Part 2 book “Handbook of personality disorders” has contents: An attachment perspective on callous and unemotional characteristics across development, empirically validated diagnostic and assessment methods, clinical assessment, clinical features of borderline personality disorder, clinical aspects of antisocial personality disorder and psychopathy,… and other contents.
CH A P TER 19 An Attachment Perspective on Callous and Unemotional Characteristics across Development Roseann M. Larstone, Stephanie G. Craig, and Marlene M. Moretti There is an extensive history of research on the etiology and course of serious conduct problems and treatment outcomes among antisocial and violent youth (e.g., Moffitt et al., 2008) A consistent finding from this work is that children and adolescents with conduct problems display considerable heterogeneity in the type and severity of their behavior problems, social and interpersonal functioning (e.g., quality of interpersonal relationships; school dropout, incarceration), and response to treatment This heterogeneity suggests that there are meaningful subgroups (e.g., child vs adolescent onset; see Moffitt, 2006) and multiple pathways to serious and persistent conduct problems and aggression (e.g., Frick & Viding, 2009; Moffitt, 1993, 2006) The identification of heterogeneous clusters in the etiology and developmental course of severe conduct problems has become a pressing research priority (Frick & Marsee, 2006; Frick & White, 2008) with important implications for intervention One well-developed line of research that has shed light on heterogeneity among children with serious behavior problems focuses on callous–unemotional (CU) traits (Frick & White, 2008; Waller et al., 2012) Historically, CU traits (e.g., lack of empathy and guilt; shallow affect; uncaring attitudes) (Cleckley, 1941; Hare, Hart, & Harpur, 1991) have been thought to represent a core deficit that is associated with early-onset and persistent antisocial and aggressive behavior Children and teens who have high levels of CU traits have been shown to demonstrate more severe, chronic and aggressive patterns of behavior than children who show conduct problems in the absence of CU traits (e.g., Frick & White, 2008; Kimonis, Bagner, Linares, Blake, & Rodriguez, 2014) Conduct problems in conjunction with high levels of CU traits are associated with low punishment sensitivity and lack of responsiveness to others’ emotions (particularly fear; see Blair, Leibenluft, & Pine, 2014; Dadds & Rhodes, 2008) CU traits are predominant in current conceptualizations of psychopathy, suggesting a link between the developmental literature on CU traits and aggression in youth on the one hand, and the clinical literature on psychopathy on the other (Hare, 1993; Kimonis, Frick, Cauffman, Goldweber, & Skeem, 2012) Apart from CU traits, the affective component of psychopathy, there are two additional defining features of psychopathy: the interpersonal (e.g., arrogant and deceitful; narcissistic view of self and manipulative behavior) and the behavioral features (e.g., impulsive/irresponsible; see Frick & White, 2008) Youth with high levels of CU traits show low levels of fearfulness and a preference for thrillseeking, novel, and dangerous activities in both 324 Attachment Perspective on Callous–Unemotional Characteristics 325 nonreferred (Frick, Cornell, et al., 2003) and referred samples (Pardini, 2006) Compared to youth with low levels of CU traits, those with high levels of such traits are less sensitive to punishment cues, show lower levels of empathy, express less emotion, and show less reactivity to threatening and emotionally distressing stimuli from a young age This may reflect a genetic basis to their CU traits and aggressive/ antisocial behavior (Dadds & Rhodes, 2008) Given these findings, it is unsurprising that CU traits are described as dispositional and have been shown to be relatively stable from late childhood to early adolescence, particularly according to parent report (Frick & White, 2008) Importantly, however, at least two studies have reported decreases over longitudinal follow up in nonreferred youth with initially high levels of CU traits (e.g., Frick, Kimonis, Dandreaux, & Farell, 2003; Pardini, Lochman, & Powell, 2007) There is no question that CU traits are central to the development of serious conduct disorder and a core component of psychopathology, particularly antisocial personality disorder (ASPD) and psychopathy, but are there multiple pathways to CU traits? The current chapter presents two contemporary and sometimes competing views regarding the etiological and developmental trajectory of CU traits in relation to aggression and related empirical findings The first model, which is dominant in the literature, adopts a developmental genetic and neurobiological perspective This etiological perspective of CU traits in childhood and adolescence is congruent with, but not identical to, the construct of primary psychopathy in adults Primary psychopathy is characterized by trait fearlessness, impulsivity, high social dominance, high self-esteem, and low anxiety, a constellation of features that are generally viewed as an expression of underlying genetic influences (e.g., Blair, Peschardt, Budhani, Mitchell, & Pine, 2006) Of particular interest relative to this discussion is a second developmental model, originally proposed by Karpman (1941, 1948) and based on an emerging literature that conceptualizes CU features or characteristics as an “acquired adaptation” to environmental influences, particularly exposure to chronic trauma and adverse social contexts (Bennett & Kerig, 2014; Kerig & Becker, 2010; Porter, 1996) This variant of CU traits is commonly conceptualized as being analogous to secondary psychopathy Secondary psychopathy in adults is linked with trauma exposure and occurs in conjunction with posttraumatic stress disorder (PTSD) symptoms (Hicks, Vaidyanathan, & Patrick, 2010) Based on the field of developmental traumatology, the central premise of this view is that children exposed to severe maltreatment, especially when perpetrated within their primary relationships with caregivers (i.e., betrayal trauma), cope through avoidance, emotional detachment, and the development of callousness (see also Ford, Chapman, Mack, & Pearson, 2006; Karpman, 1941; Kerig, Bennett, Thompson & Becker, 2012; Porter, 1996) Respectively, these two etiological models can be referred to as describing the development of “primary” versus “acquired” CU traits In this chapter, we selectively review newly emerging research focused on the heterogeneity in developmental pathways to CU traits Where the literature specific to CU traits is sparse, we supplement our discussion with research on the etiological factors that distinguish primary and secondary psychopathy in adolescence, which encompasses interpersonal, behavioral, and affective features We discuss what we term “broad” CU traits, in which the literature does not distinguish between the two variants and specify primary and acquired CU, where appropriate, to reflect the available evidence Using a developmental traumatology framework, we examine the shared and unique clinical features, etiological factors, including attachmentrelated processes and treatment response associated with primary versus acquired CU We argue that these two pathways are not mutually exclusive; however, understanding distinctive features will undoubtedly improve the quality and effectiveness of our prevention and treatment efforts We also discuss limitations in the current state of the literature and future directions for research Clinical Features A considerable body of research demonstrates that antisocial youth with CU traits differ developmentally on behavioral, emotional, and neural indices from antisocial and aggressive individuals who not show CU traits (Frick, Ray, Thornton, & Kahn, 2014; Frick & White, 2008) Below we review the available evidence that has furthered our understanding of how primary versus acquired CU traits are expressed 326 E tiology and D evelopment from studies investigating these constructs in samples of youth diagnosed with conduct disorder and those involved in the juvenile justice system Conduct disorder describes a heterogeneous group of children and adolescents, only a small minority of whom develops severe and chronic forms of antisocial behavior (e.g., Frick et al., 2014) The inclusion of CU traits as a modifier in DSM-5 (American Psychiatric Association [APA], 2013) was to identify a clinically meaningful subtype of conduct disorder (i.e., limited prosocial emotions specifier; APA, 2013), although the diagnostic criteria not distinguish between primary and acquired CU variants Primary CU is defined by shallow affect; deficient empathy, guilt, and remorse; callousness toward the feelings of others; and deficits in emotion processing that give rise to low emotional arousal—characteristics that are evident at a young age (e.g., Blair et al., 2006, 2014) In studies specifically examining primary CU traits in relation to psychopathology, these features are associated with less severe conduct problems, lower levels of physical aggression, and less emotional and behavioral dysregulation compared to the acquired variant (Kahn et al., 2013) Compared to the acquired CU variant, primary CU has been found to be associated with lower anxiety, greater self-esteem and lower behavioral inhibition in communitybased and clinic-referred youth (Fanti, Demetriou, & Kimonis, 2013; Kahn et al., 2013) There is evidence of the emergence of punishment insensitivity in early childhood, particularly in contexts where perpetrating antisocial or aggressive behavior may lead to a reward or achievement of a social goal (Dadds & Salmon, 2003) Individuals with acquired CU features also show shallow affect and low empathy; however, such youth often report greater previous exposure to trauma than youth showing the primary CU variant (Bennett & Kerig, 2014; Kahn et al., 2013; Kimonis et al., 2012) Compared to the primary variant, acquired CU has been found to be associated with greater levels of anxiety, impulsivity, negative affect (depression), and reactive aggression (Gill & Stickle, 2016; Kimonis et al., 2012) In a community sample, youth with acquired CU were found to have lower self-esteem, higher anxiety, and greater narcissism (Fanti et al., 2013) Porter (1996) proposed that salient clinical features associated with callousness–unemo- tionality emerge differently in children with acquired CU, with low empathy appearing first, eventually followed by the emergence of overt behavior problems; whereas in the case of primary CU, the core personality characteristics associated with the CU construct and related behavior problems (e.g., lying) theoretically emerge concurrently The onset of acquired CU features in children who have been chronically exposed to early adverse events including victimization is now thought to represent an adaptive response to overwhelming interpersonal trauma For example, symptoms such as affective numbing are associated with reductions in distress associated with trauma exposure However, at the same time, emotional numbing increases risk for perpetrating aggression because, over time, children and youth become impervious to recognizing others’ distress, thus reducing the interpersonal signaling functions of affective cues (e.g., facial expressions) that would inhibit aggression This pathway to CU traits differs from that presumed to underlie primary CU traits in several ways, as we discuss in later sections Importantly, trauma exposure is not a typical hallmark in children with primary CU traits, and the onset of behavior problems typically occurs in close conjunction with the emergence of CU features (Kahn et al., 2013) Despite limited evidence, taken together, research suggests that there may be overlapping and distinctive clinical features in individuals showing primary versus acquired CU traits These differences in clinical presentation suggest that there may be diverse etiological factors that give rise to both variants Specifically, primary CU traits may represent the early expression of genetic and neurodevelopmental factors, and acquired CU features may in greater measure reflect the influence of environmental factors We review in the next section the available evidence on established and newly identified etiological factors across both variants Etiology There is a long history of research on the etiology of psychopathy (see Patrick & Brislin, Chapter 24, this volume) Some perspectives emphasize biological (e.g., Blair et al., 2006, 2014; Blair, 2007) and others environmental or social origins (e.g., Karpman, 1941; Porter, 1996) of the disorder and related personality Attachment Perspective on Callous–Unemotional Characteristics 327 characteristics (i.e., psychopathic traits including novelty seeking, low affective empathy, impulsivity, and fearlessness) The last decade has seen the emergence and refinement of developmental theories and models that have pointed to underlying affective and cognitive deficits that precede the manifestation of CU traits in youth This is a rich area of investigation, as recent research has just begun to distinguish between the developmental origins of primary and acquired CU traits Below we review recent studies from genetic, emotional and moral development, and social-relational (i.e., parenting and trauma) perspectives that describe the emergence of CU traits generally, then across the two subtypes, where evidence is available Environmental and Genetic Influences Studies examining genetic contributions to broad CU traits in adolescents and young adults suggest that genetic influences on developmental trajectories (e.g., stable high; increasing; decreasing; stable low) and stability of such traits may be high (Fontaine, Rijsdijk, McCrory, & Viding, 2010) For example, a recent populationbased longitudinal study of twin pairs in middle childhood (i.e., ages 7–12 years) reported a high degree of heritability in male twins showing stable high levels of CU traits as assessed by teacher report (Fontaine et al., 2010) Studies examining CU traits in samples of identical and fraternal twins using different informants (i.e., self-, parent-, and teacher-report) and assessing heritability in childhood and adolescence, show that approximately 40–67% of the variance may be attributable to genetic effects (e.g., Larsson, Andershed, & Lichtenstein, 2006; Viding, Frick, & Plomin, 2007) Although research on the role of genetic factors in the etiology of primary versus acquired CU is limited, emerging research in the field of epigenetics suggests there may be different pathways leading to the emergence of CU traits (e.g., Cecil et al., 2014) Epigenetics refers to the study of heritable changes in gene expression (i.e., which genes are active vs inactive); that is, how genetic material is expressed in different contexts (Moore, 2015; p. 10) One line of epigenetic research in the study of CU traits has focused on changes in the oxytocin (OXT) system OXT is a neuropeptide that has a role in promoting affiliative and prosocial behavior (e.g., trust, empathy, and attachment) (Cecil et al., 2014) OXT can be examined via circulating blood levels through polymorphisms in the OXT receptor gene (OXTR) and assessing its relationship with the perception of emotion and trust (Dadds et al., 2014; Meyer-Lindenberg, Domes, Kirsch, & Heinrichs, 2011) Recent research has shown that higher levels of DNA methylation (i.e., an epigenetic signaling mechanism that cells use to keep genes in the “off” position) in OXTR is related to lower levels of circulating OXT in the context of high CU in older children (Dadds et al., 2014) In a recent study that examined possible differences in developmental pathways to CU traits, Cecil and colleagues (2014) investigated a sample of youth with conduct problems, grouped according to high versus low internalizing problems (i.e., anxiety and depression) to prospectively examine associations between early environmental risk exposure and OXTR methylation in the prediction of CU traits at age 13 Pre- and postnatal environmental risks (e.g., parental psychopathology; adverse life events) were assessed Epigenetic changes (i.e., DNA methylation) to the OXTR were assessed at birth and ages and In youth with low levels of internalizing problems, CU traits at age 13 were associated with DNA methylation at the OXTR gene at birth OXTR methylation at birth was also associated with lower levels of victimization during childhood in youth with low internalizing problems In youth with high levels of anxiety and depression, OXTR methylation was not associated with CU traits at age 13 Instead, prenatal environmental risks such as family conflict were associated with higher CU traits This suggests that adolescents with low internalizing problems had higher levels of DNA methylation in the OXTR gene at birth, which may contribute to CU characteristics In contrast, in youth with high levels of internalizing problems, CU traits were found to be independently associated with prenatal environmental adversity These findings lend support to the idea there are two distinct pathways to the development of CU traits However, it is unclear to what extent such effects differentially influence the two variants Emotional Processing To better understand the heterogeneity of CU features, researchers have examined differences in emotion regulation processes, includ- 328 E tiology and D evelopment ing emotion recognition (Bennett & Kerig, 2014; Kimonis, Frick, Cauffman, Goldweber, & Skeem, 2012; Kimonis, Frick, Fazekas, & Loney, 2006; Kimonis, Frick, Muñoz & Aucoin, 2008) As noted earlier, CU traits are associated with fundamental deficits in emotional arousal in response to others’ expressions of fear and distress In a recent review of the CU literature in children and youth, impairments in emotion recognition were noted across 26 studies, with samples of children varying in age and across studies using different measurements and methodologies (Frick et al., 2014b) Although few studies have examined emotion regulation in cases of primary versus acquired CU, the results of those that have done so are consistent with the dual pathway notion of development More specifically, different types of emotion regulation deficits have been associated with primary versus acquired CU characteristics (Bennett & Kerig, 2014; Kimonis et al., 2006, 2008, 2012) In a sample of adjudicated adolescents (26% female, Mage = 16.15 years) Bennett and Kerig (2014) found that compared to youth identified as having primary CU, youth with acquired CU (i.e., high CU features, trauma exposure and elevated posttraumatic stress symptoms) showed significantly less acceptance of emotions, less ability to identify and differentiate their own emotions, and greater emotional numbing Acquired CU was also associated with greater sensitization to detecting the expression of negative affect in others’ facial expression, specifically, disgust In other words, compared to youth with primary CU, those with the acquired variant were more likely to detect negative affect in others and were more distressed by it CU features in these youth may be evoked to buffer or protect them from distress In contrast, youth with primary CU are less likely to detect negative affect in others and are less distressed as a function of this deficit For example, Kimonis and colleagues (2012) found that in a sample of male juvenile offenders (Mage = 16 years) boys with secondary psychopathy were more likely to report negative emotionality (e.g., depression, anxiety, anger, attention problems) than those identified as having primary psychopathy They were also more likely to attend to negative emotional stimuli than their counterparts with primary psychopathy (e.g., a picture of a crying child) in laboratory-based tasks These findings are consistent with the adult psychopathy literature indicating that those with second- ary psychopathic traits demonstrate less severe emotion recognition deficits as compared to individuals with primary psychopathy (e.g., Prado, Treeby, & Crowe, 2015) These studies support the idea that those with primary CU have a deficit in emotion recognition and emotion deficits (e.g., less sensitivity to negative stimuli), which is believed to be at the core of psychopathic personality On the other hand, a person with the acquired variant may be overly sensitive or overwhelmed by emotional stimuli and may therefore have difficulty processing emotions (e.g., show less acceptance of emotions and more emotional numbing) Moral Development The specific emotion recognition and emotion regulation deficits noted in primary versus secondary CU have important implications for understanding developmental trajectories in aggressive and antisocial behavior from childhood to early adulthood As noted by Blair, Colledge, Murray, and Mitchell (2001), normative processing of emotions is a prerequisite for adaptive social and moral development According to Kimonis and colleagues (2008), developmental theories of moral socialization posit that during early normative development, a child’s transgression (e.g., acts of aggression toward peers) is typically met with distress cues from the victim (e.g., crying) or with a parent’s response (e.g., anger or disapproval) that signals a threat of punishment Both responses typically result in increased anxiety or discomfort in the child that is coded as a moral emotion The child is therefore conditioned or learns over time to avoid negative behaviors As a result of this process, strong emotions of fear and guilt are typically elicited in the child at even the thought of a future transgression, which acts as a socializing agent even in the absence of a parent or caregiver (Kimonis et al., 2008) However, children who show a reduced negative emotional response to the distress of others (i.e., primary variant) not experience this conditioning in the same way and therefore not develop the associated empathic concern (Blair et al., 2006) On the other hand, children who are hyperresponsive and highly reactive (i.e., acquired variant) may have impairments in conscience development (Kochanska, 1993) This model of moral development has been important in framing and understanding the devel- Attachment Perspective on Callous–Unemotional Characteristics 329 opment of CU traits, as it emphasizes an essential developmental process that is disrupted in the development of empathy In the context of etiological theories of psychopathy, Blair (2001) proposed a Violence Inhibition Mechanism (VIM), a biologically based system that has been implicated in the development of primary psychopathy and CU traits (Frick et al., 2014b) This theory suggests that a neurocognitive deficit plays an important role in the development of emotional processing and moral development: “At its simplest, the VIM is thought to be a system that when activated by distress cues, the sad and fearful expressions of others, results in increased autonomic activity, attention and activation of the brain stem threat response system (usually resulting in freezing) According to the model, moral socialisation occurs through the pairing of the activation of the mechanism by distress cues with representations of the acts which caused the distress cues (moral transgressions—for example, one person hitting another).” (Blair, 2001, p. 730) The primary neurocognitive mechanism in relation to deficits in affective empathy in the context of broad CU traits involves reduced amygdala and ventromedial prefrontal cortex responsiveness to others’ distress cues (Blair, 2007) Dysfunction in the ventromedial prefrontal cortex and striatum is associated with impairments in decision making (Blair, 2013) Due to this biological deficit, Blair suggests that individuals with primary psychopathy have a developmental disorder that results in a breakdown of social moralization In relation to acquired CU, youth who have experienced trauma, particularly in relation to caregivers, might also go on to show dysregulated affect (i.e., hyperarousal) and may go on to experience disruptions in moral development due to an active attempt to avoid interpersonal cues as they become emotionally overwhelmed (Kerig & Becker, 2010) Recent research with adjudicated youth identified as having secondary psychopathy were shown to have higher levels of past PTSD symptoms including hyperarousal versus youth identified as having the primary variant (Tatar, Cauffman, Kimonis, & Skeem, 2012) Affective hyperarousal may have a deleterious effect on children’s and youths’ ability to effectively attend to and process socialization cues from caregivers (Frick & Morris, 2004) This process may impact the typical development of social-cognitive skills and moral socialization In other words, children and youth with primary CU traits (i.e., emotional deficits) may be insufficiently aroused by emotional cues, while those with acquired CU traits may learn to avoid attending to emotional cues because they are emotionally overwhelming (e.g., parental anger; Frick & Morris, 2004) Trauma Trauma and child maltreatment have been shown to disrupt normative processes of emotional recognition and processing (Young & Widom, 2014) The presence of ongoing and chronic trauma or maltreatment may interrupt the normal socialization process of moral development by emotionally overwhelming a youth with negative interpersonal stimuli The importance of trauma in the definition of acquired CU traits is demonstrated by the presence of anxiety and higher rates of trauma (e.g., physical abuse, sexual abuse, neglect) as differentiating factors (e.g., Bennett & Kerig, 2014; Kahn et al., 2013) There is emerging support for distinguishing between primary and acquired CU traits on the basis of maltreatment histories For example, a study with 227 incarcerated adolescent boys with secondary psychopathy showed greater incidence of sexual abuse compared to the primary variant, whereas those individuals identified as having the primary variant reported higher rates of parental neglect compared to the secondary variant (Kimonis, Fanti, Isoma, & Donoghue, 2013) Youth classified in this study as having primary CU were differentiated from individuals in the secondary group on the basis of lower anxiety and showed higher scores on the unemotional subscale of the Inventory of Callous and Unemotional Traits (ICU) In studies we discussed previously (Bennett & Kerig, 2014; Kahn et al., 2013; Kimonis et al., 2012), researchers also found higher rates of trauma in those with acquired versus primary CU Likewise, there is evidence from the adult literature that incarcerated individuals with secondary psychopathy have more extensive trauma histories, including child abuse (Blagov et al., 2011) than those with primary psychopathy (Tatar et al., 2012) Although some studies indicate that individuals with primary CU traits or psychopathy have experienced trauma (e.g., Hicks et al., 2010), trauma has not been found to be a robust predictor of primary CU traits 330 E tiology and D evelopment Although much of this research focuses on general traumatic experiences or negative life events (e.g., Sharf, Kimonis, & Howard, 2014), other studies indicate that interpersonal trauma, particularly actions perpetrated by someone close to the individual (i.e., betrayal trauma), may have a more profound effect on emotional development Kerig and colleagues (2012) found that numbing of fear and sadness mediated the relationship between betrayal trauma and CU features in an adjudicated sample of youth (Mage = 16.16, 25% female) Coping with trauma through emotional numbing and inhibition of empathy for others is reinforced because this strategy effectively lowers distress (e.g., reduced psychological distress and somatic symptoms) and may be especially adaptive in contexts where children cannot escape trauma By extension, reexperiencing trauma via memory is also minimized through children’s use of avoidance and emotional numbing of their own negative emotions (Porter, 1996) Porter’s developmental model suggests that when youth effectively inhibit their capacity to feel, they experience a deactivation or dissociation from processes involved with emotional development and moral reasoning, and as a result not develop age-appropriate skills in these domains Parenting The quality of the parent–child relationship remains a necessary factor in the development of emotional regulation and moral development, and it has been implicated in the development of broad CU traits Retrospective studies have shown that adolescents with high levels of broad CU traits tend to recall early family environments characterized by parental rejection; poor parental bonding, neglect, or separation; and inconsistent or severe punishment (e.g., Gao, Raine, Chan, Venables, & Mednick, 2010) Some longitudinal research indicates that exposure to harsh and inconsistent parenting practices is associated with higher levels of broad CU traits over time (e.g., Barker, Oliver, Viding, Salekin, & Maughan, 2011) However, some recent findings suggest that parenting factors such as harshness, coerciveness, and inconsistency may be more associated with conduct problems without CU traits (Barker & Maughan, 2009), whereas low warmth specifically has been found to be consistently associated with chronically elevated levels of broad CU traits (e.g., Pardini et al., 2007; Waller et al., 2014) Parental warmth has emerged as a particularly salient correlate for youth high on broad CU traits and is associated with the development of both primary and acquired CU traits The relationship between low parental warmth and broad CU traits has been demonstrated in preschool-age children (Waller et al., 2012), school-age children (ages 4–12; Larsson, Viding, & Plomin, 2008; Pasalich, Dadds, Hawes, & Brennan, 2011), and adolescents (Kimonis, Cross, Howard, & Donoghue, 2013) In a sample of toddlers (age at baseline), parental warmth was related to CU behavior at age 3, over and above associations with behavior problems (Waller et al., 2014) Kimonis, Cross, and colleagues (2013) found that adolescent male offenders with high levels of CU traits retrospectively reported lower levels of maternal warmth and involvement Specifically, low maternal warmth and involvement were related to the uncaring dimension (i.e., low psychophysiological responding to others’ distress), which is the core of the CU construct This relationship remained significant after the researchers accounted for other important environmental influences, such as maltreatment Although there is a scarcity of findings on specific parenting practices and acquired CU traits, it has been suggested that unemotional or harsh parenting, or parental deficits in emotion communication and regulation, negatively impact the development of emotion recognition and sensitivity in children, placing children at greater risk for developing CU traits (Daversa, 2010) The evidence suggests that maternal warmth is an important protective factor in both primary and acquired variants; however, this hypothesis has yet to be tested Attachment Processes Kochanska, Aksan, Knaack, and Rhines (2004) suggested that normal socialization (e.g., emotional and moral development) requires a two-step process The first process involves attachment According to Bowlby (1944), “attachment” is a biologically based regulatory system that promotes survival by ensuring that children effectively communicate distress to their caregivers, who in turn provide protection When children experience their parents as sensitive and responsive, they trust that their caregivers will provide reliable care, and they Attachment Perspective on Callous–Unemotional Characteristics 331 derive security from the relationship that allows them to explore the world Over time, transactions within the parent–child relationship form a regulatory system that modulates the child’s behavior and affect Disruptions to the attachment system may occur as a function of parents’ responsiveness to their child Bowlby also recognized the impact of disrupted attachment on moral development and child aggression He argued that early experiences of extended parental rejection or separation could disrupt the attachment system and give rise to “affectionless” offending, a pattern of aggression that stemmed from the inability to detect or respond to pain and suffering in victims There are many similarities between Bowlby’s descriptions of youth who engaged in affectionless offending and youth now described as possessing CU features Primary and acquired CU features are associated with different types of disruptions to the attachment system One possibility is that deficits in the detection and identification of emotional cues place children at risk for insecure attachment because of a fundamental disruption in communication between the parent and child Compared to other children, those with primary CU may experience less intense emotions related to fear and distress and/or be less effective in communicating these emotions to their parent In turn, the parent may be less responsive to the child, or their response may not be synchronous with the child’s affective states and needs Over time, this primary deficit in emotion detection and communication disrupts the pattern of communication between parent and child At the same time, the child is less inclined to turn to the parent for support and comfort and does not perceive the parent as a secure base from which to explore the world It is therefore possible that children with primary CU traits will show deficits in reciprocal eye gazing, disrupting the development of shared partnership and derailing the development of attachment security Consistent with this view, Dadds, Jambrak, Pasalich, Hawes, and Brennan (2011) found that boys (N = 92, Mage = 8.9 years) with high CU traits showed impaired reciprocal eye gazing with both maternal and paternal attachment figures Although this study did not differentiate between primary and acquired CU traits, the theoretical rationale proposed by the authors is most consistent with problems most distinctive in cases of primary CU Attachment disruption may arise quite differently in children with acquired CU traits In such cases, children show typical emotion detection or communication; however, their caregivers are likely respond in ways that discourage or punish the direct expression of bids for safety and security Children who experience parental rejection or maltreatment in response to their bids for safety and security are less likely to develop an organized and secure attachment strategy Exposure to profound maltreatment is associated with the child’s lack of an organized attachment strategy, which may be expressed in features that resemble affective numbing and emotion avoidance Repeated exposure to trauma in the absence of safe haven with a caregiver provokes intense fear in the child, who has little recourse other than to inhibit feelings through emotional numbing and to curb the direct expression of need for parental comfort and support Over time, such experiences effectively deactivate the attachment system, reducing a child’s motivation to seek proximity to and to derive comfort and security from attachment figures If an organized attachment strategy emerges, it is likely to be anxious/avoidant (i.e., fearful attachment) and characterized by indirect or masked expressions of emotion Without the presence of a secure attachment system, there is likely to be disruption to the emotion regulation system, specifically in the form of emotion dysregulation, which has been implicated in the development of both externalizing (Moretti & Obsuth, 2009) and internalizing symptoms (Moretti & Craig, 2013) For example, in a treatment study examining an attachment-based parenting intervention, changes in emotion dysregulation were found to mediate the relationship between both attachment avoidance and attachment anxiety in adolescents with behavioral concerns (Moretti, Osbuth, Craig, & Bartolo, 2015) However, there is currently a lack of available studies specifically investigating the relationship between CU traits and attachment (Frick et al., 2014b) to support these speculations Treatment The presence of CU traits may designate a group of children or adolescents who are particularly resistant to treatment and intervention Much of the available evidence suggests that CU traits, particularly in combination with oppositional defiant disorder (ODD) features, predict poorer treatment outcomes for children 332 E tiology and D evelopment when compared to those with conduct problems and low levels of CU traits For example, based on a large-scale review of the available literature, Frick and colleagues noted that youth with CU traits are more resistant to and less likely to participate in treatment (Frick et al., 2014b) Hawes and Dadds (2005) examined a 10-week parenting intervention (Integrated Family Intervention for Child Conduct Problems) for boys between the ages and with ODD or CD and found that CU traits predicted poor treatment outcomes Recently developed treatments have shifted the focus from managing behavior to addressing specific etiological factors that have been found to be associated with primary versus acquired CU Although no treatment studies to date have examined primary versus acquired CU, different treatments may be more effective depending on the variant of CU under investigation The quality of parent–child interactions is implicated as one of the core etiological factors in youth with acquired CU traits (e.g., Kerig et al., 2012) In concordance with findings we discussed earlier in relation to parental warmth, treatment studies show that interventions that promote improvements in harsh and inconsistent parenting, and parental warmth and involvement, are associated with reductions in symptoms of psychopathy and CU traits in children (e.g., McDonald, Dodson, Rosenfield, & Jouriles, 2011; Pasalich, Witkiewitz, McMahon, Pinderhughes, & the Conduct Problems Prevention Research Group, 2016) Given the differences in emotional processing and related trauma history (particularly betrayal trauma; see Kerig et al., 2012), children and youth may respond well to treatments that target the rebuilding of secure attachment relationships Although treatment studies have improved with the increased understanding of the etiology of CU traits, few studies have examined the differential treatment effects of primary and acquired CU traits; therefore, there is little we can conclude based on the available evidence Future Directions This chapter has provided an overview of the literature and newly emerging theoretical perspectives that further our understanding of the development of CU traits, both generally and across primary and acquired variants There is some evidence to support a two-step process in the case of acquired CU traits that begins with the attachment relationship, which in turn affects socialization processes (e.g., emotional regulation and moral development) through the parent–child relationship There is evidence that exposure to chronic trauma or maltreatment may impact and alter the attachment relationship and/or the socialization processes that are salient in normal development Despite emerging evidence of two distinct developmental pathways to CU traits, there are a number of limitations in the literature that require careful attention before we are able to draw more definitive conclusions Foremost among these, there is considerable behavioral, developmental, and trait heterogeneity within the construct of conduct problems including the presence of CU traits (Frick et al., 2014a; Klahr & Burt, 2014) Such heterogeneity makes it difficult to draw conclusions regarding PD-related outcomes, including ASPD and psychopathy In addition to this, although the construct of secondary psychopathy is well established in the literature, the notion of “acquired” CU traits is a relatively new concept Hence, we may expect that CU traits will for some time be conceptualized as a unitary construct in the literature Furthermore, research on CU traits has been typified by inconsistencies in the measurement and conceptualization of the construct As discussed elsewhere (see Patrick & Brislin, Chapter 24, this volume), CU traits in children and youth have been assessed with psychopathy measures (e.g., Psychopathy Checklist—Revised [PCL-R]; Hare, 1991), measures assessing empathy, and more recently, the ICU (Frick, 2004) Limitations regarding measurement using such instruments include, in the case of the PCL-R, conflating affective (e.g., CU traits), interpersonal (e.g., arrogance), and behavioural components (e.g., aggression and delinquency) of psychopathy, which could have theoretical and practical implications With respect to terminology, in using the PCL-R as an accepted measure in developmental studies of CU traits and the term “psychopathy” interchangeably with “CU traits,” it is possible that researchers are failing to identify a subsample of youth who not show interpersonal and behavioral components of the same kind and severity as youth with clinically elevated levels of psychopathic features There is a growing interest in the emergence of CU traits in the absence of aggression and conduct problems Porter (1996) theorized that those Attachment Perspective on Callous–Unemotional Characteristics 333 with acquired CU or secondary psychopathy may show a delay in the development of conduct problems and severe patterns of aggression as they learn to dampen their emotional expression and experience during childhood Unfortunately, there is no empirical evidence to support this theory, and this remains an open question Future research needs to address the issue of conflating the components of psychopathy and to parse the components to better understand the emergence and development of CU traits independent of conduct problems Future research should adopt consistent terminology and avoid using the terms “psychopathy” and “CU traits” interchangeably In order to address many of these concerns, there are a number of methodological considerations that need to be addressed There have been several cross-sectional studies examining varied associations among parenting, antisocial behavior, and CU traits in children (see Waller, Gardner, & Hyde, 2013), and identifying highversus low-anxiety CU subtypes in adolescents (e.g., Kimonis et al., 2012); however, a smaller but growing body of longitudinal research has examined CU traits and possible pathways across development Longitudinal research that examines risk factors (e.g., trauma), and protective factors (e.g., parental warmth) will help researchers understand the differential and shared environmental risk factors for both primary and acquired CU traits Another growing concern in the research field is the lack of diversity in the populations being examined The majority of research on CU traits, and indeed on psychopathy, has been primarily with males involved with the justice system Although it is likely that this population is selected for the increased likelihood of sampling youth high on CU traits, selecting youth samples involved with the justice department conflates aggressive and antisocial behavior with CU traits In addition, the scarcity of females in sampling does not allow many opportunities for examining gender differences; it is possible that there are significant gender differences in the development and expression of primary and acquired CU traits Conclusion It may appear from our discussion that there are two distinct and nonoverlapping pathways to CU traits—one that is more biologically driven and another that is more environmentally based However, as we described earlier, individuals showing primary CU traits indeed report exposure to negative/harsh parenting and trauma; similarly, it is unclear as to whether youth with acquired CU features are significantly impacted by more biologically based mechanisms Clearly, both biological and environmental influences shape developmental pathways Even models that hold to the idea that the magnitude of genetic effects remain latently stable over development but the expression of genetic influences varies from one age versus another may be in question The field of epigenetics points to the need for more transactional models whereby the potential for genetic expression is shaped and reshaped through environmental influences The next few decades will usher in new innovative frameworks, each with its own challenges, but with the cumulative impact of pushing the field further Perhaps the most exciting ripple effect of these new frameworks will be the revision of our understanding of what interventions, for whom, and most importantly at what points in development, exert the most powerful and lasting therapeutic benefits Revisiting these key questions about the impact of psychological interventions with a new understanding of the dynamic transactions of 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classification; Dimensional approaches to classification; individual diagnostic manuals and their editions Clinical assessment See Assessment Clinical correlates, 186–189, 192–193 Clinical interviews measures for, 342t–343t overview, 376, 377t, 380, 389 schema-focused therapy (SFT) and, 557 stability and change and, 357–358 structural interview, 378–380 transference-focused psychotherapy (TFP) and, 574–575 See also Assessment Clinical utility of PD categories, 72, 73–74 Clinician factors assessment and, 375–376, 388–389 integrated modular treatment and, 652–654 interpersonal reconstructive therapy (IRT) and, 412 mentalization-based treatment (MBT) and, 550–551 schema-focused therapy (SFT) and, 564–565 systems training for emotion predictability and problem solving (STEPPS) and, 593–594 violence reduction treatment and, 633–634 See also Therapist stance Subject Index Cluster A personality disorders, 219, 504, 504t See also individual personality disorders Cluster B personality disorders, 219, 252, 504–506, 504t, 555 See also individual personality disorders Cluster C personality disorders, 219, 504t, 506, 555, 556 See also individual personality disorders Cognitive analytic therapy (CAT) borderline personality disorder and, 494–503, 495f, 498f case example of, 496–497 early intervention and, 222 features of, 493–494 integrated modular treatment and, 658f outcome evidence and, 503–507, 504t overview, 481–482, 483–484, 489–492, 507–508 theoretical orientations and, 492–493 Cognitive biases, 144–148, 145f, 560 See also Biases Cognitive functioning, 104–105, 283–284, 420, 422 Cognitive interventions assessment and, 377–378 integrated modular treatment and, 657f, 658f, 668 schema-focused therapy (SFT) and, 563–564, 565 Cognitive modification, 533, 535–536 Cognitive processes cognitive disorganization, 246 cognitive distortion, 535–536, 563 cognitive dysregulation, 370t, 371t, 385 comorbidity and, 163 development of new cognitions in CBTpd, 516 diagnosis and, 30–31 flexibility, 124–125, 286–287, 295 integrated modular treatment and, 663–664 interactions of with emotion, 292–294 mentalization and, 124, 125f overview, 28–29, 149, 277 schema-focused therapy (SFT) and, 560 schemas and, 132, 650–651 self and, 102–103 Cognitive psychology, 110–111 Cognitive restructuring, 466, 563, 637, 657f Cognitive theory causal status and, 149 clinical implications, 149–150 cognitive biases and, 144–148, 145f overview, 30, 31–32, 44, 141–143, 142f, 150–151 Cognitive therapy assessment and, 377–378 comparisons among the cognitive therapies and, 520, 521f medical model and, 19 obsessive–compulsive personality disorder and, 466 treatment methods, 522–523 violence reduction treatment and, 637–638 Cognitive-affective processing (CAP) system, 388, 452, 577 Cognitive-behavioral therapy (CBT) antisocial personality disorder and, 453–454 comparisons among the cognitive therapies and, 520, 521f emotion regulation and, 278 integrated modular treatment and, 657f interpersonal reconstructive therapy (IRT) and, 410, 411f, 412 intervention strategies and methods of, 515–520, 516f–517f obsessive–compulsive personality disorder and, 466 overview, 143, 150, 512–513, 650 research support for, 523–525, 524t schema-focused therapy (SFT) and, 556, 568 systems training for emotion predictability and problem solving (STEPPS) and, 587 theoretical orientations and, 513–515, 514f treatment methods, 522–523 violence reduction treatment and, 636, 637–638 See also Cognitive-behavioral therapy for PDs (CBTpd) Cognitive-behavioral therapy for PDs (CBTpd) comparisons among the cognitive therapies and, 520, 521f overview, 481–482, 484, 512–513, 525 research support for, 523–525, 524t theoretical orientations and, 513–515, 514f therapeutic relationship and, 520–522 treatment methods, 522–523 See also Cognitive-behavioral therapy (CBT) Coherence, 112t, 116, 118, 131–132 Collaboration cognitive analytic therapy (CAT) and, 490–491 cognitive-behavioral therapy for PDs (CBTpd) and, 521–522 dialectical behavior therapy (DBT) and, 537 integrated modular treatment and, 652–653, 654–655 mentalization-based treatment (MBT) and, 543, 549–550 violence reduction treatment and, 638, 639 Collaborative Longitudinal Study of Personality Disorders (CLPS) assessment and, 357–358 emotion regulation and, 273 historical overview of classification systems and, 59, 60 methodological differences among studies, 201–208 obsessive–compulsive personality disorder and, 461, 462–463, 468 overview, 200t, 201, 210 Collectivism cultural factors and, 94–95, 97 future directions and, 97–98 identity and, 108 individualism-collectivism cultural syndrome and, 93–94 modernization and, 95 Commitments, 112t–113t, 667 Common factor approaches, 134, 647–648 Communication, 134–136, 536–537, 589–590, 637, 652 Communities that Care system, 222 Comorbidity antisocial personality disorder and, 450–451 assessment and, 357 biological factors and, 160–164 borderline personality disorder and, 420 change and, 162–164 clinical correlates and, 186–189 cognitive analytic therapy (CAT) and, 499–500 diagnosis and assessment and, 339 dialectical behavior therapy (DBT) and, 528, 538–539 interpersonal reconstructive therapy (IRT) and, 409–410 limitations of categorical approaches and, 72, 73 mentalization-based treatment (MBT) and, 545 neurotransmitter function and, 260 obsessive–compulsive personality disorder and, 463 overview, 156–160, 158t, 192–193 risk factors and, 219 structural analysis of social behavior (SASB) model and, 403, 408–409, 409t, 413 See also Co-occurance of PD and other mental disorders Comparative Psychotherapy Process Scale (CPPS), 412 Competence in CAT measure (CCAT), 502–503, 505–506 Complication/scar model, 158, 158t See also Bivariate models Composite International Diagnostic Interview (CIDI), 175t, 176 Compulsive personality disorder, 34–35, 50t Compulsivity developmental factors and, 312t, 313–314, 319–320 diagnostic classification and, 20–21 dimensional approaches and, 77t overview, 417 trait assessment and, 370t validity and, 13–14 Computerized Adaptive Test of Personality Disorder (CAT-PD), 350 Conduct disorder antisocial personality disorder and, 429, 436, 446 comorbidity and, 159 developmental factors and, 216 parental psychopathology and, 303 See also Conduct problems Conduct problems antisocial personality disorder and, 433, 436 callous–unemotional (CU) traits and, 326, 332–333 overview, 371t trait assessment and, 370t See also Behavior; Conduct disorder Confident-narcissistic personality, 35, 35t Conners’ Continuous Performance Test–II (CPT), 288, 290–291 Conscientiousness antisocial personality disorder and, 434–435 cultural factors and, 91–92 Subject Index 699 developmental factors and, 311–312, 312t, 316–317, 319–320 obsessive–compulsive personality disorder and, 468–469 overview, 41–42, 74, 371t, 417 personality traits and, 315, 370t See also Five-factor model (FFM) Consolidation, 379, 517, 669–670 Constraint, 311–312, 417, 469 Construct Repertory Test (CRT), 42–43 Consultation, 529–530, 537 Containment, 646, 657f, 659–660 Contempt towards others, 446, 636 Contextual influences, 316–317, 320 Contingency management, 533, 534–535, 546–547 Control, 470, 636, 660–666 Controlled mentalizing, 124, 125f See also Mentalization Co-occurance of PD and other mental disorders, 104–105 See also Comorbidity Cooperativeness, 244, 374–375 Coping styles assessment and, 379–380 callous–unemotional (CU) traits and, 325 clinical implications, 150 cognitive biases and, 145f cognitive-behavioral therapy for PDs (CBTpd) and, 518 memory bias and, 149 overview, 19, 142–143 schema-focused therapy (SFT) and, 557, 560 CORDS label, 397, 398, 409–410, 413 Core beliefs, 141–142, 142f, 513–515, 514f, 518, 522–523 See also Beliefs Core Conflict Relationship Theme (CCRT), 497 Cortisol functioning, 260, 262 Countertransference, 497, 550 Course of personality disorders antisocial personality disorder and, 452–453 borderline personality disorder and, 423, 604 developmental psychopathology model and, 320 obsessive–compulsive personality disorder and, 462–463 overview, 170–171, 208–211, 217–218, 223, 231 psychoeducation and, 604 See also Change in personality disorders; Longitudinal studies; Outcomes; Stability of personality disorders Criminal behavior antisocial personality disorder and, 452–453 neurotransmitter function and, 254, 259–260 overview, 629 treatment and, 629–641, 635f violence reduction treatment and, 631–632, 634–638, 635f See also Antisocial behaviors; Behavior; Violence Cultural factors classification systems and, 89 clinical considerations, 97 DSM personality disorders across, 90–91 five-factor model (FFM) and, 39–40 future directions and, 97–98 identity and, 107–108 immigration and modernization and, 95–96 individualism-collectivism cultural syndrome and, 93–94 overview, 41, 88–89, 96–97 personality and cultural interactions and, 94–95 Cyclothymic personality disorder, 50t, 52 Daily diary card See Diary cards Dangerous behavior, 324–325 Danish Adult Reading Test (DART), 285 Deceitfulness, 394–395, 429, 636 Decision making, 288–290, 294–295, 375–376 Deductive theory, 31–32 Defense mechanisms, 114, 379, 574t Demographics correlates, 189–191, 192–193 Dependency, 13–14, 345, 373, 385, 559t, 650, 666 Dependent personality disorder (DPD) clinical correlates and, 186, 189 cognitive-behavioral therapy for PDs (CBTpd) and, 514 comorbidity and, 158 demographic correlates, 189–191 epidemiological studies, 178 five-factor model (FFM) and, 76 genetic factors and, 240 historical overview of classification systems and, 50t, 52, 59–60, 61 interpretational bias and, 146 overview, 28, 417 prevalence, 184, 185t schema-focused therapy (SFT) and, 567, 568, 569 structural analysis of social behavior (SASB) model and, 409t theoretical orientations and, 30, 32–33 Depression antisocial personality disorder and, 450 borderline personality disorder and, 420 cognitive analytic therapy (CAT) and, 504 cognitive-behavioral therapy for PDs (CBTpd) and, 515, 525 comorbidity and, 157, 159 cultural factors and, 94–95 dialectical behavior therapy (DBT) and, 528, 539 emotion regulation and, 277 genetic factors and, 244 interpersonal reconstructive therapy (IRT) and, 396 memory bias and, 294 negative thoughts and, 519 neurotransmitter function and, 257, 260 obsessive–compulsive personality disorder and, 461, 463 perfectionism and, 469 pharmacotherapy and, 256, 277–278, 616, 617, 618–619, 620, 623 schema-focused therapy (SFT) and, 555, 556 structural analysis of social behavior (SASB) model and, 408–409, 409t transference-focused psychotherapy (TFP) and, 581 700 Depressive personality disorder (DPD), 32–33, 56–57, 221 Detached Protector mode, 561, 562t See also Schema mode Detached Self-Soother/Self-Stimulator mode, 562t Detachment, 76, 77t, 78f, 325, 373 Developmental factors antisocial personality disorder and, 432–435, 433 borderline personality disorder and, 422–423 callous–unemotional (CU) traits and, 332, 333 childhood adversity and, 127–129, 301 cognitive analytic therapy (CAT) and, 492–493 cognitive theories and, 150 early intervention and, 221–223 identity and identity diffusion and, 107–108, 114, 116–117, 118f interpersonal reconstructive therapy (IRT) and, 398 mentalization and, 124, 127–129, 133, 542, 545 moral development and, 328–329 overview, 17–18, 32, 215, 223, 229–233, 651 personality and, 215–217, 310–314, 312t precursor signs and symptoms, 218–220 prevalence and, 221 risk factors and, 218–220 schema-focused therapy (SFT) and, 558 stability and change and, 217–218 temperament and, 215–216 traits relevant to personality disorders, 314–319 See also Adolescence; Adulthood; Childhood; Personality development Developmental psychopathology model overview, 232–233, 309–310, 319–320 personality traits and, 310–314, 312t role of personality traits and, 317–319 traits relevant to personality disorders, 314–319 Diagnosis antisocial personality disorder and, 445–446, 451–452 approaches to, 367, 368–373, 370t, 371t–372t borderline personality disorder and, 419–422, 494–495 case formulation and, 397 cognitive analytic therapy (CAT) and, 491–492 cognitive heuristics and, 15 cultural factors and, 96, 97 dialectical behavior therapy (DBT) and, 530–531 DSM era and, 7–8 early conceptualizations of personality disorder and, epidemiology and, 193 essentialism and, 14–15 future research and, 83–84 genetic factors and, 235–236 historical overview of classification systems and, 48–49 immigration and, 95 limitations of categorical approaches and, 72–74 Subject Index longitudinal studies and, 198 measures for, 342t medical model and, 9–11 mentalization-based treatment (MBT) and, 543 neurotransmitter function and, 264 outcomes and, 170–171 overview, 22, 231, 337–339, 382 psychiatric syndromes and, 155–156 psychoeducation and, 601–603, 602t schema-focused therapy (SFT) and, 557–558 structural analysis of social behavior (SASB) model and, 403, 405–408, 406t–407t transference-focused psychotherapy (TFP) and, 572–575, 573f, 574t validity and, 11–14 in young people, 220–221 See also Assessment; Classification systems; individual personality disorders Diagnostic and Statistical Manual of Mental Disorders (DSM) antisocial personality disorder and, 445 borderline personality disorder and, 419 comorbidity and, 156–157, 162–164 cultural factors and, 90–91, 96 diagnostic classification and, 21 early conceptualizations of personality disorder and, 6–7 evolution of, 28 five-factor model (FFM) and, 38 medical model and, 9–11 overview, 7–8, 25–26, 169–170, 171 theoretical orientations and, 34–35 validity and, 13–14 Diagnostic and Statistical Manual of Mental Disorders (DSM-I), 49, 50t, 51 Diagnostic and Statistical Manual of Mental Disorders (DSM-II), 50t, 51–52, 426 Diagnostic and Statistical Manual of Mental Disorders (DSM-III) antisocial personality disorder and, 426–427 assessment and, 341 borderline personality disorder and, 419 childhood and adolescence and, 220 comorbidity and, 156–157 DSM era and, 7–8 early conceptualizations of personality disorder and, 6–7 epidemiology and, 173–174, 174, 175t, 176 historical overview of classification systems and, 50t, 52–53, 56 medical model and, 9–10 obsessive–compulsive personality disorder and, 461 overview, 4, 25–26 Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R) antisocial personality disorder and, 427 comorbidity and, 156–157 DSM era and, 7–8 epidemiology and, 173, 174, 175t, 176 historical overview of classification systems and, 50t, 53–54, 56 obsessive–compulsive personality disorder and, 460, 461 theoretical orientations and, 31 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) antisocial personality disorder and, 427 assessment and, 341 borderline personality disorder and, 419 cognitive theories and, 150–151 comorbidity and, 156–157, 159 DSM era and, 7–8 epidemiology and, 173, 174, 175t, 176–177 five-factor model (FFM) and, 38, 39–40, 75 genetic factors and, 241–242 historical overview of classification systems and, 50t, 55–57 medical model and, 9–10 obsessive–compulsive personality disorder and, 459–460, 461, 462–463, 467–468, 471 structural analysis of social behavior (SASB) model and, 403 theoretical orientations and, 30–31, 31, 32–33 transference-focused psychotherapy (TFP) and, 572, 581 validity and, 14 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) comorbidity and, 156–157, 161 DSM-5 and, 63–64 future editions and, 64, 65 historical overview of classification systems and, 50t, 57 longitudinal studies and, 198 obsessive–compulsive personality disorder and, 461 theoretical orientations and, 31 Diagnostic and Statistical Manual of Mental Disorders (DSM-5) antisocial personality disorder and, 427, 429, 436, 437, 444, 445–447 assessment and, 337–338, 341, 344, 389 borderline personality disorder and, 419, 421, 494–495 callous–unemotional (CU) traits and, 326 childhood and adolescence and, 220 cognitive heuristics and, 15 cognitive theories and, 142, 150–151 comorbidity and, 159, 162–164 cultural factors and, 88–89 developmental factors and, 312–313 developmental psychopathology model and, 233, 309, 319, 320 diagnosis and, 21, 221, 337–338 differentiating traits from other aspects of personality functioning, 318 DSM era and, 7–8 early conceptualizations of personality disorder and, 6–7 epidemiology and, 174, 177–178 five-factor model (FFM) and, 38, 39–40, 76, 78–80, 78f, 80t future editions and, 63–64, 65 genetic factors and, 246 historical overview of classification systems and, 50t, 57–63 identity and, 108–109 interpersonal reconstructive therapy (IRT) and, 394–395, 413 lexical hypothesis and, 42 longitudinal studies and, 198 medical model and, 10–11 mentalization and, 130 obsessive–compulsive personality disorder and, 459–460, 471 overview, 26, 47–48, 648 psychiatric syndromes and, 155 psychoeducation and, 602 psychopathology and, 101, 428 schema-focused therapy (SFT) and, 560 systems training for emotion predictability and problem solving (STEPPS) and, 589 theoretical orientations and, 31, 32–33 transference-focused psychotherapy (TFP) and, 572 See also Alternative Model Diagnostic classification comorbidity and, 162–164 cultural factors and, 90–92 DSM-5-III Trait Model and, 80–82, 81t epidemiology and, 173–174 future research and, 83–84 limitations of categorical approaches and, 72–74 overview, 20–22, 65–66, 169–170 theoretical orientations and, 30–31 See also Classification systems; individual diagnostic manuals and their editions Diagnostic Interview for Borderlines— Revised (DIB-R), 421 Diagnostic Interview Schedule (DIS), 175t, 176 Dialectical behavior therapy (DBT) diagnosis, assessment, and formulation and, 377–378, 377t, 387–388, 530–531 domains of psychopathology and, 527–528 emotion regulation and, 278 obsessive–compulsive personality disorder and, 467 overview, 481–482, 483–484, 527 research support for, 538–539 strategies, 533–537 systems training for emotion predictability and problem solving (STEPPS) and, 586 theoretical foundation of, 531–533 therapeutic relationship and, 537–538 transference-focused psychotherapy (TFP) and, 572, 580–581 treatment stages and targets, 528–530 Dialectical behavior therapy prolonged exposure (DBT-PE) protocol, 530 See also Dialectical behavior therapy (DBT) Dialectics, 531, 532–533, 537–538 Dialogic sequence analysis (DSA), 499 Diary cards, 387–388, 528–529, 530–531 Diathesis–stress model, 232–233, 303, 306, 513–514 Dichotomous thinking, 147–148 Differential diagnosis, 403, 405–408, 406t–407t See also Diagnosis Differentiation, 375, 382, 384 Subject Index 701 Digit Symbol subtest, 284 Dimensional approaches to classification advantages to, 74 antisocial personality disorder and, 437–438, 446–447 assessment and, 357–359, 369–373, 370t, 371t–372t comorbidity and, 163 cultural factors and, 91–92 developmental factors and, 313, 320 diagnosis and, 369–373, 370t, 371t–372t future research and, 83–84 genetic factors and, 236–237, 236f, 237f limitations of categorical approaches and, 72–74 neurotransmitter function and, 264 overview, 43–44, 72 transference-focused psychotherapy (TFP) and, 572 See also Classification systems; Five-factor model (FFM); Traitdimensional model Dimensional Assessment of Personality Pathology (DAPP), 77t, 239–240, 241 Dimensional Assessment of Personality Pathology—Basic Questionnaire (DAPP-BQ), 217, 370 Dimensional Personality Symptom Item Pool (DIPSI), 77t, 217, 349 Dimensional trait model, 60–61 See also Trait models Disability, 356–357 Disagreeableness, 312, 312t, 313–314 Disconnection, 558, 559t Disease model, 3–4, 26, 31 Disinhibition antisocial personality disorder and, 429, 433–434, 434, 435, 446, 451 assessment and, 373 dimensional approaches and, 77t factor hierarchy and, 78f obsessive–compulsive personality disorder and, 471 Disinhibition (DIS) versus conscientiousness domain, 76 Dispositional dimensions, 437–438 Disruptive behavior disorder, 63–64, 219 Dissocial behavior diagnostic classification and, 20–21 integrated modular treatment and, 666 overview, 417 trait assessment and, 370t validity and, 13–14 Dissociative symptoms childhood adversity and, 305 cognitive analytic therapy (CAT) and, 493–494, 497 identity diffusion and, 114 neurotransmitter function and, 260 schema mode and, 561 Distraction, 590, 662–663 Distress, 126, 330 Dopamine system, 244, 257–259 See also Neurotransmitter systems DSM-5 Clinicians’ Personality Trait Rating Form (DSM-5 CPTRF), 354 DSM-5 Personality and Personality Disorders Work Group (PPDWG) comorbidity and, 162 five-factor model (FFM) and, 76 future editions and, 63–64 historical overview of classification systems and, 58, 59–63 overview, 66 DSM-5 Section III Alternative Model for PD See Alternative Model DSM-5 Work Groups, 459 DSM-5-III Informant Personality Trait Rating Form (DSM-5 IPTRF), 354 DSM-5-III Trait Model, 78–79, 78f, 80–84, 80t, 81t Dyssocial reaction personality disorder, 50t Dysthymia, 56–57 Early experiences See Childhood experiences Early intervention, 221–223 See also Interventions Early maladaptive schemas (EMSs), 142–143, 144, 558–560, 559t Eating disorders borderline personality disorder and, 420 cognitive analytic therapy (CAT) and, 499 dialectical behavior therapy (DBT) and, 528, 539 identity diffusion and, 113, 114 obsessive–compulsive personality disorder and, 463, 467, 469 perfectionism and, 469 schema-focused therapy (SFT) and, 569 Eccentric perceptions, 79, 373 Ecological momentary assessment (EMA) strategies, 381, 421 Effortful control, 386t, 434, 576 Egocentrism, 370t, 371t Ego-identity, 111, 113, 114, 115, 636 See also Identity EIC scale, 592, 594 Elemental Psychopathy Assessment (EPA), 427 Emotion regulation assessment and, 388 cognitive-behavioral therapy for PDs (CBTpd) and, 517–518 dialectical behavior therapy (DBT) and, 532–533, 539 personality impairment and, 318–319 psychotherapy and pharmacotherapy and, 277–278 skills training and, 222 Emotional abuse, 128–129 See also Childhood experiences Emotional dysregulation borderline personality disorder and, 420–421 cognitive-behavioral therapy for PDs (CBTpd) and, 517–518 diagnostic classification and, 20–21 integrated modular treatment and, 660–665 overview, 417 validity and, 13–14 Emotional intensity disorder (EID), 588, 590 Emotional interventions, 669 Emotional processing, 232, 246, 271–272, 327–328, 664–665 Emotional reactivity, 370t, 371t, 664–665 702 Emotional regulation cognitive processing in BPD and, 277 dialectical behavior therapy (DBT) and, 527, 531 dysregulation in patients with PD, 273 in healthy subjects, 272–273 integrated modular treatment and, 664–665 neuroimaging studies in BPD and, 274–276 neuropsychological mechanisms and, 274 overview, 232, 271–272 parental psychopathology, 303 skills training and, 589–590, 591 trait assessment and, 369–370, 370t violence reduction treatment and, 637 Emotional unstable personality disorder, 50t Emotions dialectical behavior therapy (DBT) and, 530 inhibition and, 559t instability and, 312t, 313 integrated modular treatment and, 661–662 intensity and, 370t, 371t interactions of with cognition, 292–294 lability, 79, 370t, 385 overview, 271–272 schema-focused therapy (SFT) and, 560 Empathy antisocial personality disorder and, 435, 446 callous–unemotional (CU) traits and, 327 interpersonal reconstructive therapy (IRT) and, 395 mentalization-based treatment (MBT) and, 546–548, 550–551 overview, 371t schema-focused therapy (SFT) and, 564 trait assessment and, 370t triarchic model and, 430 validation and, 550–551 violence reduction treatment and, 636 Empirically based treatments, 367, 481–485, 566–568, 602t Engagement, 515–516, 545, 546 Entitlement, 373, 559t, 636 Environmental factors antisocial personality disorder and, 429, 435–437 callous–unemotional (CU) traits and, 326–327 childhood adversity and, 127, 301–303 cultural factors and, 92, 94–95 developmental psychopathology model and, 320 dialectical behavior therapy (DBT) and, 531, 537 genetic factors and, 237, 239, 306 mentalization and, 127, 132, 545 overview, 229, 513 personality and, 242–243, 319 psychoeducation and, 602–604, 602t risk factors and, 219 traits relevant to personality disorders, 316 twin studies and, 239 violence reduction treatment and, 638 See also Family factors Subject Index Epidemiologic Catchment Area Study (ECA), 90–91, 174, 176 Epidemiology assessment and, 191–192 borderline personality disorder and, 422 childhood adversity and, 306 epidemiological studies, 174–180, 175t longitudinal studies and, 198 obsessive–compulsive personality disorder and, 462 overview, 169–171, 173–174, 192–193 See also Prevalence Epigenetics, 333 See also Genetic factors Episodic memory, 285–286, 294–295 See also Memory processes Epistemic choices, 26–29, 45 Epistemic distrust, 103–104 Epistemic hypervigilance, 130, 135, 136 Epistemic openness, 134 Epistemic rigidity, 545 Epistemic trust, 123, 130, 132–133, 135–136, 545 Epistemic vigilance, 130, 133 Equifinality, 233, 309 Error detection, 272–273 Error-related negativity (ERN), 160, 433 Etiology borderline personality disorder and, 422–423, 603–604 callous–unemotional (CU) traits and, 326–327 moral development and, 329 obsessive–compulsive personality disorder and, 464–465 overview, 229–233, 651 psychoeducation and, 603–604 See also Biological factors; Causal factors; Psychosocial factors Evaluation bias, 145f, 147–148, 149 Event-related potentials (ERPs), 160, 433 Evidence-based approach to personality disorder, 417–418 Evidence-based practice (EBP), 503–507, 504t Evidence-Based Practice in Psychology (EBPP), 412–413 Evidence-based psychotherapies borderline personality disorder and, 605 cognitive-behavioral therapy for PDs (CBTpd) and, 523–525, 524t interpersonal reconstructive therapy (IRT) and, 412–413 mentalization and, 134, 551–552 overview, 482 psychoeducation and, 605, 607 systems training for emotion predictability and problem solving (STEPPS) and, 597 transference-focused psychotherapy (TFP) and, 580–582 See also Treatment; individual treatment approaches Evolutionary factors cultural factors and, 92, 98 diagnostic classification and, 21 five-factor model (FFM) and, 39 mentalization and, 131 overview, 17–18, 27, 34–35, 44 Experiential techniques, 563–564, 565 Exploitativeness, 370t, 371t, 446, 636 Exploration, 548, 646, 659, 666–670 Explosive aesthenic personality disorder, 50t, 52 Exposure approaches, 277, 463, 530, 533, 536 External features of self, 124, 125f Externalizing spectrum (ES) model, 451 Externalizing Spectrum Inventory (ESI), 430–431 Externalizing symptoms comorbidity and, 159, 187 cultural factors and, 97 factor hierarchy and, 78f obsessive–compulsive personality disorder and, 470 schema-focused therapy (SFT) and, 569 Extraversion cultural factors and, 91–92 developmental factors and, 311, 312t developmental psychopathology model and, 319–320 future editions of classification systems and, 65 overview, 41–42, 74 transference-focused psychotherapy (TFP) and, 573f See also Five-factor model (FFM) Eysenck Personality Questionnaire (EPQ), 74, 77t, 240 Factor analysis antisocial personality disorder and, 429 assessment and, 373 developmental factors and, 217 five-factor model (FFM) and, 39 lexical hypothesis and, 42 overview, 36–37, 417 schema-focused therapy (SFT) and, 566 Factor hierarchy, 78–79, 78f Factor models, 35–44, 36f Failure, 559t Family factors borderline personality disorder and, 420 childhood adversity associated with mental disorders and, 301–303 dysfunctional families, 303–304 epidemiological studies, 179–180 genetic analyses, 237–243 obsessive–compulsive personality disorder and, 464 personality impairment and, 318–319 risk factors and, 218–220 traits relevant to personality disorders, 315–317 See also Environmental factors; Genetic factors Fast Track program, 222 Fear antisocial personality disorder and, 437 fear-based disorders, 159 mentalization and, 126 neurotransmitter function and, 252 schema-focused therapy (SFT) and, 560 triarchic model and, 430 Fearlessness, 325, 327, 433, 434–435, 437 Fight–flight–freeze process, 142–143 See also Coping styles Fight–flight–freeze system (FFFS), 311 Five Dimensional Personality Test (5DPT), 77t, 348 Five-factor model (FFM) classification systems and, 61–62, 65 cultural factors and, 91–92 developmental factors and, 216–217, 311–312, 312t developmental psychopathology model and, 233 obsessive–compulsive personality disorder and, 460, 468–469 overview, 37–44, 43–44, 74–76, 77t trait assessment and, 370 traits described in DSM-5 and, 76, 78–80, 78f, 80t See also Agreeableness; Big Five personality model; Conscientiousness; Extraversion; Neuroticism; Openness to Experience Flexibility, 132, 494, 495f, 664 Forensic treatment settings, 499, 568, 569 Functional impairments, 21, 337, 373, 461–462 Functional magnetic resonance imaging (fMRI) See Neuroimaging technologies Galton, Sir Francis, 36 Game of Dice Task, 289–290 Gamma-aminobutyric acid (GABA), 260–262 See also Neurotransmitter systems Gender, 112t, 189–190, 193, 293, 315 Gene–environment interactions, 306 See also Environmental factors; Genetic factors General Assessment of Personality Disorders (GAPD), 352 Generalization, 669–670 Generalized anxiety disorder (GAD), 159, 216, 463 See also Anxiety disorders Genetic factors antisocial personality disorder and, 433, 435–437 callous–unemotional (CU) traits and, 325, 327, 333 developmental psychopathology model and, 315–316, 317, 320 future directions in, 246–247 gene–environment interactions and, 306 genetic analyses, 237–243 identifying putative genes, 243–246 interpersonal reconstructive therapy (IRT) and, 399 mentalization and, 126 obsessive–compulsive personality disorder and, 464 overview, 17–19, 161, 217, 229, 231, 235, 247 phenotype, 235–237, 237f, 238f psychoeducation and, 603–604 traits relevant to personality disorders, 315–316 See also Family factors; Phenotypic features Genomewide association (GWA) studies, 436 Gift of Love (GOL), 396–397, 398, 410, 412 Global Assessment of Functioning (GAF) score, 369, 551 Glutamate, 260–261 See also Neurotransmitter systems Goals assessment and, 384 dialectical behavior therapy (DBT) and, 530, 532–533 Subject Index 703 identity and, 108–109, 112t integrated modular treatment and, 652, 656 personality impairment and, 318 systems training for emotion predictability and problem solving (STEPPS) and, 590 violence reduction treatment and, 633 Go/no-go task, 277, 290–291 Grandiosity, 59–60, 79, 559t, 636 Group treatments dialectical behavior therapy (DBT) and, 527, 529 mentalization-based treatment (MBT) and, 552 obsessive–compulsive personality disorder and, 466 peer psychoeducation, 606–607 psychoeducation and, 606 schema-focused therapy (SFT) and, 555, 568 systems training for emotion predictability and problem solving (STEPPS) and, 591–595 Growth hormone (GH), 259–260 Guilt, 467, 560 Hare Self-Report Psychopathy Scale (SRPIII), 427, 430–431 Harm avoidance, 243–244, 245 Helping Young People Early (HYPE) program, 222 Heterogeneity borderline personality disorder and, 419 callous–unemotional (CU) traits and, 325, 332 diagnosis and assessment and, 368 limitations of categorical approaches and, 72, 73 longitudinal studies and, 207–208, 207f mentalization and, 126 Hexaco Dark Triad, 40–41 Histrionic personality disorder (HPD) clinical correlates and, 186, 187, 188 cognitive analytic therapy (CAT) and, 504t, 506 demographic correlates, 189–191 emotion regulation and, 273 epidemiological studies, 176 future editions of classification systems and, 63–64 genetic factors and, 240 historical overview of classification systems and, 50t, 59–60 overview, 28 prevalence, 182, 183–184, 183t schema-focused therapy (SFT) and, 567, 568 structural analysis of social behavior (SASB) model and, 405, 406t–407t, 409t theoretical orientations and, 32–33 Honesty-Humility, Emotionality, Extraversion, Agreeableness, Conscientiousness, Openness (HEXACO), 26, 40–41, 42, 43–44, 77t, 349–350 Hospitalization, 605 See also Inpatient treatment Hostile-dominance, 370t, 371t, 469 Hostility, 394–395, 623 Human Connectome Project, 161 Hybrid model, 64, 65, 163, 357, 373 Identification of feelings, 549, 661 Identity assessment and, 379, 386t clinical implications, 118–119 definitions of, 110–113, 112t–113t development of, 116–117, 118f integrated approach and, 381, 658f layers of, 111 mentalization and, 130, 131 overview, 103, 107–109, 649 personality impairment and, 318 schema-focused therapy (SFT) and, 558 the self and, 109–110 transference-focused psychotherapy (TFP) and, 574t, 575 See also Identity diffusion; Self; Selfconcept Identity diffusion assessment and, 379 clinical implications, 118–119 development of, 116–117, 118f inferred self and, 102–103 mentalization and, 130 overview, 108–109, 112t–113t, 113–116 See also Identity Imagery work, 523, 557, 563–564, 565 Immigration, 95–96, 97 Implicit Association Test (IAT), 147 Implicit processes, 146–147 Impulse control, 94–95, 386t See also Impulsivity Impulsive Child mode, 561, 562t See also Schema mode Impulsivity antisocial personality disorder and, 429, 433, 446, 452 assessment and, 373 borderline personality disorder and, 275, 420–422, 423 callous–unemotional (CU) traits and, 325, 327 genetic factors and, 246 identity and, 113, 114 interpersonal reconstructive therapy (IRT) and, 394–395 mentalization and, 126 neurotransmitter function and, 252, 253–254, 256–257, 261 obsessive–compulsive personality disorder and, 469 overview, 104–105, 371t pharmacotherapy and, 616, 617 psychoeducation and, 603 risk factors and, 219 schema mode and, 561 trait assessment and, 370t transference-focused psychotherapy (TFP) and, 581 violence reduction treatment and, 636 Inadequate personality disorder, 50t, 52 Individual differences, 20, 42, 310–311 Individual therapy, 465, 507, 528–529 Individualism, 93–94, 93–95, 97–98 Individuation process, 117 Inductive approach, 27–28, 42–45 Inductive-lexical-factor-trait tradition, 36–37 Inferred self, 102–103 704 Informants in assessment, 191–192, 220–221, 353–354, 354 See also Assessment Information processing, 141–142, 144–148, 145f, 246 Inhibition developmental psychopathology model and, 316–317 neurotransmitter function and, 252 obsessive–compulsive personality disorder and, 471 overview, 104–105, 370t, 371t schema-focused therapy (SFT) and, 558, 559t Inpatient treatment, 116, 499, 605 See also Treatment Insecure attachment mentalization and, 127–128, 545 overview, 371t, 417 trait assessment and, 370t validity and, 13–14 See also Attachment Insight-oriented approach, 465–466 Integrated Family Intervention for Child Conduct Problems, 332 Integrated modular treatment assessment and, 377t containment phase, 646, 659 exploration and change phase, 646, 659, 666–670 integration and synthesis phase, 646, 659, 670–673 overview, 645–648, 673 regulation and modulation phase, 646, 659, 660–666 safety phase, 646, 659 treatment modules, 651–657, 657f, 658f See also Integrated treatment approach Integrated treatment approach assessment and, 381–387, 383t, 386t interpersonal reconstructive therapy (IRT) and, 410–412, 411f mentalization-based treatment (MBT) and, 542 overview, 16–17, 373–375, 483 rationale for, 646–647 routes to, 647–648 See also Cognitive analytic therapy (CAT); Integrated modular treatment Integration assessment and, 379, 383t, 384 clinical definition of PD and, 375 integrated modular treatment and, 646, 659, 670–673 See also Integrated treatment approach Intelligence assessment and, 283–284 comorbidity and, 159 developmental factors and, 312, 312t, 319–320 overview, 41–42 risk factors and, 219 Interdependence, 94–95 Intermittent explosive disorder (IED), 275 Internal features of self, 124, 125f Internalizing symptoms cognitive analytic therapy (CAT) and, 494 comorbidity and, 159 factor hierarchy and, 78f Subject Index obsessive–compulsive personality disorder and, 470 schema-focused therapy (SFT) and, 569 Internalizing–externalizing model, 105, 159–160 International Affective Picture System (IAPS), 275, 276, 277 International Classification of Diseases (ICD), 96, 419 International Classification of Diseases (ICD-6), 49, 51 International Classification of Diseases (ICD-8), 51–52 International Classification of Diseases (ICD-9), 52–53 International Classification of Diseases (ICD-10), 47–48, 55–57, 220, 408, 421 International Classification of Diseases (ICD-11) assessment and, 355, 356 early diagnosis and, 221 epidemiology and, 174 historical overview of classification systems and, 57–63 overview, 47–48, 65, 648 psychopathology and, 101 International Classification of Functioning, Disability, and Health (ICF), 356 International Personality Disorder Examination (IPDE), 90, 175t, 176, 180, 198 Internet-based treatment, 607 Interpersonal Dependency Inventory (IDI), 345 Interpersonal diagnostic criteria, 30–31 See also Diagnostic classification Interpersonal factors adaptive impairment and, 374–375 assessment and, 384–385, 386t borderline personality disorder and, 420–421 callous–unemotional (CU) traits and, 324 dialectical behavior therapy (DBT) and, 530–531 emotion regulation and, 278 expectations and, 132 integrated approach and, 374, 381, 658f, 666, 672–673 interpersonal circle and, 32–33, 43–44, 370 intervention and, 669 mentalization and, 126, 131–132 obsessive–compulsive personality disorder and, 469 overview, 28–29, 44, 107–108, 123, 648, 649 problems with, 13–14, 338, 383t, 384–385 sensitivity, 257 violence reduction treatment and, 631 See also Social factors Interpersonal psychotherapy (IPT), 277, 278, 658f Interpersonal reconstructive therapy (IRT) case formulation and, 395–399 comorbidity and, 408–409, 409t diagnosis and assessment and, 339 evidence-based practice and, 412–413 natural biology in, 398–399 overview, 394–395, 413 structural analysis of social behavior (SASB) model and, 399–408, 400f, 402f, 404f, 406t–407t treatment model, 409–412, 411f Interpersonal theory, 30, 377t, 380–381 Interpretation cognitive biases and, 145f integrated modular treatment and, 664 overview, 141–142 personality impairment and, 318–319 transference-focused psychotherapy (TFP) and, 578, 579 Interpretational bias, 145f, 146–147, 149 Interventions callous–unemotional (CU) traits and, 331–332 cognitive-behavioral therapy for PDs (CBTpd) and, 515–520, 516f–517f cultural factors and, 97 DBT strategies, 533–537 diagnosis and, 220–221, 337 early intervention and, 221–223 integrated modular treatment and, 652–653, 656–657, 657f, 658f, 668–669 mentalization-based treatment (MBT) and, 543, 546–549 schema-focused therapy (SFT) and, 563–566 transference-focused psychotherapy (TFP) and, 577–578, 578t violence reduction treatment and, 632–634 See also Treatment; individual treatment approaches Interviews, clinical See Clinical interviews Intimacy, 112t, 395, 460 Intrapsychic level, 35t Introjections, 117, 401 Introversion, 312t, 313, 319–320, 417, 573f Inventory of Callous and Unemotional Traits (ICU), 329, 448t, 449–450 Iowa Gambling Task (IGT), 288–289 Irreverent communication, 536–537 Irritability, 255, 429, 581 Labeling of feelings, 549, 661 Language processing, 284–285 Law of initial values, 203–204 Learning borderline personality disorder and, 295 cognitive analytic therapy (CAT) and, 494, 501 neurotransmitter function and, 260 personality impairment and, 318–319 Leary circle, 32–33 Level of Personality Functioning Scale (LPFS), 82, 83, 351, 355, 430–431 Levenson Self-Report Psychopathy Scale (LSRP), 427 Lexical models, 36–37, 42–43, 44 Lifestyle habits, 590–591 Limits, 558, 559t Linnaeus, Carl, 27 London Parent–Child Project, 127–128 Lonely Child mode, 562t Longitudinal course of personality disorder See Course of personality disorders Subject Index 705 Longitudinal studies designing, 199 methodological differences among studies, 201–208, 207t overview, 197–198, 209–210, 217 overview of four major studies of PD, 199–201, 200t See also Course of personality disorders Longitudinal Study of Personality Disorders (LSPD), 199–201, 200t, 201–208 Loss, feelings of, 561 Major depressive disorder (MDD), 157, 159, 277, 294 See also Depression Maladaptive beliefs, 141–142, 142f, 560 See also Beliefs Maladaptive coping styles, 560 See also Coping styles Maltreatment associated with mental disorders, 301–303 callous–unemotional (CU) traits and, 325, 331 mentalization and, 128–129, 545 risk factors and, 219 schemas and, 144 See also Childhood experiences Manic-depression concept, 420 Manipulativeness, 79, 373, 394–395, 446 Marital status, 190–191, 193 Masochistic personality disorder, 35, 54 McLean Study of Adult Development (MSAD), 200t, 201, 201–208, 211 Meaning, sense of, 384, 649 Mean-level stability, 206–207, 315, 320 See also Stability of personality disorders Meanness, 434, 435, 436, 446, 451 See also Callous–unemotional (CU) traits Measure of Disordered Personality Functioning (MDPF), 351–352 Medical model alternative versions of, 16, 19–20 cultural factors and, 89 influence of, 14–15 overview, 3–4, 8–11, 26 theoretical orientations and, 31 validity and, 11–14 See also Disease model Medications See Pharmacotherapy Memory processes borderline personality disorder and, 285–286, 293–294, 295 cognitive biases and, 145f development of identity and, 117 memory bias, 148–149, 293–294 neurotransmitter function and, 259, 260 overview, 19, 141–142 schema-focused therapy (SFT) and, 560 Mental disorders, 301–303 See also individual disorders Mental representations, 115, 271, 318–319, 572, 575 Mental states, 104, 133 Mentalization approach to personality disorders and, 124–127, 125f assessment and, 380, 386t attachment and, 103, 126–127 childhood adversity and, 127–129 clinical implications, 133–136 cognitive theories and, 150 development of identity and, 117 disruptions in, 544–545 epistemic trust and, 132–133 integrated modular treatment and, 655, 665 overview, 104, 109–110, 123–124, 136 the self and, 129–132 transference-focused psychotherapy (TFP) and, 576 See also Mentalization-based treatment (MBT); Self-reflective thinking Mentalization-based treatment for adolescents (MBT-A), 222, 551–552 Mentalization-based treatment (MBT) assessment and, 377t diagnosis, assessment, and formulation and, 543 integrated modular treatment and, 664 intervention strategies and methods of, 546–549 overview, 133–134, 481–482, 483–484, 541–543 process of, 550–551 research support for, 551–552 theoretical orientations and, 543–544 therapeutic relationship and, 549–550 transference-focused psychotherapy (TFP) and, 572 Metacognitive processes, 373, 657f, 658f Metacognitive therapy, 466–467, 664 Millon Clinical Multiaxial Inventory (MCMI), 77t Millon Inventory of Personality Styles (MIPS), 77t Millon’s model, 39, 43–44, 74 Mindfulness skills, 529, 536, 661–662, 664 Minnesota Multiphasic Personality Inventory (MMPI), 74, 239, 254 Mistrust, 373, 559t See also Trust Modulatory system, 648, 649, 657f, 659, 660–666 Molecular genetics, 436 See also Genetic factors Monoamine oxidase inhibitors (MAOIs), 618, 619, 622f, 623 See also Antidepressants; Pharmacotherapy Mood affective disorder (MAD), 259–260 Mood disorders antisocial personality disorder and, 450 borderline personality disorder and, 420 cognitive analytic therapy (CAT) and, 499 comorbidity and, 187 epidemiological studies, 179–180 historical overview of classification systems and, 56–57 obsessive–compulsive personality disorder and, 461–462 schema-focused therapy (SFT) and, 556, 569 Mood Disorders Work Group, 56–57 Mood stabilizers See Pharmacotherapy Moral development, 328–329 Moral reconation therapy (MRT), 453 Moral values, 379–380, 574, 574t Motivation, 632–633, 655–656 MRI studies See Neuroimaging technologies Multidimensional Personality Questionnaire (MPQ), 242–243, 287, 582 Multidisciplinary team, 638 Multifinality, 233, 309 Multiple self-states model (MSSM) case example of, 496–497 cognitive analytic therapy (CAT) and, 495–496, 498f, 507–508 research support for, 497 screening and, 499 Multisource Assessment of Personality Pathology (MAPP), 345–346 Multisystemic therapy (MST), 638 Multivariate models, 105, 159–160, 247 Narcissism assessment and, 345, 347–348 callous–unemotional (CU) traits and, 326 coping styles and, 142 inferred self and, 102–103 overview, 372t psychopathy and, 428 theoretical orientations and, 30 trait assessment and, 370t Narcissistic personality disorder (NPD) assessment and, 347–348 demographic correlates, 189–191 five-factor model (FFM) and, 75–76 genetic factors and, 240 historical overview of classification systems and, 52, 59–60, 61 interpersonal reconstructive therapy (IRT) and, 394–395 interpretational bias and, 147 obsessive–compulsive personality disorder and, 463 overview, 28, 35, 35t prevalence, 182–183, 183t schema-focused therapy (SFT) and, 556, 561, 567, 568 structural analysis of social behavior (SASB) model and, 405, 406t–407t, 409t in young people, 221 Narcissistic Personality Inventory (NPI), 345 Narratives historical overview of classification systems and, 59 integrated modular treatment and, 657f, 658f, 664, 665, 671 narrative formation, 515–516, 516f–517f narrative psychology, 110 overview, 18–19 See also Self-narrative National Comorbidity Survey (NCS), 156–157, 176 National Comorbidity Survey Replication (NCS-R) cultural factors and, 90 epidemiological studies, 176 gender and, 189 longitudinal studies and, 205 obsessive–compulsive personality disorder and, 460–461 overview, 157 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), 177, 189, 460–461 706 Natural biology, 398–399, 410 See also Biological factors Negative affectivity antisocial personality disorder and, 452 developmental factors and, 313, 319–320 dimensional approaches and, 77t factor hierarchy and, 78f mentalization and, 126 overview, 417 Negative core beliefs, 513–515, 514f Negative emotionality, 316–317, 446 Negativistic depressive personality disorder, 50t Negativistic personality disorder, 33, 35 Negativity, 147–148, 559t Neglect, 128–129, 219, 304 See also Childhood experiences NEO Five-Factor Inventory (NEO-FFI), 162 NEO Personality Inventory (NEO PI, NEO PI-R, and NEO-PI-3) environmental factors and, 242 five-factor model (FFM) and, 74, 75–76 genetic factors and, 240, 245 obsessive–compulsive personality disorder and, 468–469 overview, 37, 346–347 Neo-Kraepelinian movement, 4, 8, 19, 156, 157 Neurobiological factors antisocial personality disorder and, 433, 433–434, 435, 438 borderline personality disorder and, 420 callous–unemotional (CU) traits and, 326 emotion regulation and, 272–273, 274–276 genetic factors and, 246 interpersonal reconstructive therapy (IRT) and, 395 mentalization-based treatment (MBT) and, 546 obsessive–compulsive personality disorder and, 464–465, 469–470 overview, 18–19, 229, 251–252 pharmacotherapy and, 621–623, 622f psychoeducation and, 602t transference-focused psychotherapy (TFP) and, 581–582 See also Biological factors; Neurotransmitter systems Neurogenesis, 244 See also Genetic factors Neuroimaging technologies comorbidity and, 161 emotions and, 271, 274–276, 277 genetic factors and, 246 neurotransmitter function and, 252, 255–256, 264 transference-focused psychotherapy (TFP) and, 582 Neuroleptics, 623–624 See also Pharmacotherapy Neuropsychological mechanisms borderline personality disorder and, 232, 283–284, 287–295 cognition and emotion interactions and, 292–294 emotion regulation and, 274 measuring discrete cognitive abilities and, 287–291 Subject Index neuropsychological testing using conventional test batteries, 284–287 obsessive–compulsive personality disorder and, 465 overview, 18–19, 229, 283, 294–295 psychoeducation and, 602t transference-focused psychotherapy (TFP) and, 581–582 Neurotic personality organization, 108–109 Neuroticism assessment and, 379 cultural factors and, 91–92 developmental factors and, 216, 311, 312t, 316–317, 319–320 five-factor model (FFM) and, 41 genetic factors and, 245 obsessive–compulsive personality disorder and, 468–469 overview, 74, 417 traits relevant to personality disorders, 315 transference-focused psychotherapy (TFP) and, 574t See also Five-factor model (FFM) Neurotransmitter systems emotion regulation and, 277–278 genetic factors and, 244 overview, 229, 231–232, 251–252, 264 See also Dopamine system; Gammaaminobutyric acid (GABA); Glutamate; Neurobiological factors; Norephinephrine; Serotonin system Niche expression, 672–673 NIMH Research Domain Criteria (RDoC) See Research Domain Criteria (RDoC) Nonsuicidal self-injury (NSSI), 253 See also Self-harm Norephinephrine, 244, 259–260 See also Neurotransmitter systems Normal personality assessment and, 358–359 emotion regulation and, 272–273 integrated approach and, 374 overview, 16–17 personality impairment and, 319 stability and change and, 217–218 trait assessment and, 370 Norwegian Institute of Public Health Twin Panel, 240 “Not otherwise specified” (NOS) designation, 72, 73, 211 Novelty seeking, 243–244, 324–325, 327 Numbness, 326, 561 Nurse Family Partnership program, 222 Object relations, 132, 379, 574t, 578, 579–580 Object relations theory Alternative Model and, 350 borderline personality disorder and, 30 cognitive analytic therapy (CAT) and, 489 cognitive-behavioral therapy for PDs (CBTpd) and, 514 identity diffusion and, 114 overview, 30 transference-focused psychotherapy (TFP) and, 571, 572, 575, 576, 577 Observing limits, 533, 535 Obsessive–compulsive disorder (OCD) comorbidity and, 159, 160 emotion regulation and, 277 obsessive–compulsive personality disorder and, 461, 463 pharmacotherapy and, 624 Obsessive–Compulsive Overcontroller mode, 563t Obsessive–compulsive personality disorder (OCPD) clinical correlates and, 186, 187, 188 cognitive analytic therapy (CAT) and, 504t, 506 construct validity and, 467–468 cultural factors and, 90, 94–95 demographic correlates, 189–191 epidemiological studies, 176 etiology and, 464–465 five-factor model (FFM) and, 76 genetic factors and, 240 historical overview of classification systems and, 50t interpersonal reconstructive therapy (IRT) and, 394–395, 409–410, 413 interpretational bias and, 146, 147 neurotransmitter function and, 253–254 overview, 417, 459–463, 471–472 prevalence, 184, 185, 185t schema-focused therapy (SFT) and, 567, 568, 569 structural analysis of social behavior (SASB) model and, 409 theoretical orientations and, 30 traits linked to, 468–471 treatment and, 465–467, 471–472 Occupation, 191, 193, 356 Older adults, 539 See also Adulthood Omega-3 fatty acids, 617–618, 622f See also Pharmacotherapy Openness to Experience cultural factors and, 91–92 developmental factors and, 312, 312t, 319–320 dimensional approaches and, 77t five-factor model (FFM) and, 39–40 overview, 41–42, 74 See also Five-factor model (FFM) Oppositional behavior, 370t, 372t Oppositional defiant disorder (ODD), 159, 331–332 Orderliness, 41, 370t, 372t, 467, 468–469 Organic personality disorder (OPD), 285 Other-orientation, 34–35, 124, 125f, 558, 559t Other-representations, 379, 388 Outcomes antisocial personality disorder and, 452–453 borderline personality disorder and, 423 cognitive analytic therapy (CAT) and, 503–507, 504t interpersonal reconstructive therapy (IRT) and, 413 overview, 170–171, 649 risk factors and, 218–219 transference-focused psychotherapy (TFP) and, 580 treatment and, 484–485 violence reduction treatment and, 640–641 See also Course of personality disorders Subject Index 707 Overcompensation, 142–143, 563t Overgeneralization, 147–148 Overvigilance, 558, 559t Oxytocin (OXT), 262, 263, 327 See also Neurotransmitter systems Paranoid Overcontroller mode, 563t Paranoid personality disorder (PPD) clinical correlates and, 186, 188 cognitive analytic therapy (CAT) and, 504, 504t coping styles and, 143 demographic correlates, 189–191 epidemiological studies, 178, 179 future editions of classification systems and, 63–64 genetic factors and, 240 historical overview of classification systems and, 50t, 59–60 obsessive–compulsive personality disorder and, 463 prevalence, 180, 181t, 182 schema-focused therapy (SFT) and, 567, 568 structural analysis of social behavior (SASB) model and, 409t theoretical orientations and, 30, 32–33 Parasuicidality, 90 See also Suicidality Parental Bonding Instrument (PBI), 304 Parental factors, 302, 303, 330 See also Family factors; Parenting Parent–child relationships, 218, 330–331, 332, 435, 470 Parenting associated with personality disorders, 304 callous–unemotional (CU) traits and, 325, 330–331, 333 developmental psychopathology model and, 316–317 moral development and, 328 overview, 32 personality impairment and, 318–319 psychoeducation and, 602–604 Parenting interventions, 332 See also Interventions; Treatment Passive-aggressive personality disorder (PAPD) clinical correlates and, 188 demographic correlates, 190–191 historical overview of classification systems and, 49, 50t interpersonal reconstructive therapy (IRT) and, 409–410 neurotransmitter function and, 254 prevalence, 184, 185t structural analysis of social behavior (SASB) model and, 409t Pathological identity, 112t–113t See also Identity Pathological Narcissism Inventory (PNI), 347–348 Pathoplasty/exacerbation, 158, 158t See also Bivariate models Perceptions, 104–105, 376, 581 Perfectionism, 460, 469–470 Performance impairment, 558, 559t Perinatal factors, 218–219 Personality cognitive structure of, 650–651 course of personality disorders and, 210–211 cultural interactions and, 94–95 developmental factors and, 215, 215–217 developmental psychopathology model and, 233 diagnosis and assessment and, 338–339 differentiating traits from other aspects of personality functioning, 317–318 environmental factors and, 242–243 five-factor model (FFM) of, 37–44 individualism-collectivism cultural syndrome and, 93–94 mentalization and, 126, 131, 132 overview, 44–45, 648–650 theoretical orientations and, 33–34 Personality and Personality Disorders Work Group (PPDWG), 356 Personality Assessment Inventory, 380 Personality Assessment Schedule (PAS), 77t Personality constructs and dispositions, 18–19 Personality development, 114, 492–493 See also Developmental factors Personality Diagnostic Questionnaire (PDQ), 175t, 180, 192 Personality Diagnostic Questionnaire–4 (PDQ-4), 90 Personality Disorder Beliefs Questionnaire (PDBQ), 146 Personality Disorder Examination (PDE), 175t Personality Disorders and Relational Disorders Work Group, 57 Personality disorders in general, 3–14, 15–20, 648–651 See also individual disorders Personality functioning Alternative Model and, 350–352 assessment and, 355, 378–381 developmental factors and, 318–319 historical overview of classification systems and, 50t, 58–59 integrated approach to characterizing, 373–375 overview, 26 See also Personality traits Personality Inventory for DSM-5 (PID-5), 76, 78–79, 78f, 162, 178, 353 Personality Inventory for DSM-IV (PIDIV), 90 Personality Psychopathology Five (PSY-5), 77t, 78, 79, 460 Personality Structure Questionnaire (PSQ), 491–492 Personality traits assessment and, 352–354, 355, 385–387, 386t in childhood, adolescence, and adulthood, 312t cultural factors and, 91–92 developmental psychopathology model and, 310–314, 320 historical overview of classification systems and, 50t integrated modular treatment and, 669–670 role of in the development of personality disorders, 317–319 traits relevant to personality disorders, 314–319 See also Personality functioning; Trait models Pessimistic anhedonia, 370t, 372t PET studies See Neuroimaging technologies Pharmacotherapy anticonvulsants, 611–613 antidepressants, 256, 277–278, 618–619, 622f atypical antipsychotics, 613–617 borderline personality disorder and, 420, 605, 611–624, 619t, 622f cognitive analytic therapy (CAT) and, 499–500 emotion regulation and, 277–278 integrated modular treatment and, 657f neurotransmitter function and, 256, 261 omega-3 fatty acids and, 617–618, 622f overview, 482–483, 611, 620–624, 622f psychoeducation and, 605 research regarding, 619–620, 621 resources for, 626–628 trait assessment and, 369–370 See also Treatment Phenomenology, 35t, 107, 111 Phenotypic features, 230, 235–237, 237f, 238f See also Genetic factors Phobias, 159, 160 Physical abuse, 219, 305 Physical health, 221–222 Picture Arrangement Test, 284 PID-5 Brief Form (PID-5-BF), 353 See also Personality Inventory for DSM-5 (PID-5) PID-5 Informant Rating Form (PID-5IRF), 353–354 See also Personality Inventory for DSM-5 (PID-5) Planning, 290, 294–295, 311–312 Porteus Maze Test, 290 Posttraumatic stress disorder (PTSD) borderline personality disorder and, 420 dialectical behavior therapy (DBT) and, 530, 536, 539 emotion regulation and, 277 memory bias and, 294 moral development and, 329 neurotransmitter function and, 260 Practice-based evidence (PBE), 503–507, 504t Predisposition/vulnerability model, 158, 158t See also Bivariate models Prevalence antisocial personality disorder and, 450 childhood adversity and, 305 early diagnosis and, 221 obsessive–compulsive personality disorder and, 460–461 overview, 169–170, 180–186, 181t, 183t, 185t, 186t, 192–193 See also Epidemiology Prevention, 221–223 Primary traits, 385–387, 386t Problem solving borderline personality disorder and, 290, 294–295 dialectical behavior therapy (DBT) and, 533–536 memory bias and, 294 systems training for emotion predictability and problem solving (STEPPS) and, 590 violence reduction treatment and, 637 708 Procedural sequence object relations model (PSORM), 491 Prognosis, 170–171 See also Outcomes Program implementation, 639–640 Progress monitoring, 387–388 Prosocial behavior, 373, 374–375 Proximity seeking, 126, 544–545 Psychiatric syndromes, 155–156, 160–164 See also Comorbidity Psychiatry model, 7–8, 20 Psychic equivalence mode, 129 See also Mentalization Psychoanalytic domain, 28–29, 30, 72, 102–103 Psychodynamic domain, 44, 111, 465–466, 636, 658f Psychodynamic-interpersonal techniques (PI), 412 Psychoeducation dialectical behavior therapy (DBT) and, 533 goals and contents of, 601–606, 602t integrated modular treatment and, 660–661, 667 overview, 482, 600–601, 607 peer psychoeducation, 606–607 resources for, 607t–609t schema-focused therapy (SFT) and, 557–558, 563–564 systems training for emotion predictability and problem solving (STEPPS) and, 587, 594 Psychological mechanisms, 18–19, 96, 319 Psychopathic Personalities (Schneider, 1923), Psychopathic Personality Inventory (PPI) antisocial personality disorder and, 433–434, 435–436 overview, 427, 429, 448–449, 448t triarchic model and, 430–431 Psychopathic Personality Inventory— Revised (PPI-R), 344–345 Psychopathy assessment and, 359, 447–450, 448t, 629 biological factors and, 160–164 callous–unemotional (CU) traits and, 324–325, 333 childhood adversity and, 301–303 clinical correlates and, 186–189 cultural factors and, 90–91, 96 early conceptualizations of personality disorder and, etiology and, 431–437 factor hierarchy and, 78f historical overview of, 426–427 inattention to in the medical model, 11 integrated modular treatment and, 666 mentalization and, 131, 542, 545–546 overview, 101–105, 155–156, 417, 426–429, 629–630 schema-focused therapy (SFT) and, 569 subdimensions of, 427–429, 437–438 traits relevant to personality disorders, 314 transference-focused psychotherapy (TFP) and, 572, 573f treatment and, 453–454, 482, 629–641, 635f triarchic model, 429–431 See also Antisocial personality disorder (ASPD); Comorbidity; Developmental psychopathology model Subject Index Psychopathy Checklist—Revised (PCL-R) antisocial personality disorder and, 427, 433–434, 450–451, 453 callous–unemotional (CU) traits and, 332–333 overview, 344, 428, 429, 447–448, 448t, 449 schema-focused therapy (SFT) and, 567 triarchic model and, 431 violence reduction treatment and, 633, 634, 641 Psychopathy Checklist—Youth Version (PCL-YV), 448t Psychosis, 48–49, 246, 259 Psychosocial factors course of personality disorders and, 210–211 historical overview of classification systems and, 51 obsessive–compulsive personality disorder and, 463 overview, 8–9, 229, 230–231, 651 violence reduction treatment and, 637 Psychotherapy, 277–278, 483, 605, 616 See also Treatment Psychoticism developmental factors and, 313, 314 factor hierarchy and, 78f, 79 neurotransmitter function and, 257 Punitive Parent mode, 561, 562t See also Schema mode Punitiveness, 535, 559t Purpose to life, 384 Questionnaires, 342t–343t, 376, 557 See also Assessment Rank-order stability, 206, 314, 320 See also Stability of personality disorders Rapport, 387, 466 Reasoning and rehabilitation (R&R) therapy, 453 Recidivism antisocial personality disorder and, 452–454 schema-focused therapy (SFT) and, 568 treatment and, 453–454, 630–631, 640–641 Reciprocal role procedure (RRP), 491, 496, 499 Reciprocation, 495f, 536–537 Recognition, 501–502, 559t, 667 Reenactments, 490–491 Reflective mentalizing, 124–125 See also Mentalization Reformulations, 499, 500–501 Regulatory processes callous–unemotional (CU) traits and, 330–331 comorbidity and, 163 integrated approach and, 381 integrated modular treatment and, 657f, 659, 660–666 overview, 648, 649 Reinforcement, 535, 588–589 Rejection, 331, 558, 559t, 603 Relationships borderline personality disorder and, 420, 422 cognitive analytic therapy (CAT) and, 490–491 development of identity and, 117 dialectical behavior therapy (DBT) and, 528 mentalization and, 125–126, 133 multiple self-states model and, 496 obsessive–compulsive personality disorder and, 460, 469 schema-focused therapy (SFT) and, 564 systems training for emotion predictability and problem solving (STEPPS) and, 588, 591 Relaxation techniques, 591, 663 Reliability, 12, 397–398 Remorselessness, 370t, 429, 636 Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), 286 Representations of other people, 143–144 Representations of the self, 103–104, 143–144 Representations of the world, 143–144 Reproducibility Project, 26 Research Domain Criteria (RDoC), 64–65, 155, 163–164, 355, 359 Resiliency, 41–42, 131–132, 302, 446 Response control, 294–295 Response inhibition, 290–291 Response styles, 145f, 148 Responsiveness, 316–317 Restricted emotional expression, 370t, 372t, 460, 672 Revised NEO Personality Inventory (NEO PI-R), 240 See also NEO Personality Inventory (NEO PI, NEO PI-R, and NEO-PI-3) Revision, 501–502 Reward processing, 244, 310 Rigidity integrated modular treatment and, 655 mentalization and, 132, 136, 545 obsessive–compulsive personality disorder and, 460, 467, 470 violence reduction treatment and, 636 Risk factors borderline personality disorder and, 231 childhood adversity and, 301–302, 303, 305 cultural factors and, 94–95 early intervention and, 221–223 gene–environment interactions and, 306 overview, 218–220, 223, 233 schema-focused therapy (SFT) and, 558 suicidality and, 470 violence reduction treatment and, 634–636, 635f Risk taking, 394–395, 528 Risk–need–responsivity (RNR) framework, 630, 634–635, 640, 641 Robust mentalizing, 134–135 See also Mentalization Role procedures, 116, 117, 493–494, 496 Rorschach test, 283 Ruff Figural Fluency Test, 287 Rule following, 311–312, 429, 467 Ryle, Tony, 489n SAAB model, 408 SACB model, 408 Sadism, 370t, 372t Sadistic personality disorder, 35, 54 Sadness, 560 Subject Index 709 Safety antisocial personality disorder and, 429 callous–unemotional (CU) traits and, 331 integrated modular treatment and, 646, 659 interpersonal reconstructive therapy (IRT) and, 398, 399 Sampling, 42, 203–205, 210 SASB Intrex, 405 Schedule for Affective Disorders and Schizophrenia—Lifetime Version (SADS-L), 175t, 178, 180 Schedule for Interviewing Borderlines (SIB), 178 Schedule for Nonadaptive and Adaptive Personality (SNAP), 75, 77t, 370 Schema mode cognitive-behavioral therapy for PDs (CBTpd) and, 514–515, 514f interventions and, 565–566 overview, 104, 143, 567 schema-focused therapy (SFT) and, 560–561, 562t–563t See also Schema-focused therapy (SFT); Schemas Schema Mode Inventory, 557 Schema therapy See Schema-focused therapy (SFT) Schema therapy conceptual model, 566–567 Schema-focused therapy (SFT) cognitive-behavioral therapy and, 512, 514 comparisons among the cognitive therapies and, 520, 521f diagnosis, assessment, and formulation and, 557–558 integrated modular treatment and, 658f intervention strategies and methods of, 564–566 overview, 143, 481–482, 483–484, 525, 555–557, 568–569 research support for, 566–568 systems training for emotion predictability and problem solving (STEPPS) and, 587 theoretical orientations and, 558–564, 559t, 562t–563t treatment methods, 522–523 See also Schemas Schemas cognitive biases and, 144–148 integrated modular treatment and, 658f, 666, 667–669 origins and content of, 143–144 overview, 141–142, 142f, 150, 558, 648, 650–651 schema activation, 144 schema avoidance, 560 systems training for emotion predictability and problem solving (STEPPS) and, 589 See also Schema mode; Schema-focused therapy (SFT); Self-schemas Schizoid personality disorder (SPD) clinical correlates and, 186, 187, 188, 189 demographic correlates, 189–191 epidemiological studies, 178 future editions of classification systems and, 63–64 historical overview of classification systems and, 50t, 59–60 mentalization and, 129 neurotransmitter function and, 253–254 overview, 34–35, 417 parental psychopathology and, 303 perinatal factors and, 218–219 prevalence, 180–181, 181t, 182 theoretical orientations and, 32–33 Schizophrenia clinical correlates and, 188 comorbidity and, 158 epidemiological studies, 179–180 future editions of classification systems and, 63–64 identity diffusion and, 113 neurotransmitter function and, 258, 259 obsessive–compulsive personality disorder and, 461 overview, 104–105 Schizotypal personality disorder (STPD) clinical correlates and, 186, 188, 189 comorbidity and, 158, 159 epidemiological studies, 178, 179 five-factor model (FFM) and, 75–76 future editions of classification systems and, 63–64 genetic factors and, 240, 246 historical overview of classification systems and, 50t interpersonal reconstructive therapy (IRT) and, 394–395 neuropsychological mechanisms and, 283 neurotransmitter function and, 252, 257–259 parental psychopathology and, 303 perinatal factors and, 218–219 prevalence, 181, 181t, 182 in young people, 221 Schizotypy, 77t Screening, 198, 499–500 Secure attachment, 127–128, 132–133 Secure base, 400–401 Security, 331, 380–381 Selective serotonin reuptake inhibitor (SSRI), 256, 277–278, 619, 622 See also Antidepressants; Pharmacotherapy Self assessment and, 386t cognitive analytic therapy (CAT) and, 492–493 integrated approach and, 381, 658f, 670–672 mentalization and, 124, 125f, 129–132 overview, 648–649 schema-focused therapy (SFT) and, 559t transference-focused psychotherapy (TFP) and, 575 See also Identity Self pathology assessment and, 382, 383t, 384, 385 clinical definition of PD and, 375 diagnosis and assessment and, 338 Self-Aggrandizer mode, 563t Self-awareness, 109, 661–662 Self-concept cultural factors and, 88 identity diffusion and, 115 lexical hypothesis and, 42 mentalization and, 136 overview, 109–110 psychopathology and, 101–105 See also Identity Self-Concept and Identity Measure (SCIM), 115 Self-control, 316–317, 318–319, 559t Self-criticism, 467, 561 Self-defeating personality disorder, 54 Self-defeating sadistic personality disorder, 50t Self-destructive behaviors identity diffusion and, 114 interventions and, 566 psychoeducation and, 603 schema mode and, 561 schema-focused therapy (SFT) and, 564, 566 transference-focused psychotherapy (TFP) and, 580 Self-directedness, 244, 373, 383t, 384, 394–395 Self-discipline, 559t Self-disclosure, 536–537, 564 Self-efficacy, 384 Self-esteem assessment and, 380–381, 386t callous–unemotional (CU) traits and, 325 cultural factors and, 94 interpretational bias and, 147 overview, 649, 651 Self-expression, 672–673 Self-harm assessment and, 373, 386t borderline personality disorder and, 420, 421–422, 423 childhood adversity and, 305 cultural factors and, 90 dialectical behavior therapy (DBT) and, 528, 528–529 mentalization and, 136 neurotransmitter function and, 253, 256–257, 261 overview, 372t pharmacotherapy and, 617 schema mode and, 561 schema-focused therapy (SFT) and, 567 trait assessment and, 369–370, 370t See also Nonsuicidal self-injury (NSSI) Self-identity, 18–19, 575 Self-injurious behavior (SIB), 276 See also Self-harm Self-knowledge, 101–102, 375, 650, 655 Self-narrative, 110, 117, 649, 671 See also Narratives Self-observation, 536 Self-orientation, 34–35 Self-perception, 376, 581 Self-referential knowledge, 101, 102, 670–671 Self-reflective thinking, 109–110, 373, 386t, 496, 654–655 See also Mentalization Self-regulation childhood adversity and, 128 clinical implications, 118–119 developmental factors and, 217 developmental psychopathology model and, 317 identity and, 103, 113 710 Self-regulation (cont.) integrated modular treatment and, 646, 655, 657f, 659, 660–666 overview, 103, 648 transference-focused psychotherapy (TFP) and, 576, 577 Self-Report Psychopathy Scale-III (SRPIII), 448, 448t Self-report questionnaires assessment and, 380 identity diffusion and, 115 overview, 351–353, 373, 376, 389 psychopathy and, 428 schema-focused therapy (SFT) and, 557 stability and change and, 357–3598 trait assessment and, 370 See also Assessment Self-representations assessment and, 379, 388 childhood adversity and, 128 identity diffusion and, 115 integrated modular treatment and, 670–671 mentalization and, 131 transference-focused psychotherapy (TFP) and, 576–577 Self-schemas, 102, 386t, 667 See also Schemas Self-soothing skills, 662–663 Self-states cognitive analytic therapy (CAT) and, 492–494, 500–501 identity diffusion and, 114 multiple self-states model and, 496 overview, 104 Self-talk, 663–664 Semistructured interview, 575 See also Clinical interviews Sensation seeking, 370t, 372t, 636 Sensitivity, 316–317, 397–398 Sequential diagrammatic reformulations (SDR) cognitive analytic therapy (CAT) and, 490, 492, 493–494, 501 multiple self-states model and, 495–496, 497, 498f Serotonin system arginine vasopressin (AVP) and, 262 borderline personality disorder and, 275 emotion regulation and, 277–278 genetic factors and, 244, 245–246 glutamate and, 260–261 overview, 252–257 See also Neurotransmitter systems Serotonin-norepinephrine reuptake inhibitors (SNRIs), 619, 621–623, 622f See also Pharmacotherapy Severity assessment and, 382, 383t, 384 dimensions of, 369 transference-focused psychotherapy (TFP) and, 573f, 574, 576 treatment and, 484–485 Severity Indices of Personality Problems (SIPP), 352 Sexual abuse, 116, 219, 304–305, 576 Sexual deviation personality disorder, 50t Sexuality, 108–109, 112t, 370t, 371t Shame, 518, 559t, 560 Shyness, 93, 316–317 Subject Index Single-nucleotide peptide polymorphisms (SNPs), 243, 245–246 Skills training dialectical behavior therapy (DBT) and, 527, 529, 533–536 integrated modular treatment and, 662–663 systems training for emotion predictability and problem solving (STEPPS) and, 589–591, 593–595 violence reduction treatment and, 636, 637–638 Sleep problems, 623 Social anxiety, 94–95, 319, 624 Social apprehensiveness, 370t, 372t Social avoidance, 13–14, 20–21, 370t, 417, 666 See also Avoidance Social factors callous–unemotional (CU) traits and, 325, 326–327 disability and, 356 genetic factors and, 246 identity and, 107–108, 111, 113t integrated modular treatment and, 658f, 672–673 isolation and, 559t learning and, 124, 135–136 mentalization and, 131, 135–136 moral development and, 328–329 overview, 97, 135, 163, 305–306 transference-focused psychotherapy (TFP) and, 581 withdrawal and, 93, 417 See also Withdrawal See also Interpersonal factors Social phobia, 94, 158, 216 Socialization, 316, 328–329, 330–331, 332 Sociopathic personality disturbance, 50t Solution analysis, 533, 534 Specificity, 397–398 Spectrum model, 158, 158t See also Bivariate models Splitting, 114, 587–588, 634 Stability of personality disorders assessment and, 357–359 borderline personality disorder and, 420–421 cognitive analytic therapy (CAT) and, 494 developmental psychopathology model and, 320 longitudinal studies and, 205–208, 207f overview, 197, 208–211, 217–218 traits relevant to personality disorders, 314–315, 316 See also Course of personality disorders Stages of change, 667 See also Change STAIRWAYS program, 587, 594, 595, 595–596 See also Systems training for emotion predictability and problem solving (STEPPS) Standardized Psychiatric Examination (SPE), 175t Standards, unrelenting, 559t State models, 125–126, 130–131 State–Trait Anger Expression Inventory (STAXI), 611–612 State–Trait Anxiety Inventory, 505 STEPPS See Systems training for emotion predictability and problem solving (STEPPS) Stopping rules, 38–42, 43 Stop-signal tasks, 290–291 Strange Situation, 127–128 Stress, 125f, 126, 244, 259–260, 302–303, 544–545 Stroop task, 276, 287, 290–291, 292 Structural analysis of social behavior (SASB) model case formulation and, 396, 397–398 clinical applications of, 401–403, 402f comorbidity and, 408–409, 409t diagnosis and, 403, 405–408, 406t–407t diagnosis and assessment and, 339 overview, 32–33, 394n, 399–400, 400f, 413, 414 predictive principles, 401 secure base and, 400–401 structure of, 401 Structural Analysis of Social Behavior— Cyclic Maladaptive Pattern (SASBCMP), 497 Structural interview, 378–380 See also Interviews, clinical Structural model of psychopathology, 159 Structured clinical interview See Clinical interviews Structured Clinical Interview for DSMIII-R Personality Disorders (SCIDII), 178, 180 Structured Clinical Interview for DSMIII-R (SCID), 175t, 178 Structured Clinical Interview for DSM-IV Axis II (SCID-II) case formulation and, 397 epidemiological studies, 176–177 longitudinal studies and, 198 overview, 354 structural analysis of social behavior (SASB) model and, 405, 408 transference-focused psychotherapy (TFP) and, 575 Structured Interview for DSM-III-R Personality Disorders (SIDP), 179, 192, 193, 198, 467 Structured Interview for DSM-III-R Personality Disorders-Revised (SIDP-R), 176 Structured Interview for DSM-IV Personality Disorders (SIDP-IV), 217, 241–242 Structured Interview for Personality Organization (STIPO), 379–380 Structured Interview for Personality Organization—Revised (STIPO-R), 379–380 Structured Interview for Schizotypy (SIS), 175t Structured Interview of Personality Organization (STIPO), 115, 575 Structured interviews, 115 See also Assessment Submissiveness, 59–60, 370t, 372t, 417, 469 Substance abuse antisocial personality disorder and, 433, 450–451 borderline personality disorder and, 420 cognitive analytic therapy (CAT) and, 494, 499 cultural factors and, 90 Subject Index 711 dialectical behavior therapy (DBT) and, 528, 538–539 early intervention and, 221–222 identity diffusion and, 114 obsessive–compulsive personality disorder and, 463 overview, 667 psychopathy and, 428 violence reduction treatment and, 636 Suicidality antisocial personality disorder and, 450 assessment and, 386t borderline personality disorder and, 274, 422, 423 cognitive-behavioral therapy for PDs (CBTpd) and, 525 cultural factors and, 90 dialectical behavior therapy (DBT) and, 527, 528–529, 538, 539 integrated modular treatment and, 663–664 memory bias and, 294 neurotransmitter function and, 252–254, 256–257, 261–262 obsessive–compulsive personality disorder and, 461–462, 469–470 psychopathy and, 428 schema mode and, 561 transference-focused psychotherapy (TFP) and, 581 Supervision, 529–530 Supportive dynamic therapy, 483–484 Suppression, 273, 665 Surrender, 142–143 Suspiciousness, 370t, 372t Symptoms antisocial personality disorder and, 445–446 assessment and, 386t clinical correlates and, 186–189 cultural factors and, 96 developmental psychopathology model and, 320 disease model and, early intervention and, 221–223 integrated approach and, 381, 657f medical model and, 19–20 obsessive–compulsive personality disorder and, 459–460 overview, 649 precursor signs and symptoms, 218–220 psychoeducation and, 602t traits relevant to personality disorders, 314–317 Synthesis, 646, 659, 670–673 Systematic Treatment Selection (STS), 377t, 378, 388 Systems approach, 587, 588–589 Systems training for emotion predictability and problem solving (STEPPS) case example of, 595–596 components of, 589–591 format of, 591–595 overview, 481–482, 586–587, 597 research support for, 597 theoretical orientations and, 587–588 Taxonomy, 28, 31–35, 35t, 36f See also Classification systems Teleological mode, 129 See also Mentalization Telephone consultation, 529 Temperament antisocial personality disorder and, 432–433, 434–435 assessment and, 373 developmental factors and, 215–217 genetic factors and, 243–244 overview, 28–29, 30, 65, 311, 513 risk factors and, 219 Temperament and Character Inventory (TCI), 77t Temporal instability, 72, 73, 112t Termination, 502 Thematic Apperception Test (TAT), 146, 283 Theoretical integration, 647 See also Integrated treatment approach Theoretical orientations cognitive analytic therapy (CAT) and, 492–493 dialectical behavior therapy (DBT) and, 531–533 epistemic choices for structuring, 26–29 inductive-factor-trait models, 35–44, 36f mentalization-based treatment (MBT) and, 543–544 multiple perspectives, 30–31, 33–35, 35t overview, 29, 29f, 44–45 schema-focused therapy (SFT) and, 558–564, 559t, 562t–563t single perspective, 29–30, 31–33 systems training for emotion predictability and problem solving (STEPPS) and, 587–588 taxonomically focused, 31–35, 35t transference-focused psychotherapy (TFP) and, 575–577 Therapeutic alliance assessment and, 387 integrated modular treatment and, 652–653, 656 mentalization and, 135, 136 motivation and, 656 obsessive–compulsive personality disorder and, 466 ruptures in, 653 violence reduction treatment and, 633 See also Therapeutic relationship Therapeutic community (TC) approaches, 636 Therapeutic relationship cognitive analytic therapy (CAT) and, 490–491, 495f, 502, 503 cognitive-behavioral therapy for PDs (CBTpd) and, 515–516, 520–522 dialectical behavior therapy (DBT) and, 530–531, 537–538 integrated modular treatment and, 652–653, 654, 656 mentalization-based treatment (MBT) and, 546, 549–550 motivation and, 656 schema-focused therapy (SFT) and, 564–565 transference-focused psychotherapy (TFP) and, 578–579 validation and, 654 See also Therapeutic alliance Therapist ratings, 115 See also Assessment Therapist stance, 543, 547–548, 578–579, 633–634 See also Clinician factors Thoughts, 116, 466, 663–664 Threat perceptions, 145–146, 399 Threshold liability model, 236–237, 236f Tolerance, 662 Tower of Hanoi task, 290 Tower of London task, 289, 290 Trail Making Test—Part B, 287 Trait constellations, 385–387, 386t Trait models antisocial personality disorder and, 446–447 assessment and, 337–338, 352–354, 355, 358 callous–unemotional (CU) traits and, 332 comorbidity and, 163 diagnosis and, 337–338 gene–environment interactions and, 306 integrated modular treatment and, 669–670 lexical hypothesis and, 42–43 longitudinal studies and, 198 measures for, 343t mentalization and, 125–126 obsessive–compulsive personality disorder and, 468–471 overview, 35–44, 36f, 648, 650 See also Personality traits Trait-dimensional model, 72, 74, 91–92, 369–370 See also Dimensional approaches to classification Transactional models, 333 Transdiagnostic approach, 232, 539 Transference, 550 See also Transferencefocused psychotherapy (TFP) Transference-focused psychotherapy (TFP) assessment and, 377t diagnosis, assessment, and formulation and, 572–575, 573f, 574t identity and identity diffusion and, 118–119 intervention strategies and methods of, 577–578, 578t overview, 481–482, 483–484, 485, 571–572 process of, 579–580 research support for, 580–582 schema-focused therapy (SFT) and, 568 theoretical orientations and, 575–577 treatment relationship and, 578–579 Transtheoretical conceptualization, 104, 647 Trauma callous–unemotional (CU) traits and, 325, 329–330, 331 childhood adversity associated with mental disorders and, 301–303 early experience of, 304–305 mentalization and, 126, 128–129 mentalization-based treatment (MBT) and, 544–545 neurotransmitter function and, 260, 263 overview, 232–233 schema-focused therapy (SFT) and, 558 Treatment antisocial personality disorder and, 453–454 assessment and, 377–378, 377t, 386t, 387–388 712 Treatment (cont.) borderline personality disorder and, 422, 604–605, 621–624 callous–unemotional (CU) traits and, 331–332 childhood adversity and, 306 clinical implications, 423 cognitive theories and, 149–150 comorbidity and, 163 cultural factors and, 97 diagnosis and, 21, 220–221, 337 early intervention and, 221–223 emotion regulation and, 277–278 empirically based treatments, 481–485 identity diffusion and, 116, 118–119 integrated approach and, 381–387, 383t, 386t, 651 interpersonal reconstructive therapy (IRT) and, 409–413, 411f mentalization and, 133–136 neurotransmitter function and, 261 obsessive–compulsive personality disorder and, 465–467, 471–472 overview, 648 psychoeducation and, 604–605 psychopathy and, 453–454 self-development and, 651 violence and, 629–641, 635f See also Interventions; Pharmacotherapy; individual treatment approaches Treatment planning, 367, 376, 381, 574 Treatment-resistant depression, 528, 539 See also Depression Treatment-resistant PD, 339 Triarchic model, 429–431, 437, 438, 446–447, 451 Triarchic Psychopathy Measure (TriPM), 448t, 449, 452 Tridimensional model, 251–252 Tridimensional Personality Questionnaire (TPQ), 243–244 Subject Index TriPM, 430–431, 433–434 Trust, 103–104, 327, 373, 545, 587 Twin studies antisocial personality disorder and, 436–437 callous–unemotional (CU) traits and, 327 childhood adversity and, 306 identifying putative genes, 243 obsessive–compulsive personality disorder and, 464 overview, 238–243 traits relevant to personality disorders, 315–316 See also Family factors; Genetic factors Uncertainty, 103–104 Validation, 533, 550–551, 558, 654 Values, 97, 108–109 Venturesomeness, 446 Verbal abuse, 219 Verbal episodic memory, 285–286 See also Memory processes Violence antisocial personality disorder and, 452–453 neurotransmitter function and, 253–254, 259–260 overview, 629 treatment and, 629–641, 635f See also Aggression; Antisocial behaviors; Violence reduction treatment Violence Inhibition Mechanism (VIM), 329 Violence reduction treatment outcome evidence and, 640–641 overview, 630–631, 641 psychopathy and, 631–638, 635f treatment delivery, 638–640 See also Treatment; Violence Violence Risk Scale (VRS), 634–636, 635f, 640–641 Visual episodic memory, 286 See also Memory processes Visual probe tasks, 292–293 Vocational aspirations, 108–109 VRS—Sexual Offender version (VRS-SO), 640–641 Vulnerabilities, 301–302, 559t, 566 See also Risk factors Wakefulness, 259 Web-based treatment, 607 Wechsler Adult Intelligence Test—Revised (WAIS-R), 283–284, 285 Wechsler Memory Scale (WMS), 285–286 Weekly diary cards See Diary cards Wide Range Achievement Test, 285 Wideband Cross-Language Six (WCL6), 41–42, 44 Wisconsin Card Sorting Task (WCST), 259, 286–287 Wisconsin Personality Disorders Inventory (WISPI), 403, 405, 408, 413 Withdrawal, 79, 93, 417 WMS Logical Memory Test, 285–286 Working alliance See Therapeutic alliance Working memory, 259, 273 See also Memory processes Young Parenting Inventory, 557 Young Schema Questionnaire, 515 Youth Psychopathic Traits Inventory (YPI), 240, 427, 430–431, 448t, 450 Youth Self-Report (YSR), 92 Zanarini Rating Scale for Borderline Personality Disorder (ZAN-BPD), 288 Zen, 531, 532 Zone of proximal development (ZPD), 494, 501–502 ... 75(4), 122 9– 124 2 Larsson, H., Andershed, H., & Lichtenstein, P (20 06) A genetic factor 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R., & Tyrer, P (20 11) Classifying personality disorder according to severity Journal of Personality Disorders, 25 , 321 –330 Livesley, W J (20 01) Commentary on reconceptualising personality disorder