughly 50% heritable (Ferguson, 2010), and that the genetic contribution to antisocial behavior is stronger for offenders with a lifelong persistent pattern (similar to ASPD) as compared with adolescents with a limited pattern of offending (Barnes, Beaver, & Boutwell, 2011). Furthermore, genetic influences interact with environmental factors to facilitate ASPD.

Early imaging research had suggested functional and structural brain anomalies among individu- als with ASPD, including reduced prefrontal gray matter and abnormal patterns (hypo- and hyper- activation) of limbic response to emotional stimuli (McCloskey, Phan, & Coccaro, 2005). Findings from more recent studies have qualified these initial results, suggesting that the relationship between ASPD and structural prefrontal lobe deficits may be, in part, driven by psychopathy, substance use, and other comorbidities (Glenn, Johnson, & Raine, 2013; Gregory et al., 2012). Likewise, individuals high on the interpersonal–affective dimension of psychopathy show lower limbic (e.g., amygdala) activity to emotional/salient stimuli, whereas indi- viduals higher on the antisocial-lifestyle dimension often show increased limbic activity to emotional stimuli (Seara-Cardoso & Viding, 2015). Individu- als higher on affective-interpersonal psychopathic traits show reduced neural responses to others’ pain, whereas those higher on antisocial-lifestyle traits show increased neural responses to others’ pain (Seara-Cardoso, Viding, Lickley, & Sebas- tian, 2015). Conversely, increased striatal response to reward seems to be present among those with high antisocial traits independent of psychopathy, though the psychopathic group showed greater connectivity between the striatum and dorsome- dial prefrontal cortex during reward (Geurts et al., 2016). These studies highlight the need to disam- biguate ASPD and psychopathy when conducting research on antisocial behavior, consistent with calls to consider CD with and without CU traits (i.e., DSM–5 limited prosocial emotions specifier to the CD category).

Individuals with ASPD (and antisocial behavior in general) also show deficits in a variety of higher order cognitive processes (e.g., planning, decision

making, cognitive control/impulsivity, attention) often referred to collectively as executive function- ing (e.g., Morgan & Lilienfeld, 2000), consistent with adolescents with CD. Regarding decision mak- ing, individuals with ASPD are overly influenced by the prospect of large rewards (Mazas, Finn, & Stein- metz, 2000) and have difficulty altering behavior in response to punishment cues and/or changing con- tingencies (De Brito, Viding, Kumari, Blackwood, & Hodgins, 2013). These difficulties appear to be, in part, associated with a general tendency toward impulsive behavior (Chamberlain, Derbyshire, Leppink, & Grant, 2016; Swann, Lijffijt, Lane, Steinberg, & Moeller, 2009), but also may reflect general information processing difficulties as indi- viduals with ASPD made poorer choices even after taking longer to deliberate on their decision than a comparison group (DeBrito et al., 2013). Prelimi- nary research also suggests that these deficits occur (at least among young adults with ASPD) even in the absence of substance use disorder (Chamberlain et al., 2016), and are not limited to those who are elevated on psychopathy (Zeier, Baskin-Sommers, Hiatt Racer, & Newman, 2012). In psychopathy, these learning deficits have been linked to physi- ological and neural underarousal to aversive stimuli that impairs learning (Birbaumer et al., 2005; Veit et al., 2013). However, this physiological under- arousal appears to be more linked to affective-inter- personal facets of psychopathy than to antisocial behavior (Veit et al., 2013), as the association between antisocial behavior is more complicated and includes increased reactivity to some negative stimuli (Lorber, 2004). There appear to be similari- ties in terms of correlates for (a) CD and ASPD and (b) CD with CU traits and psychopathy, suggesting that there also may be higher levels of developmen- tal continuity among these conditions from adoles- cence to adulthood.

intermittent explosive Disorder Most research on correlates of IED has focused on cognitive–affective processes and their underlying neurobiological and neurochemical mechanisms. Individuals with IED consistently show heightened levels of anger and anger reactivity supporting the conceptualization of IED as a disorder of “affective”

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aggression (McCloskey, Berman, Noblett, & Coc- caro, 2006; McCloskey, Lee, Berman, Noblett, & Coccaro, 2008). However, emotion regulation problems in IED are not limited to anger, with several studies showing increased global affective lability relative to individuals with other psycho- logical disorders (Fettich, McCloskey, Look, & Coccaro, 2015; McCloskey et al., 2006; McCloskey, Lee, et al., 2008). Furthermore, those with IED also show greater intensity in their negative emotions than other psychiatric comparison groups (Fettich et al., 2015).

Problems with emotion regulation in IED are exacerbated by difficulties in socioemotional infor- mation processing. Like others with aggression problems, individuals with IED tend to demon- strate a hostile attribution bias, in which benign or ambiguous acts are seen as hostile and/or intention- ally malicious (Crick & Dodge, 1996). As evidence of this, individuals with IED exhibit difficulty in reading ambiguous facial expressions, emotional cues, and intention-based cues, all of which lead to the misattribution of nonhostile actions as threaten- ing (Best et al., 2002; Coccaro et al., 2014; Coccaro, Noblett, & McCloskey, 2009). Further, those with IED are more likely to have a negative emotional response to situations in which an ambiguously intended act is directed toward them, evincing their reduced cognitive empathy, which appears to be a driving factor in aggression (Coccaro, Lee, & Kavoussi, 2009; Murray-Close et al., 2010). There is also some evidence that these socioemotional infor- mation processing deficits may go beyond hostile attributions as those with IED also show generalized deficits in correctly identifying facial expressions across emotions (Best et al., 2002).

Research using self-report measures of impul- sivity suggests that individuals with IED are more impulsive (McCloskey, Lee, et al., 2008), but these findings are not consistent with equivocal results from behavioral impulsivity tasks (e.g., Best et al., 2002). It has been suggested that individuals with IED may not be more impulsive across all impulsiv- ity domains, but may show more negative urgency (Puhalla, Ammerman, Uyeji, Berman, & McClos- key, 2016). That is, individuals with IED are more impulsive specifically in the context of a significant

negative emotion. This is consistent with the find- ings on IED and emotion dysregulation (Fettich et al., 2015) and it would also explain the previous self-report and behavioral impulsivity findings. The combination of information processing deficits, emotional dysregulation, and emotional impulsiv- ity is reflected in the tendency of individuals with IED to react disproportionately aggressively to provocation situations (McCloskey, Ben-Zeev, Lee, Berman, & Coccaro, 2009; McCloskey et al., 2006; McCloskey, Lee, et al., 2008).

IED has been linked to several biological cor- relates. Regarding neurochemistry, IED is most strongly associated with serotonin, as multiple indices of impaired serotonin functioning (e.g., lower serotonin levels, lower platelet serotonin content, and decreased number of serotonin trans- porter binding sites) have been found among individuals with IED (Coccaro, 2012), whereas serotonin-enhancing drugs have been shown to reduce affective aggression in IED (Coccaro, Lee, & Kavoussi, 2009). Functional and structural brain abnormalities are also present among those with IED. Functional magnetic resonance imaging stud- ies show increased amygdala activation (Coccaro, McCloskey, Fitzgerald, & Phan, 2007; McCloskey et al., 2016) and reduced prefrontal cortex (PFC) activation (Coccaro et al., 2007) in IED when look- ing at angry faces and negative evocative pictures, suggesting an increased limbic (and potentially decreased prefrontal) response to social threat. Dysregulation of this fronto-cortical circuit that is thought to govern emotion regulation is supported by the lack of a negative amygdala-PFC coupling in IED when responding to emotional stimuli (Coccaro et al., 2007; McCloskey et al., 2016). These functional deficits may reflect structural brain abnormalities. Magnetic resonance imaging studies have revealed that individuals with IED showed sig- nificantly lower grey matter volume in fronto-limbic brain structures as well as inward shape deforma- tions of the amygdala and hippocampus (Coccaro, Fitzgerald, Lee, McCloskey, & Phan, 2016; Coccaro, Lee, McCloskey, Csernansky, & Wang, 2015).

Few studies have examined familial and con- textual factors as related to IED. Though limited in number, research findings show that adverse

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childhood experiences are associated with IED. Increased and earlier exposure to trauma was asso- ciated with IED (Nickerson, Aderka, Bryant, & Hofmann, 2012), with IED participants reporting more physical and emotional abuse and neglect and lower parent care (particularly maternal) relative to psychiatric controls (Fanning, Meyerhoff, Lee, & Coccaro, 2014; Lee, Meyerhoff, & Coccaro, 2014). More research on these and other contextual factors is needed.

DeveloPmental Pathways

It is important to consider normative or typical development in determining whether behavior is problematic among adolescents. In addition, it is critical to consider developmental relations among these disorders and co-occurring conditions over time, as some disorders may confer risk for other conditions and/or sequelae that in turn lead to other psychological disorders. In the following section, we consider normative levels of externalizing behaviors, as well as the developmental relations among these conditions.

oppositional Defiant Disorder and conduct Disorder Some ODD and CD behaviors are normative dur- ing different developmental periods (e.g., opposi- tional behavior among toddlers and adolescents; Drabick, 2009; Steinberg, 2008). As such, criteria often include explicit statements that compare individuals with others of the same developmental level to determine whether behaviors are atypical or problematic relative to peers. The developmental pathways and interrelations among these condi- tions also should be considered during adolescence, though a number of different pathways may be evidenced. For example, there may be a common underlying process that underpins many external- izing conditions, but the behaviors manifested change over time in accordance with developmental changes and opportunities for exhibiting external- izing behaviors (Beauchaine & Hinshaw, 2016; Frick & Nigg, 2012). Another possibility is that cor- relates or sequelae of one condition may confer risk for another condition and facilitate successive or

concurrent comorbidity among disorders (Drabick, Beauchaine, Gadow, Carlson, & Bromet, 2006). For example, adolescents with ADHD often experience interpersonal and academic difficulties, which may confer risk for ODD. Adolescents with ADHD and ODD may be rejected by typically developing peers and be more likely to select and/or to be socialized by deviant peers, increasing risk for CD.

When considering potential developmental path- ways among conditions, ODD onset generally occurs prior to age 10 (retrospective self-reported onset of ODD begins at age 4 and increases steadily into adolescence; Nock et al., 2007). Childhood-onset CD requires at least one symptom prior to age 10; this CD subtype can occur with other earlier-onset conditions, now that the CD hierarchical exclusion criterion has been removed for ODD in the DSM–5. In particular, behavioral symptoms of ODD are expected to be associated with CD (Frick & Nigg, 2012; Stringaris & Goodman, 2009).

To be consistent with the diagnostic nomen- clature, ASPD cannot be diagnosed prior to age 18 and requires that individuals meet criteria for CD prior to age 15. Accordingly, continuity between CD and ASPD is expected among some individuals. However, it is unclear whether ASPD is more likely to be continuous with CD when the latter is exhib- ited with or without limited prosocial emotions. Given that CU traits and this specifier are expected to identify adolescents with a more persistent and pernicious course (Frick et al., 2014a, 2014b), it is possible that continuity will be associated with ado- lescents with CD with limited prosocial emotions, though research is wanting.

antisocial Personality Disorder Independent of its relation to CD, ASPD has a very high level of comorbidity, with some community studies showing over 90% of individuals with ASPD have another DSM disorder (e.g., Swanson, Bland, & Newman, 1994). The greatest comorbid- ity is with psychopathy, as many studies indicate that almost all individuals with psychopathy also meet criteria for ASPD (Hare, 1996), though the reverse is not true; in fact, only a portion of those with ASPD also meet criteria for psychopathy (e.g., 32%; Coid & Ullrich, 2010). As such, psychopathy

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has been conceptualized as a severe subtype of ASPD, and this is supported by studies showing ASPD with (vs. without) comorbid psychopathy is associated with greater impairment and poorer treatment response (Glenn et al., 2013; Gregory et al., 2012; Ogloff, 2006). However, findings of different cognitive and neurobiological impair- ments associated with ASPD vs. psychopathy (e.g., differences in fear reactivity) suggest a more com- plex relationship between ASPD and psychopathy (Anton et al., 2012). Among DSM disorders, ASPD is most related to substance use disorders with estimates of 50% for alcohol use disorders and over 80% for any substance disorder (Glenn et al., 2013; Trull et al., 2010). This comorbidity is important when considering research on ASPD as many of the cognitive and neurobiological deficits associ- ated with ASPD are also associated with substance use disorders (e.g., executive functioning), though some of these deficits are likely present prior to substance use initiation given that these corre- lates are associated also with CD. Like ODD and CD, ASPD co-occurs with several other disorders including mood disorders, anxiety disorders, and other personality disorders (e.g., borderline per- sonality disorder). The specific comorbidity for ASPD seems to vary somewhat as a function of gen- der; men with ASPD are more likely to meet criteria for comorbid mood disorders, whereas women with ASPD are more likely to meet criteria for comorbid histrionic or borderline personality disorder (Sher et al., 2015). For most of these disorders, the pres- ence of comorbid ASPD is associated with a more severe and treatment-refractory course (Glenn et al., 2013).

intermittent explosive Disorder IED typically has an onset in adolescence (ages 12–21), with a slightly earlier onset in boys (Coc- caro, 2012). Similar to ODD, CD, and ASPD, most individuals (75%–80%) with IED meet criteria for another psychological disorder. These comor- bidities are especially high for anxiety, depressive, disruptive (i.e., CD and ODD), and substance use disorders, all of which are 2.5 to 4 times more likely to occur among those with IED (Kessler et al., 2006). Personality disorders also have a high rate

of comorbidity with IED, particularly borderline personality disorder and ASPD, with about 25% of those with IED meeting criteria for borderline personality disorder and/or ASPD in community samples and much higher rates in research samples (Coccaro, 2012). This extensive comorbidity raises questions about IED as a distinct disorder. However, like ODD, IED tends to precede any comorbid disor- ders (e.g., Kessler at al., 2006) suggesting that rather than a symptom of another disorder, IED promoted the development of comorbid psychopathology. Supporting the differentiation between IED and its many comorbidities, the underlying nature of IED appears to be qualitatively different from subclinical aggression (Ahmed, Green, McCloskey, & Berman, 2010), whereas many of IED’s comorbid disorders (including ASPD) appear more dimensional in nature (Marcus, Lilienfeld, Edens, & Poythress, 2006). There also appears to be some specificity in the heritability of IED in that family members of an individual with IED were more likely to have a diagnosis of IED relative to other potentially related disorders (e.g., ASPD; Coccaro, 2012). Finally, the presence of IED seems to exacerbate the impairment associated with comorbid disorders rather than vice versa (Keyes, McLaughlin, Vo, Galbraith, & Heimberg, 2016).

assessment anD intervention

Considering the prevalence, impact, correlates, courses, comorbidity, and sequelae of these dis- orders, the utility of valid and reliable assessment approaches, as well as evidence-based interventions, is clear. It is important to use multiple informants and assessment approaches during adolescence, given that informants often have access to differ- ent information and their responses may not be grounded in developmental processes (e.g., teachers may be more likely to determine whether a behavior is problematic than parents who have less experi- ence with typically developing adolescents). How- ever, at least regarding treatment, the evidence is mixed at best, with somewhat more positive results for ODD and CD relative to IED and ASPD. Next, we review current knowledge regarding best prac- tices for these disorders.

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oppositional Defiant Disorder and conduct Disorder A multimethod, multi-informant assessment approach is typically recommended to determine whether adolescents meet criteria for ODD or CD, as well as to identify risk factors and correlates that can inform prognosis and interventions (De Los Reyes et al., 2015; McMahon & Frick, 2005). The use of behavioral checklists from multiple informants (e.g., parents, teachers, older children), diagnostic interviews, and observational methods is recom- mended to assess ODD behaviors. This approach is particularly important for assessing ODD given the necessity of determining whether these behaviors occur often relative to peers and the addition to DSM–5 of a severity indicator (i.e., number of set- tings). Given the covert nature of many CD behav- iors and potential issues related to social desirability in responding, it is important to obtain information from multiple informants for CD through behav- ioral checklists and/or diagnostic interviews. CD is a particularly heterogeneous disorder; assessments should take this issue into account and consider aspects related to this heterogeneity (e.g., presence of CU traits, co-occurring ADHD, aggressive and nonaggressive behaviors, age of onset).

Commonly used behavioral checklists that assess for ODD and CD behaviors include the Achenbach Child Behavior Checklist family of instruments, the Behavioral Assessment System for Children, Con- ners Rating Scales, and the Child and Adolescent Symptom Inventory. The most frequently used and empirically supported structured interviews for ODD and CD are the Diagnostic Interview Sched- ule for Children and the Diagnostic Interview for Children and Adolescents, although other struc- tured interviews contain ODD and CD modules. In terms of observational coding systems for ODD, the Behavioral Coding System and Dyadic Parent–Child Interaction Coding System II are structured, micro- analytic observation methods for assessing parental interactions with younger children. Another valid and reliable observational method for assessing ODD among preschool children is the Disruptive Behavior Diagnostic Observation Schedule, which is designed to assess problems in behavioral regulation and anger modulation in a laboratory setting. The

Revised Edition of the School Observation Coding System can be useful for evaluating ODD behaviors in the school setting. To assess for CU behaviors, reliable and valid questionnaires that have been used in a variety of settings (e.g., community, clini- cal, forensic) and among adolescents include the Antisocial Process Screening Device and Inven- tory of Callous/Unemotional Traits (for a review of assessment instruments and approaches, see McMahon & Frick, 2005).

The most effective treatment approaches for ODD and CD involve cognitive–behavioral strategies and multiple levels of functioning, with combined parent and child involvement typically superior to either component alone and to control conditions (for a review, see Eyberg, Nelson, & Boggs, 2008; P. C. Kendall, 2012). Several parent and family treatments have been shown to be effective among children with ODD. Parent–Child Interaction Train- ing (Brinkmeyer & Eyberg, 2003) is designed for children ages 2–7 years and uses (a) child-directed interactions to develop nondirective play skills and thereby improve the quality of parent–child inter- actions and (b) parent-directed interaction, which involves improving parenting skills related to giv- ing instructions, addressing noncompliance, and rewarding compliance. Helping the Noncompliant Child (McMahon & Forehand, 2003) is a second- ary prevention program designed for children ages 3–8 years with noncompliant behavior. Parents learn skills that can decrease coercive parent–child interactions, improve parents’ provision of posi- tive feedback and clear directions, and increase use of appropriate discipline strategies. The Incred- ible Years intervention (Webster-Stratton & Reid, 2003) includes treatment programs designed for parents, children (ages 2–10), and teachers. The Incredible Years program is designed to reduce children’s behavior problems and increase social competence, which is addressed by improving parental monitoring and discipline strategies, as well as children’s problem-solving skills. Parent Management Training–Oregon Model (Patterson, Chamberlain, & Reid, 1982) involves teaching parents behavioral principles for modifying and monitoring child behavior and for implementing behavior modification programs for their children

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(ages 3–12 years). Sanders’s (1999) Positive Parent- ing Program (Triple P) is a multilevel system that includes universal prevention (Level 1); provision of parenting skills that vary on the basis of the number of sessions, format, and content (Levels 2–4); and a behavioral family intervention that targets family stressors in addition to children’s disruptive behaviors (Level 5).

A variety of child-focused cognitive–behavioral interventions for adolescent behavior problems (including aggression and CD) also have received support, particularly among children in elementary school and early adolescence. These include Loch- man et al.’s Anger Control Training, which is the predecessor for the Coping Power Program (Loch- man, Barry, & Pardini, 2003). Both programs are based on the social information-processing model of anger control and include problem-solving approaches. In Kazdin’s (2003) Problem-Solving Skills Training, adolescents are taught problem- solving strategies and encouraged to generalize these strategies to real-life problems. As another example, Group Assertive Training (Huey & Rank, 1984) is a school-based intervention designed to address aggressive classroom behavior among adolescents.

Regarding CD and delinquency, Multidimen- sional Treatment Foster Care (Chamberlain & Smith, 2003) is an efficacious community-based program that involves placing adolescents who have engaged in delinquent behavior in a foster home for 6 to 9 months during which time the adolescent receives treatment. The foster parents obtain preservice training that focuses on behav- ioral reinforcement and consistent discipline, and caregivers to whom the adolescent will return fol- lowing the foster care placement receive intensive parent management training. This intervention has been shown to be superior to typical group home care for adolescents with histories of chronic delin- quency. Multisystemic Therapy (Henggeler & Lee, 2003) is an individualized and flexible intervention that addresses the many domains in which adoles- cents with CD exhibit difficulties. This interven- tion involves cognitive–behavioral approaches, pragmatic family therapies, and pharmacologi- cal interventions as appropriate and is delivered within the child’s context (e.g., school, home) with

at least weekly meetings with the therapist over a period of 3 to 5 months.

Little research has examined mediators and mod- erators of treatment outcome among adolescents with ODD or CD. However, changes in parenting behaviors (e.g., increased parental monitoring) and, among older adolescents, changes in social informa- tion processing and peer relationships likely medi- ate treatment effects (Lochman & Wells, 2002). Regarding treatment moderators, harsh parental behaviors, parental psychological functioning, mari- tal adjustment, family stressors, and child comorbid internalizing symptoms moderate treatment effects (Beauchaine, Webster-Stratton, & Reid, 2005), and not only confer risk for externalizing behaviors, but also may have implications for intervention outcomes.

antisocial Personality Disorder Diagnostic interviews are the gold standard assess- ment measure for ASPD. The Structured Clinical Interview for DSM Personality Disorders (SCID–II; First, Spitzer, Williams, & Gibbon, 1997) and the Structured Interview of Disorders of Personality (SID–P; Pfohl, Blum, & Zimmerman, 1995) are semi-structured interviews that are designed to diagnosis ASPD (as well as all other DSM personal- ity disorders) by asking questions directly relevant to the seven ASPD criteria and additional questions relevant to CD. The full SCID–II and SID–P take 45 to 90 minutes to administer, but the ASPD ques- tions themselves take only about 10 to 15 minutes. There are always risks associated with using just a portion of a measure that has some validation data on the full measure. However, if one were to do that, the SCID–II would be the easier of the two measures as the SCID–II, but not the SID–P, organizes its questions by diagnosis. Likewise, the 20-item Hare Psychopathy Checklist—Revised (Hare, 1991) and its adolescent (ages 12–18) complement (Forth, Kosson, & Hare, 2003) consist of two primary factors that assess both behaviors associated with ASPD (antisocial lifestyle) and more interpersonal–affective traits that are considered the core of psychopathy (e.g., lack of empathy). The checklist is widely used in criminal and psy- chiatric settings to assess risk of reoffending and/

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or engaging in violent behavior, and is considered the gold standard in this regard (Salekin et al., 1996), though a more recent meta-analysis that found it had the lowest predictive validity of nine risk assessment tools (median: area under the curve = .66, positive predictive value = .52, negative pre- dictive value = .68) has called this into question (Singh, Grann, & Fazel, 2011). Several omnibus questionnaire inventories assess ASPD including the Personality Assessment Inventory (Morey, 2007), Personality Diagnostic Questionnaire (Hyler, 1994) and the Millon Clinical Multiaxial Inventory (Mil- lon, Grossman, & Millon, 2015). Overall, these measures correlate moderately well at the symptom level, but only modestly at the diagnostic level with interview measures of ASPD (e.g., Guy, Poythress, Douglas, Skeem, & Edens, 2008).

ASPD is considered among the most treatment- resistant psychological disorders in part because of the lack of desire among individuals with ASPD to seek treatment. For this reason, treatments for ASPD often occur within the context of the justice system. This research, which suggests modest to moderate effects of cognitive–behavioral and related interventions, has limited applicability to ASPD in that ASPD is not required (or often assessed) for treatment (National Institute for Health and Clinical Excellence, 2010). In addition, these studies typi- cally focus on reducing criminal recidivism rather than the treatment of ASPD. There are few well-con- trolled trials examining the efficacy of treatments for ASPD. An early exploratory randomized control trial of 59 male community participants with ASPD found that cognitive–behavioral therapy (CBT) was not better than treatment as usual in reducing ASPD symptoms (e.g., anger, aggression, substance use). Relatedly, only 11 of the 25 men in the CBT condition completed 10 or more of the scheduled 15 to 30 treatment sessions (Davidson et al., 2009). A second study of a behavioral intervention for opioid dependent outpatients with ASPD found improvement on family/social adjustment relative to standard care for the behavioral treatment group, but no difference between behavioral and treatment as usual groups on either the rate of drug negative specimens or the substance use scales of the addiction severity index (Neufeld et al., 2008).

A mentalization-based treatment was found to reduce mood symptoms and self-harm among indi- viduals with ASPD and comorbid borderline per- sonality disorder (Bateman, O’Connell, Lorenzini, Gardner, & Fonagy, 2016), but it is not clear to what extent the treatment affected ASPD pathology outside of general aggressiveness. Studies of phar- macological interventions for ASPD are similarly limited, with a few “poor quality” studies generally showing no difference between psychotropic medi- cation (e.g., antidepressants) and placebo (Khalifa et al., 2010). Overall, the findings reflect a paucity of research on treatments specifically for ASPD independent of age, let alone in late adolescence/ early adulthood, where the behavioral symptoms of ASPD may be most severe.

intermittent explosive Disorder The Structured Clinical Interview for DSM–5 (First, Williams, Karg, & Spitzer, 2015) includes a mod- ule that assesses for IED. Otherwise, there are few published measures to assess IED. The Intermittent Explosive Disorder Interview (IED-I) is an unpub- lished instrument that has been used in several research studies of IED (McCloskey & Coccaro, 2003) and distinguishes between individuals with IED and psychiatric controls (Kulper et al., 2015). In addition, two measures of aggression frequency are often used in IED research. The Life-History of Aggression (LHA; Coccaro, Berman, & Kavoussi, 1997) is an 11-item self-report measure of aggres- sion, self-harm, and antisocial behavior that is used to assess frequency of lifetime verbal and physi- cal aggression. The five-item aggression scale of the LHA has been shown to be a valid and reliable measure of aggression frequency (Coccaro et al., 1997). Complementing this, the Overt Aggression Scale–Modified (OAS-M; Coccaro, Harvey, Kupsaw- Lawrence, Herbert, & Bernstein, 1991) is an inter- view that assesses the frequency and intensity of aggressive acts in which an individual engaged over the past week. Items on the OAS-M are weighted so that a more intense act of aggression (e.g., punching someone vs. yelling at them) contributes more to the total aggression score. The OAS-M has adequate psychometric properties with reported interra- ter reliabilities (ICC) > .90 for the aggression and

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irritability scales (Coccaro et al., 1997), as well as significant correlations between the OAS-M aggres- sion scale and lifetime measures of aggression fre- quency (r = .45–.52; Coccaro, Berman, & Kavoussi, 1997; see McCloskey & Coccaro, 2003, for a full review of the OAS-M). The OAS-M has also been found to be sensitive to change. For this reason, the OAS-M is used in most IED treatment studies (e.g., Coccaro, Lee, & Kavoussi, 2009; McCloskey, Noblett, Deffenbacher, Gollan, & Coccaro, 2008).

Despite the prevalence and impact of IED, there is a dearth of treatment research on the disorder. A double-blind placebo-controlled trial found that fluoxetine reduced aggression (Coccaro, Lee, & Kavoussi, 2009); however, a more recent (albeit smaller) study did not find an effect of fluoxetine on aggression (Coccaro, Lee, Breen, & Irwin, 2015). Likewise, there has been inconsistent support for the use of anticonvulsants in the treatment of IED, with randomized clinical trials showing that Dival- proex (Hollander et al., 2003) and Oxcarbazepine (Mattes, 2005), but not Levetiracetam (Mattes, 2008), reduced aggression among patients with IED. There has been even less research on psychologi- cal interventions for IED. A study of a brief (four 90-min sessions) cognitive–behavioral program for aggressive drivers found drivers with IED tended to improve less than drivers without IED, leading the authors to suggest that IED individuals may benefit from longer, more intensive therapy (Galovski & Blanchard, 2002). A later randomized clinical trial of a 12-session cognitive–behavioral treatment for IED found that cognitive–behavioral treatment was superior to waitlist in reducing anger, aggression, and hostility in IED (McCloskey, Noblett, et al., 2008). However, this study was limited to adults ages 25–53. It is still unknown if this intervention is effective for adolescents with IED.

controversies anD Future Directions

For all the antisocial disorders reviewed, controver- sies remain. The DSM–5 includes several modifica- tions to the diagnostic criteria that were somewhat controversial and will require additional research to examine the utility of these changes. There are

also several gaps in the literature regarding interven- tion and interrelations among these disorders, par- ticularly during adolescence when the phenotypic presentations of these conditions may be difficult to disentangle. We present several controversies and gaps in current knowledge next, in addition to related directions for future research.

oppositional Defiant Disorder and conduct Disorder For ODD, one concern is that findings regarding the predictive utility of emotional vs. behavioral symptoms are mixed and differ depending on the informant considered and strategy for dividing emotional and behavioral symptoms (Drabick & Gadow, 2012; Stringaris & Goodman, 2009). Never- theless, changes to the DSM–5 provide a consistent framework for division of symptoms into subgroups and a foundation for future research. In addition, DSM–5 provides the first operationalization of often for ODD symptoms; however, further evaluation is needed to determine whether these descriptions can increase reliability and whether the frequency anchors represent valid comparisons to adolescents across developmental periods (Burke et al., 2010; Frick & Nigg, 2012). The addition of a severity cri- terion for ODD also requires further examination. Although there is an expectation that adolescents who exhibit ODD symptoms across settings and individuals will experience greater severity, more research is needed. Last, the addition of the specifier “with limited prosocial emotions” to the DSM–5 CD category will require further research to determine its utility, particularly in differentiating adolescents with childhood-onset CD who differ in the persis- tence of CD symptoms (Frick & Nigg, 2012; Moffitt et al., 2008).

There are several directions for future research on ODD. First, there is a need to evaluate concurrent and predictive utility of the disorder, independent of co-occurring conditions (e.g., ADHD, CD), espe- cially now that the CD exclusion criterion has been abandoned. Second, future research should continue to examine the predictive validity of ODD symptom subgroups using the DSM–5 approach to separat- ing symptoms. Third, greater operationalization of severity and pervasiveness criteria is included in the

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DSM–5, and effects on reliability and validity for ODD should be evaluated. Last, given that symptom severity and correlates of ODD differ depending on the informant used to rate symptoms, additional research regarding contextual demands, informants, and settings is needed to supplement research regarding the severity criterion added to the DSM–5 ODD category (Burke et al., 2010; De Los Reyes et al., 2015; Frick & Nigg, 2012; Moffitt et al., 2008).

For CD, continued consideration of the limited prosocial emotions specifier is an important direc- tion for future research. Given the high levels of treatment seeking among families of adolescents with ODD and/or CD, future research should evalu- ate mediators and moderators of treatment outcomes to inform assessment and modifications to exist- ing interventions, as well as improve intervention outcomes. Additional issues that have been raised regarding CD involve (a) the potential utility of a childhood-limited subgroup and (b) whether changes to the conceptualization of CD should be made to better accommodate girls (Frick & Nigg, 2012; Moffitt et al., 2008). There is considerable het- erogeneity among adolescents with childhood-onset CD in that some exhibit a more persistent path of antisocial behavior, whereas others are more likely to desist. Although the former group may exhibit higher levels of CU traits (and meet criteria for the limited prosocial emotions specifier), children who desist are not well-characterized, suggesting that future research is necessary to better understand them. To date, although discussion continues regard- ing whether different criteria, symptom thresholds, duration, or some combination would better charac- terize CD behaviors among girls, data do not support modifying diagnostic criteria for CD on the basis of sex. Finally, despite the diagnostic link between CD and ASPD, future research should evaluate continu- ity from CD to ASPD, taking into consideration age of onset for CD as well as the presence of limited prosocial emotions that might be more predictive of psychopathy than ASPD more broadly (Burke et al., 2010; Frick et al., 2014a, 2014b).

antisocial Personality Disorder The diagnosis of ASPD has been criticized as being too behaviorally focused and overemphasizing

criminal behavior (in effect making criminal behavior a psychological disorder) at the cost of affective–interpersonal characteristics associated with an “antisocial personality” (Gurley, 2009). Despite minor changes in the DSM criteria, these criticisms persisted. To address these problems, the proposed DSM–5 restructuring of personality disorders included significant changes to ASPD that would focus more on traditional psychopathic traits including callousness and lack of empathy, and would have a “with psychopathic traits” specifier that would mirror the “with limited prosocial emotions” specifier for CD (American Psychiatric Association, 2013). However, in response to con- cerns about the new approach to personality dis- orders (e.g., Shedler et al., 2010), these changes to ASPD were not enacted. Rather, they remain in the DSM–5 as an alternative (more trait-based) model of personality disorders for further research. Therefore, the actual DSM–5 criteria are identical to its DSM–IV–TR predecessor, with its heavy behavioral/criminal focus. As a result, many studies of ASPD will likely continue without full attention to the heterogeneity of these potentially core interpersonal–affective deficits.

ASPD is a heterogeneous disorder that overlaps, but is separate from, psychopathy and criminality. Though some studies have started to focus on sub- typing ASPD (Poythress et al., 2010), more research is needed to identify key subtypes of ASPD and assess to what extent genetic, cognitive, environ- mental, and neurobiological deficits are specific to an ASPD subtype or consistent across all subtypes. This includes a greater understanding of how the significant comorbidity between ASPD and other psychiatric disorders affects the course and severity of ASPD (Glenn et al., 2013). It is well-established that adolescents with CD with and without CU traits differ on many of these correlates, as well as course and severity (Frick et al., 2014a, 2014b); future research could take a similar approach to identifying consistencies and useful discriminat- ing processes among individuals with ASPD with and without various co-occurring conditions. Once key deficits associated with more homogenous subtypes of ASPD are identified, treatments can be better tailored to address those deficits. This would

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include treatment of adolescents and young adults with ASPD outside of the criminal system, an area of study that is clearly lacking.

intermittent explosive Disorder The DSM–5 included several revisions of the cri- teria for IED. Chief among these is the inclusion of verbal aggression and the related multiple path- ways (frequent minor aggression or less frequent major aggression) to meet the aggression severity/ frequency criterion. This change is consistent with research showing that frequent verbal aggres- sion can be highly impairing (e.g., McCloskey, Lee, et al., 2008). Other changes introduced in the DSM–5 improved the specificity of the disor- der. This included specifying that the aggressive outbursts are (a) anger-based, (b) cause distress or impairment, and (c) are developmentally inap- propriate (by specifying that the diagnosis cannot be given to children under age 6). Despite recent increases in research on IED, the disorder is still understudied and the changes made to the DSM–5 should increase research on the disorder, as pre- viously most research on IED did not use DSM criteria because of limitations with earlier DSM diagnoses (Coccaro, 2012).

Research on IED, though limited, has identi- fied several neurobiological deficits including serotonin dysregulation and structural and func- tional deficits of the corticolimbic circuits posited to underpin emotion regulation. Such findings are consistent with the findings that IED participants show global emotion dysregulation and impulsiv- ity in the face of negative emotion. However, the role of related cognitive and biological processes is less clear. Other areas of IED research have been given even more limited attention and require further examination. For example, very few stud- ies have considered environmental factors as they relate to IED; those few that have are cross-sectional and focused almost exclusively on abuse/trauma/ aggression as opposed to correlates of IED. In fact, there is a dearth of longitudinal research on IED. Individuals with IED present with varying levels of comorbidity, aggression presentation and severity, and associated deficits, but no research has exam- ined whether there are reliable subtypes within the

IED diagnosis. Relatedly, the IED criteria is in many ways similar to the new childhood disorder intro- duced in the DSM–5—disruptive mood dysregula- tion disorder—and research is needed to determine the extent these two disorders are related. Finally, considering the severity and prevalence of IED, more treatment research is needed, especially among adolescents.

conclusion

Adolescence is a critical period for the development of cognitive control and peer relationships, and as such, is key in the developmental trajectory of pathological, antisocial behavior. Categorical mani- festations of such pathological antisocial behaviors in adolescence include ODD, CD, ASPD, and IED. Though there are clear differences between these disorders regarding symptom presentation (e.g., ODD and IED symptoms are more focused on angry, defiant and aggressive behavior, CD and ASPD symptoms assess more global antisocial behavior), there is also significant overlap with regard to not only presentation (e.g., most include aggressiveness as a symptom), but also comorbidity, risk factors, and sequelae. All four disorders show a great deal of comorbidity, both with each other, and more generally with other mood, anxiety, and substance use disorders, suggesting more severe, global, and overlapping deficits. There are common cognitive (e.g., poor executive functioning, limited cognitive flexibility, hostile attributional biases) and neuro- biological (e.g., atypical frontal lobe activation and decreased cortico-limbic functional connectivity) impairments across the four disorders. It may be that distinctions within these disorders (e.g., the differentiation of CD with vs. without limited proso- cial emotions, ASPD with vs. without psychopathy) may be as important to differentiating developmen- tal trajectories as differences between the disorders. Regarding treatment, the findings presented here highlight the importance of early intervention for adolescents with CD/ODD, as treatments for these disorders have demonstrated efficacy in contrast to treatments for IED and ASPD, which are signifi- cantly more limited in demonstrated efficacy and effectiveness.

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