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date: 03 August 2020

(p. xvii) Preface

(p. xvii) Preface

Since publication of Robins’s (1966) landmark text almost 60 years ago, we have known that antisocial adult males usually follow a developmental trajectory that begins as early as preschool with hyperactivity/impulsivity and oppositionality, followed by conduct problems in middle school, delinquency and substance use in high school, and incarceration and recidivism by late adolescence and adulthood (see also Loeber & Hay, 1997; Moffitt, 1993). Using the prevailing classification system for psychopathology, the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5; American Psychiatric Association [APA], 2013), many of these males could be diagnosed with six psychiatric disorders over the course of their development, including attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), intermittent explosive disorder (IED), conduct disorder (CD), a substance-related/addictive disorder, and, finally, antisocial personality disorder (ASPD; Beauchaine, Hinshaw, & Pang, 2010; Beauchaine & McNulty, 2013; Beauchaine, Neuhaus, Brenner, & Gatzke-Kopp, 2008; Patrick, this volume). Although understudied until recently, girls who are reared in the same families as externalizing males—and therefore share genetic susceptibility and environmental risk—also suffer from difficulties with behavioral impulsivity very early in life and are vulnerable to subsequent depression, self-inflicted injury, and borderline personality development as they mature (Beauchaine, Klein, Crowell, Derbidge, & Gatzke-Kopp, 2009; Crowell, Beauchaine, & Linehan, 2009; Hinshaw et al., 2012).

In addition to these heterotypically continuous patterns of psychopathology across development, concurrent comorbidity rates among externalizing syndromes are extremely high (see Krueger & Tackett, this volume; Nikolas, this volume). As outlined in chapters to follow, accumulating evidence points toward both (1) shared genetic and neural mechanisms of heterotypic continuity and concurrent comorbidity (Gizer, Otto, & Ellingson, this volume; Zisner & Beauchaine, this volume), and (2) interactions between biological vulnerabilities and environmental risk factors in shaping the ultimate expression of externalizing behavior (Beauchaine, Shader, & Hinshaw, this volume; Krieger, & Stringaris, this volume). According to this transactional perspective, externalizing disorders are more accurately viewed as a spectrum of related behavioral syndromes than as discrete diagnostic categories.

Traditionally, it has been assumed that different externalizing syndromes reflect distinct disorders with separate etiologies (Kopp & Beauchaine, 2007). This is implied by the DSM (APA, 2013), which treats comorbidity as a differential (p. xviii) diagnostic concern. The assumption that different externalizing syndromes are diagnostically distinct has resulted in the development of largely separate literatures for ADHD, ODD, CD, substance-related/addictive disorders, and ASPD. Basic scientists and clinicians tend to study and treat, respectively, single, traditionally defined disorders despite clear etiological underpinnings across the externalizing spectrum (Beauchaine et al., 2008). One consequence of this fractionated approach to research and practice is the evolution of distinct treatment approaches for each behavioral syndrome. Psychostimulants are often the front-line treatment for ADHD (MTA Cooperative Group, 1999), behavioral and multisystemic interventions are preferred for CD (e.g., Nock, 2003), and motivational techniques are often favored for substance-related and addictive disorders (e.g., Masterman & Kelly, 2003). Thus, many empirically supported treatments target specific diagnostic syndromes and are limited in their capacity to address concurrent comorbidities, thus rendering them less effective than they ultimately should be (see, e.g., Conrod & Stewart, 2005).

Although treatment development is not the major focus of this volume, we assume that a comprehensive understanding of etiology and pathophysiology is a prerequisite of maximally effective interventions (Preskorn & Baker, 2002). Thus, in editing the volume, we recruited world-renowned experts and asked them to address questions about etiological and pathophysiological commonalities across the externalizing spectrum. Although traditional externalizing disorders are defined in the chapter by Drabick, Steinberg, and Hampton, the following chapter by Ahmad and Hinshaw immediately departs from the DSM and instead presents ADHD from a developmental psychopathology perspective in which individual-level vulnerabilities interact with contextual risk factors over time, resulting in development of more severe externalizing behaviors for those who are exposed to significant risk and adversity but not for those who are reared in protective environments. Although about half of the remaining chapters focus more heavily on individual-level vulnerabilities (e.g., Baker, this volume; Corr & McNaughton, this volume; Eme, this volume; Gerring & Vasa, this volume; Golmaryami & Frick, this volume; Iselin, McVey, Ehatt; this volume; Pinsonneault, Parent, Castellanos-Ryan, & Séguin, this volume; Séguin & Parent, this volume), whereas the other half focus more heavily on environmental adversity and risk (e.g., Besemer & Murray, this volume; Graham, Glass, & Mattson, this volume; Jennings & Hahn Fox, this volume; Snyder, this volume; VanZomeren-Dohm, Xu, Thibodeau, & Cicchetti, this volume), all treat externalizing behaviors as a spectrum of behavioral syndromes with common etiological mechanisms.

An externalizing spectrum is consistent with both the developmental psychopathology perspective (Hinshaw & Beauchaine, this volume), which is transactional by nature, and with the philosophy that undergirds the Research Domain Criteria (RDoC), currently being developed and used by the National Institute of Mental Health (e.g., Insel et al., 2010; Sanislow et al., 2010). Explicit objectives of RDoC are to map primary dimensions of behavior, such as trait impulsivity, and to identify their biobehavioral substrates, from genes to behavior. For (p. xix) example, as outlined by Gizer, Otto, and Ellingson (this volume), several genes that affect dopamine (DA) neurotransmission are implicated in trait impulsivity. These genes appear to confer less DA reactivity in neural structures (e.g., nucleus accumbens, caudate) that are implicated in reward processing and extinction of previously learned behaviors (Zisner & Beauchaine, this volume). Under-reactive DA responding is expressed as a behavioral propensity to reward-seeking and trait impulsivity. Importantly, this impulsivity underlies disorders across the externalizing spectrum (Beauchaine, Shader, & Hinshaw, this volume; Krueger & Tackett, this volume) yet is also observed in other forms of psychopathology not traditionally classified as externalizing, such as borderline personality (see Kaufman, Crowell, & Stepp, this volume). Identifying traits that cut across traditional diagnostic boundaries is a core objective of both the developmental psychopathology perspective (Levy, Hawes, & Johns, this volume) and of RDoC (Beauchaine et al., 2013). Major assumptions of this approach are that it will (1) identify more genetically homogenous samples for psychiatric genetics studies, an area of research that has been hampered by the current approach of mapping genes onto behavioral syndromes that arise from heterogeneous causes (Gizer, Otto, & Ellingson, this volume); (2) improve construct validity over the DSM; and (3) result in better treatments because our understanding of etiology will necessarily improve, thus providing for better matching of patients to interventions.

Following from the developmental psychopathology perspective, and given the heavy research emphasis on the RDoC initiative, the Oxford Handbook of Externalizing Spectrum Disorders is, we believe, a timely contribution to the literature. Each one of the authors is a chosen expert in the field, and each presents cutting-edge research on externalizing syndromes, including their continuities, comorbidities, and etiological underpinnings. We invite readers to challenge their assumptions about externalizing disorders as discrete diagnostic entities, and to consider how externalizing behavior develops across the life-span, as vulnerable individuals confront environmental risk and adversity.

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