Consider the following three boys, all residing in the same juvenile detention facility. Ryan is a 17-year-old male. He has never known his father and his mother has always worked multiple jobs to support Ryan and his three siblings. Ryan is known as a generally “good kid,” but has never been well supervised and has been in trouble for staying out past curfew and throwing parties with alcohol several times. Ryan was convicted of vehicular manslaughter after he was in a serious car accident following an evening of drinking with friends.

Michael is a 13-year-old male. He has an IQ in the “borderline” range and has been diag-nosed with several learning disabilities, including ADHD. These impairments are reflected in his very poor educational performance. Michael comes from a dangerous, impoverished neighborhood where drug-related violence is very common. There have been approximately two dozen shootings in his public housing complex in the past 5 years, including several that Michael either witnessed or in which he knew someone involved. Michael was incarcerated after being convicted on assault charges stemming from approximately a dozen fights at school, including one where Michael broke another boy’s nose. Michael claims to only fight in self-defense, and states that while he is sorry the other boy’s nose was broken, he still feels that the boy should not have threatened him. Teachers indicate that Michael was in fact the one threatening the other student.

John is a 12-year-old male and has been in trouble all his life. John’s parents have had him in various treatment programs since he burned his little brother when he was 9 years old “to see what would happen.” John’s parents have little trouble with their other sons and are well thought of by their community. They indicate that John is not emotionally close to them and they are frightened of him. Recently, John was convicted of murdering an elderly woman that his mother helped care for. When asked about the crime, John indicated that he set the woman on fire after she threatened to report his numerous thefts of her possessions to the police. Laughing, John told a clinician that he had, in fact, been stealing from the woman.

Antisocial behavior, particularly in adolescence, has a number of implications for adolescent health. Antisocial behavior in the context of conduct disorder, typified by aggressive behaviors, property damage, theft, and serious violations of rules (APA, 2000), is associated with increased risk of physical injury and death, incarceration, substance abuse, sexually transmitted diseases, and teen pregnancy (Moffitt, Caspi, Dickson, Silva, & Stanton, 1996). Antisocial behavior is so common in adolescents that it appears to be a part of the normal teen experience (Elliott, Ageton, Huizinga, Knowles, & Canter, 1983; Moffitt, 1993). Despite the high prevalence of adolescent antisocial behavior, most teens do not suffer lasting health and social problems from these acts; however, for the seriously antisocial and some unlucky few, the impact of delinquent behavior can have serious, long-term consequences (Frick & White, 2008; Moffitt et al., 1996).

Antisocial behavior has several different categorical designations in the current DSM-IV nomenclature, including antisocial personality disorder (APD) and conduct disorder (CD) (APA, 2000). While APD, by definition, cannot be diagnosed before age 18 (APA, 2000), evidence supports a hierarchical relationship between conduct disorder (CD) and APD, in which adults with APD are required to have at least a positive history of CD symptoms and most likely met criteria for CD during adolescence (Burke, Waldman, & Lahey, 2010). This indicates that CD should be viewed as a precursor to the onset of APD in adolescence.

Nevertheless, antisocial youth are a heterogeneous group, as shown in the case examples, with distinct causal mechanisms and correlates (Frick & White, 2008; Moffitt, 1993; 2003). Only some youth diagnosed with CD will go on to develop APD (Burke et al., 2010), with youth from some subgroups of CD much more likely than others to do so (Frick & Dickens, 2006; Moffitt, 2003). The DSM-IV recognizes two subgroups of antisocial behavior, childhood-onset CD and adolescent-onset CD (APA, 2000). Furthermore, research has identified a third subtype, CD with callous-unemotional (CU) traits, which will likely be included in DSM-V (Frick & Moffitt, 2010). The diagnostic criteria for all the subtypes are identical; however, childhood-onset CD requires the presence of symptoms before age 10, and CD with CU traits requires the presence of additional symptoms, namely, a lack of guilt and empathy; a cold, callous interpersonal style; and a willingness to manipulate others for personal gain.

In order to meet overall CD criteria, a youth must display at least three of the following symptoms in the previous 12 months, one of which must have occurred in the previous 6 months: (1) often bullies, threatens, or intimidates others; (2) often initiates physical fights; (3) has used a weapon that can cause serious physical harm to others; (4) has been physically cruel to people; (5) has been physically cruel to animals; (6) has stolen while confronting a victim; (7) has forced someone into sexual activity; (8) has deliberately engaged in fire setting; (9) has deliberately destroyed others’ property (other than by fire setting); (10) has broken into someone else’s house, building, or car; (11) often lies to obtain goods or favors or to avoid obligations; (12) has stolen items of nontrivial value without confronting a victim; (13) often stays out at night despite parental prohibitions, beginning before age 13 years; (14) has run away from home overnight at least twice while living in parental or parental surrogate home (or once without returning for a lengthy period); or (15) is often truant from school, beginning before age 13 years.

Prevalence of CD has been estimated at between 1 and 10 % of the general population (APA, 2000); however, rates vary widely depending on subtype and age of onset. In a large-scale longitudinal study of the Dunedin, New Zealand, community, Moffitt and colleagues found that approximately 7 % of the sample could be categorized as childhood-onset CD, while 23 % of the sample were categorized as adolescent-onset CD (Moffitt et al., 1996). Furthermore, they found the male to female ratio in the childhood-onset group to be 10:1, while the ratio fell to 1.5:1 in the adolescent-onset CD group (Moffitt & Caspi, 2001). Estimates of the number of youth with CD with CU traits range from 32 to 50 % of those with CD, and most in this subgroup are categorized as childhood-onset (Christian, Frick, Hill, Tyler, & Frazer, 1997; Kahn, Frick, Youngstrom, Findling, & Youngstrom, n.d.; Rowe et al., 2009).

Despite being grouped together, the subtypes of conduct disorder differ in etiology, course, and outcome. Adolescent-onset CD is proposed to be a result of failing to meet the demands of adolescence. Moffitt (1993, 2003) suggests that all adolescents show some rebelliousness and seek greater autonomy from their parents to assert their own identity. However, in adolescent-onset CD, this process is exaggerated or becomes extreme and crosses the line into antisocial delinquent behavior (Moffitt, 1993; 2003). Ryan, for example, is likely not a particularly abnormal teenager, but did not receive the necessary supervision. While youth with adolescent-onset CD tend to stop behaving antisocially by early adulthood, there are often long-term consequences to their behaviors, such as poor educational achievement and the stigma of incarceration (Moffitt et al., 1996).

Childhood-onset CD tends to be more severe and chronic relative to adolescent-onset CD (Moffitt, 1993; 2003). It can also be further subdivided into youth with or without callous-unemotional (CU) traits (Frick, 2006; Frick & White, 2008). Even within the childhood-onset CD group, the presence or absence of CU traits has important and unique implications for the severity (Frick & Dickens, 2006), emotional, cognitive (Frick & White, 2008), and neurocognitive correlates of CD (Blair, 2010), as well as unique etiological correlates (Blair, 2010; Frick & White, 2008). While DSM-IV does not currently recognize these distinctions, current DSM-V proposals include a “with CU traits” (Frick & Moffitt, 2010) specifier to acknowledge the important differences between the two groups of youth.

Most youth with childhood-onset CD do not have CU traits, but do have troubled backgrounds (Frick & Moffitt, 2010). Childhood-onset CD without CU traits is more strongly associated with poor parenting, socioeconomic hardship, and other environmental factors than is CD with CU traits (Hipwell et al., 2007; Oxford, Cavell, & Hughes, 2003; Wootton, Frick, Shelton, & Silverthorn, 1997). CD without CU traits is associated with lower IQ, particularly verbal IQ (Loney, Frick, Ellis, & McCoy, 1998; Salekin, Neumann, Leistico, & Zalot, 2004); psycho-neurological dysfunction (Moffitt, 1993); and increased levels of fear and anxiety (Frick, Lilienfeld, Ellis, Loney, & Silverthorn, 1999). It has been theorized that these types of risk factors combine to create situations that contribute to the development of antisocial behavior. For example, youth may exhibit a “hostile attribution bias,” in which the youth incorrectly perceives the actions or intentions of others as hostile even when they are not (Crick & Dodge, 1994) or a situation may arise where increasingly combative and negative interactions between youth and their parents create a dynamic in which children are inconsistently and poorly disciplined and the parent-child relationship becomes cold and distant (Patterson, Reid, & Dishion, 1998). These factors predispose children with childhood-onset CD to increased and inappropriate levels of “reactive aggression,” that is, aggression in response to perceived provocation (Berkowitz, 1993). Michael is a good example of this subtype of CD.

Conduct disorder with CU traits appears to have different causal mechanisms. In addition to reactive aggression, youth with CU traits also exhibit goal-oriented aggression (e.g., aggression with a purpose such as stealing) and, as opposed to youth with CD without CU traits, they are much less likely to feel remorse or guilt or to express empathy for their victims (Frick, 2006). As noted above, the genetic influence on antisocial behavior in CD with CU traits appears to be much higher than in CD without CU traits (Viding, Blair, Moffitt, & Plomin, 2005) and several studies show the stability of CU traits from adolescence to adulthood (Blonigen, Hicks, Kruger, Patrick, & Iacono, 2006; Burke, Loeber, & Lahey, 2007; Lynam, Caspi, Moffitt, Loeber, & Stouthamer-Loeber, 2007). Furthermore, youth with CD and CU traits do not have the IQ deficits commonly associated with CD without CU traits (Loney et al., 1998; Salekin et al., 2004) and there is preliminary evidence that the neurobiological impairment associated with CD with CU traits is specific to the amygdala and frontal lobe regions that are highly interconnected with the amygdala, including the orbitofrontal cortex and ventromedial prefrontal cortex (Blair, 2010). An emerging body of evidence suggests that this amgydala dysfunction interferes with the recognition of fear and distress in others (Blair, 2010) and thereby disrupts socialization, possibly by reducing response to punishment and normal socialization techniques (Dadds & Salmon, 2003; White & Frick, 2010) or by interfering with the normal cognitive and emotional processes that keep mammalian aggression within adaptive limits (Blair, Mitchell, & Blair, 2005). Children like John are prototypical examples of youth with CD with CU traits.

Unlike other disorders, there has not been discussion about large-scale changes to the current CD criteria. Problems of inter-rater reliability and validity that plagued earlier versions of the DSM appear to have been resolved, or are at least not pressing enough to be a major focus of the DSM-V Work Group (Pardini, Frick, & Moffitt, 2010). A wide variety of measures, including the Child Behavior Checklist (Achenbach, 1991) and the Behavior Assessment System for Children (Reynolds & Kamphaus, 2004), among others, have been found to be both reliable and valid for assessing CD across development.

Despite these improvements in assessment, whether to classify broad-based antisocial behavior as a personality disorder remains unclear. As noted previously, personality disorders are defined by DSM-IV as pervasive patterns of inner experience and behavior that differ substantially from cultural norms (APA, 2000). In adults, persistent violations of social norms and rules result in a diagnosis of antisocial personality disorder. However, given that the presence of some degree of antisocial behavior in adolescence has been described as normal (Elliot et al., 1983; Moffitt, 1993), making a case for adolescent-onset CD as a personality disorder is difficult as these behaviors are an exaggeration of, not a deviation from, culturally normative behavior. And while many youth may at first appear to meet criteria for childhood-onset CD without CU traits, there is a hurdle: The importance of environmental factors in maintaining CD symptoms and the availability of effective treatments for CD imply childhood-onset CD without CU traits is more similar to other Axis I clinical disorders. In the face of these facts it is difficult to argue that CD without CU traits can be described as a “pervasive pattern of inner experience.” Indeed, CD is currently classified as an Axis I disorder and not as a personality disorder.

Childhood-onset CD with CU traits, however, presents much more like a personality disorder. While there do appear to be strong genetic and biological risk factors for CU traits, environmental factors play a role in the etiology of CD with CU traits (White & Frick, 2010). The combination of these genetic/biological and environmental risk factors do appear to produce a pervasive pattern of inner experience (i.e., problems recognizing fear and distress in others) and behavior (i.e., antisocial behavior and violence) that violate cultural norms. Furthermore, while there is some evidence that CU traits do decrease over time and with treatment (Frick, Kimonis, Dandreaux, & Farell, 2003; Lynam et al., 2007; White, Frick, Lawing, & Bauer, 2012), treatment programs with these youth have been much less successful relative to other subtypes of CD. Furthermore, antisocial adults with CU traits commit more crimes, are much more likely to be incarcerated, and are greater institutional management problems than other antisocial adults (Frick & Dickens, 2006).

A number of treatments have been shown to be effective in treating CD. In younger youth with CD (ages 7–13), Parent Management Training, Oregon Model (Patterson, Reid, Jones, & Conger, 1975), which focuses on teaching parents effective parenting strategies and skills, and Problem-Solving Skills Training (Kazdin & Weisz, 2003), which focuses on teaching children more effective problem-solving skills, have substantial evidence to support their use (Eyberg, Nelson, & Boggs, 2008). In adolescents, multisystemic therapy (Henggeler & Lee, 2003) and Multidimensional Treatment Foster Care (Chamberlain & Smith, 2003) have a base of evidence supporting their use (Eyberg et al., 2008). Both of these interventions have an intensive, holistic approach and seek to improve a youth’s home life, both interpersonally and economically, and school life and to reduce the influence of deviant peers. However, not all youth appear to respond to treatment equally well. Youth with CD and CU traits in particular have a much poorer record in terms of treatment success than other CD youth (Falkenbach, Poythress, & Heide, 2003; Gretton, McBride, Hare, Shaughnessy, & Kumka, 2001; O’Neill, Lidz, & Heilbrun, 2003; Spain, Douglas, Poythress, & Epstein, 2004). Despite these findings, studies have shown that youth with CD and CU traits can benefit from treatment, though more intensive interventions may be required (Caldwell, Skeem, Salekin, & Van Rybroek, 2006; White, Frick, Lawing, & Bauer, 2012).

Jane is a 12-year-old female. She has been referred to an inpatient facility due to aggression toward her foster mother and others, and self-injurious behavior. She has a history of being sexually abused by her mother’s boyfriend, starting at approximately age four, and neglect by her mother. Her mother has recently given up custody and parental rights, and is thereby barred from contact with Jane until she turns 18. Jane has been in and out of foster care and inpatient care for several years prior to this hospitalization. At the facility, Jane exhibits sexual behavior that is inappropriate for her age and environment toward male staff and patients. For example, Jane regularly attempts to leave the unit wearing tops many sizes too small and/or without underwear. During her hospitalization, Jane has exhibited extreme emotional volatility. For example, she frequently rapidly goes from physical affection and touching (e.g., hugs, inappropriate touching) to angry outbursts and aggression, often triggered by any kind of redirection. Jane displays several kinds of manipulative behavior, such as offering to perform required tasks (e.g., school work and unit chores) in exchange for special treatment. Also, she attempts to gain extra favors in exchange for de-escalating aggressive behavior. In one instance, Jane threatened to hit staff members with a chair, but said that she would put it down if she were given extra free time that morning.

Borderline personality disorder (BPD) is described as one of the most “crippling and frequently lethal” psychiatric illnesses (Goodman et al., 2010). It is estimated to affect 2 % of the general population, 20 % of psychiatric inpatients (Goodman et al., 2010), and 30–60 % of psychiatric populations with personality disorders (DSM-IV-TR; APA, 2000). It is much more frequently diagnosed in women (75 % women; however, see Zlotnick, Rothschild, & Zimmerman, 2002, for a review and discussion of possible gender bias in diagnosis of BPD).

According to the criteria outlined in DSM-IV-TR, BPD comprises the following symptoms (five or more are required for diagnosis): (1) frantic efforts to avoid real or imagined abandonment; (2) a pattern of unstable and intense interpersonal relationships characterized by extremes of idealization and devaluation; (3) identity disturbance; (4) impulsivity in at least two areas that are potentially self-damaging; (5) recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior; (6) affective instability due to marked reactivity of mood; (7) chronic feelings of emptiness; (8) inappropriate, intense anger or difficulty controlling anger; or (9) transient, stress-related paranoid ideation or severe dissociative symptoms.

One aspect of BPD that makes it especially troubling (and as referred to above, potentially lethal) is its association with greater risk for suicide. According to DSM-IV-TR, up to 10 % of those meeting BPD criteria eventually commit suicide, a rate 50 times greater than that of the general population (APA, 2000).

Identification of BPD and other personality disorders during adolescence is typically discouraged. Unfortunately, this has at least two important implications: (1) important precursors may be missed, and (2) little is known about its developmental antecedents (Goodman et al., 2010).

In fact, there is mounting evidence that BPD may have discernible developmental antecedents, including a childhood onset for some people (Bernstein et al., 1993). Many BPD patients may exhibit early signs: For example, two thirds of BPD patients with a history of deliberate self-harm first started to mutilate themselves as children or adolescents (Zanarini, Frankenburg, Ridolfi et al., 2006), and signs such as abnormal moodiness (Mangelsdorf, Shapiro, & Marzolf, 1995) have been observed even in infancy in patients who later develop BPD (Goodman et al., 2010). Nevertheless, it is very important to likewise note that most children who display features of BPD do not go on to meet criteria for BPD as adults (Lofgren, Bemporad, King, Lindem, & O’Driscoll, 1991).

There is evidence that several integral risk factors for BPD occur in childhood or adolescence, making these developmental periods etiologically important. Family and early experiences appear to be important in the development of BPD in numerous ways. For one, there is some evidence of moderate heritability of BPD symptoms (e.g., Torgerson et al., 2000). Further, parental psychopathology appears to be a risk factor for development of BPD, particularly parental anxiety, substance abuse, depression, and antisocial behavior (Bradley, Jenei, & Westen, 2005; Goldman, D’Angelo, & DeMaso, 1993), which are hypothesized to reflect familial tendencies toward negative affectivity and impulsivity (Bradley et al., 2005).

Moreover, extant empirical evidence indicates that a high percentage of BPD patients report adverse environmental events such as abuse, neglect, trauma, or disturbances in family structure as part of their childhood histories, and that many of these reported events tend to co-occur. There is converging empirical evidence from large-scale epidemiological and clinical samples that the following constitute consistent risk factors for BPD (Zanarini & Frankenburg, 2007):

It is difficult to weight the importance of different types of trauma for the development of BPD; it is likely specific to the individual. Still, it is worth noting that of these factors, emotional neglect particularly distinguishes patients with BPD.

Many contemporary theorists believe that BPD is not appropriately categorized as a personality disorder. Rather, more recent conceptualizations of BPD describe it as an emotion regulation (e.g., Linehan, 1993) or affective spectrum disorder, with concurrent impulse control problems (Links, Heslegrave, & van Reekum, 1999; Zanarini, 1993). Zanarini and Frankenburg (2007) posit that BPD is defined by intense inner pain, maladaptive strategies to cope with that pain, a “hyperbolic temperament” (i.e., one that tends to go to extremes and is very reactive), emotional dysregulation, and disinhibition. They add that the interpersonal difficulties observed in BPD result from this hyperbolic temperament, in that it involves a propensity to take offense, and to insist that others pay attention to the greatness of the person’s inner pain. Although it was once thought that a “triggering” event marking symptom onset most often occurred in adolescence, Zanarini et al. add that it can also occur in childhood or young adulthood. They further suggest that the interaction of one or more triggering or “kindling” events and vulnerable or hyperbolic temperament leads to emergence of acute symptoms of BPD. Additionally, temperamental vulnerability (e.g., high neuroticism, low agreeableness, both characteristic of BPD; Clarkin, Hull, Cantor, & Sanderson, 1993; Morey & Zanarini, 2000; Trull, Widiger, Lynam, & Costa, 2003) is likely to interact with childhood adversity. Kindling events, for example, could be more or less normative events viewed through the lens of a hypervigilant child (Zanarini & Frankenburg, 2007).

There is an accumulation of preliminary evidence that suggests biological contributions to this vulnerability, including problems with neurotransmitters such as serotonin, dopamine, acetylcholine, and vasopression; deficits in hypothalamic-pituitary-adrenal (HPA) axis functioning; and dysfunction in frontolimbic brain circuitry (see Crowell, Beauchaine, & Linehan, 2009 for a synopsis).